MDedge Endocrinology

Children appear less likely than adults to be the first cases of COVID-19 within a household, based on data from families of 39 children younger than 16 years.

Courtesy NIAID

“Unlike with other viral respiratory infections, children do not seem to be a major vector of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission, with most pediatric cases described inside familial clusters and no documentation of child-to-child or child-to-adult transmission,” said Klara M. Posfay-Barbe, MD, of the University of Geneva, Switzerland, and colleagues.

In a study published in Pediatrics, the researchers analyzed data from all COVID-19 patients younger than 16 years who were identified between March 10, 2020, and April 10, 2020, through a hospital surveillance network. Parents and household contacts were called for contact tracing.

In 31 of 39 (79%) households, at least one adult family member had a suspected or confirmed SARS-CoV-2 infection before onset of symptoms in the child. These findings support data from previous studies suggesting that children mainly become infected from adult family members rather than transmitting the virus to them, the researchers said

In only 3 of 39 (8%) households was the study child the first to develop symptoms. “Surprisingly, in 33% of households, symptomatic HHCs [household contacts] tested negative despite belonging to a familial cluster with confirmed SARS-CoV-2 cases, suggesting an underreporting of cases,” Dr. Posfay-Barbe and associates noted.

The findings were limited by several factors including potential underreporting of cases because those with mild or atypical presentations may not have sought medical care, and the inability to confirm child-to-adult transmission. The results were strengthened by the extensive contact tracing and very few individuals lost to follow-up, they said; however, more diagnostic screening and contact tracing are needed to improve understanding of household transmission of SARS-CoV-2, they concluded.

Resolving the issue of how much children contribute to transmission of SARS-CoV-2 is essential to making informed decisions about public health, including how to structure schools and child-care facility reopening, Benjamin Lee, MD, and William V. Raszka Jr., MD, both of the University of Vermont, Burlington, said in an accompanying editorial (Pediatrics. 2020 Jul 10. doi: 10.1542/peds/2020-004879).

The data in the current study support other studies of transmission among household contacts in China suggesting that, in most cases of childhood infections, “the child was not the source of infection and that children most frequently acquire COVID-19 from adults, rather than transmitting it to them,” they wrote.

In addition, the limited data on transmission of SARS-CoV-2 by children outside of the household show few cases of secondary infection from children identified with SARS-CoV-2 in school settings in studies from France and Australia, Dr. Lee and Dr. Raszka noted.

“On the basis of these data, SARS-CoV2 transmission in schools may be less important in community transmission than initially feared,” the editorialists wrote. “This would be another manner by which SARS-CoV2 differs drastically from influenza, for which school-based transmission is well recognized as a significant driver of epidemic disease and forms the basis for most evidence regarding school closures as public health strategy.”

“Therefore, serious consideration should be paid toward strategies that allow schools to remain open, even during periods of COVID-19 spread,” the editorialists concluded. “In doing so, we could minimize the potentially profound adverse social, developmental, and health costs that our children will continue to suffer until an effective treatment or vaccine can be developed and distributed or, failing that, until we reach herd immunity,” Dr. Lee and Dr. Raszka emphasized.

The study received no outside funding. The researchers and editorialists had no financial conflicts to disclose.

SOURCE: Posfay-Barbe KM et al. Pediatrics. 2020 Jul 10. doi: 10.1542/peds.2020-1576.

Children appear less likely than adults to be the first cases of COVID-19 within a household, based on data from families of 39 children younger than 16 years.

Courtesy NIAID

“Unlike with other viral respiratory infections, children do not seem to be a major vector of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission, with most pediatric cases described inside familial clusters and no documentation of child-to-child or child-to-adult transmission,” said Klara M. Posfay-Barbe, MD, of the University of Geneva, Switzerland, and colleagues.

In a study published in Pediatrics, the researchers analyzed data from all COVID-19 patients younger than 16 years who were identified between March 10, 2020, and April 10, 2020, through a hospital surveillance network. Parents and household contacts were called for contact tracing.

In 31 of 39 (79%) households, at least one adult family member had a suspected or confirmed SARS-CoV-2 infection before onset of symptoms in the child. These findings support data from previous studies suggesting that children mainly become infected from adult family members rather than transmitting the virus to them, the researchers said

In only 3 of 39 (8%) households was the study child the first to develop symptoms. “Surprisingly, in 33% of households, symptomatic HHCs [household contacts] tested negative despite belonging to a familial cluster with confirmed SARS-CoV-2 cases, suggesting an underreporting of cases,” Dr. Posfay-Barbe and associates noted.

The findings were limited by several factors including potential underreporting of cases because those with mild or atypical presentations may not have sought medical care, and the inability to confirm child-to-adult transmission. The results were strengthened by the extensive contact tracing and very few individuals lost to follow-up, they said; however, more diagnostic screening and contact tracing are needed to improve understanding of household transmission of SARS-CoV-2, they concluded.

Resolving the issue of how much children contribute to transmission of SARS-CoV-2 is essential to making informed decisions about public health, including how to structure schools and child-care facility reopening, Benjamin Lee, MD, and William V. Raszka Jr., MD, both of the University of Vermont, Burlington, said in an accompanying editorial (Pediatrics. 2020 Jul 10. doi: 10.1542/peds/2020-004879).

The data in the current study support other studies of transmission among household contacts in China suggesting that, in most cases of childhood infections, “the child was not the source of infection and that children most frequently acquire COVID-19 from adults, rather than transmitting it to them,” they wrote.

In addition, the limited data on transmission of SARS-CoV-2 by children outside of the household show few cases of secondary infection from children identified with SARS-CoV-2 in school settings in studies from France and Australia, Dr. Lee and Dr. Raszka noted.

“On the basis of these data, SARS-CoV2 transmission in schools may be less important in community transmission than initially feared,” the editorialists wrote. “This would be another manner by which SARS-CoV2 differs drastically from influenza, for which school-based transmission is well recognized as a significant driver of epidemic disease and forms the basis for most evidence regarding school closures as public health strategy.”

“Therefore, serious consideration should be paid toward strategies that allow schools to remain open, even during periods of COVID-19 spread,” the editorialists concluded. “In doing so, we could minimize the potentially profound adverse social, developmental, and health costs that our children will continue to suffer until an effective treatment or vaccine can be developed and distributed or, failing that, until we reach herd immunity,” Dr. Lee and Dr. Raszka emphasized.

The study received no outside funding. The researchers and editorialists had no financial conflicts to disclose.

SOURCE: Posfay-Barbe KM et al. Pediatrics. 2020 Jul 10. doi: 10.1542/peds.2020-1576.

Children appear less likely than adults to be the first cases of COVID-19 within a household, based on data from families of 39 children younger than 16 years.

Courtesy NIAID

“Unlike with other viral respiratory infections, children do not seem to be a major vector of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission, with most pediatric cases described inside familial clusters and no documentation of child-to-child or child-to-adult transmission,” said Klara M. Posfay-Barbe, MD, of the University of Geneva, Switzerland, and colleagues.

In a study published in Pediatrics, the researchers analyzed data from all COVID-19 patients younger than 16 years who were identified between March 10, 2020, and April 10, 2020, through a hospital surveillance network. Parents and household contacts were called for contact tracing.

In 31 of 39 (79%) households, at least one adult family member had a suspected or confirmed SARS-CoV-2 infection before onset of symptoms in the child. These findings support data from previous studies suggesting that children mainly become infected from adult family members rather than transmitting the virus to them, the researchers said

In only 3 of 39 (8%) households was the study child the first to develop symptoms. “Surprisingly, in 33% of households, symptomatic HHCs [household contacts] tested negative despite belonging to a familial cluster with confirmed SARS-CoV-2 cases, suggesting an underreporting of cases,” Dr. Posfay-Barbe and associates noted.

The findings were limited by several factors including potential underreporting of cases because those with mild or atypical presentations may not have sought medical care, and the inability to confirm child-to-adult transmission. The results were strengthened by the extensive contact tracing and very few individuals lost to follow-up, they said; however, more diagnostic screening and contact tracing are needed to improve understanding of household transmission of SARS-CoV-2, they concluded.

Resolving the issue of how much children contribute to transmission of SARS-CoV-2 is essential to making informed decisions about public health, including how to structure schools and child-care facility reopening, Benjamin Lee, MD, and William V. Raszka Jr., MD, both of the University of Vermont, Burlington, said in an accompanying editorial (Pediatrics. 2020 Jul 10. doi: 10.1542/peds/2020-004879).

The data in the current study support other studies of transmission among household contacts in China suggesting that, in most cases of childhood infections, “the child was not the source of infection and that children most frequently acquire COVID-19 from adults, rather than transmitting it to them,” they wrote.

In addition, the limited data on transmission of SARS-CoV-2 by children outside of the household show few cases of secondary infection from children identified with SARS-CoV-2 in school settings in studies from France and Australia, Dr. Lee and Dr. Raszka noted.

“On the basis of these data, SARS-CoV2 transmission in schools may be less important in community transmission than initially feared,” the editorialists wrote. “This would be another manner by which SARS-CoV2 differs drastically from influenza, for which school-based transmission is well recognized as a significant driver of epidemic disease and forms the basis for most evidence regarding school closures as public health strategy.”

“Therefore, serious consideration should be paid toward strategies that allow schools to remain open, even during periods of COVID-19 spread,” the editorialists concluded. “In doing so, we could minimize the potentially profound adverse social, developmental, and health costs that our children will continue to suffer until an effective treatment or vaccine can be developed and distributed or, failing that, until we reach herd immunity,” Dr. Lee and Dr. Raszka emphasized.

The study received no outside funding. The researchers and editorialists had no financial conflicts to disclose.

SOURCE: Posfay-Barbe KM et al. Pediatrics. 2020 Jul 10. doi: 10.1542/peds.2020-1576.

Diabetes was by far the most common delayed pediatric presentation in emergency care during the COVID-19 pandemic, according to a snapshot survey of nearly 2,500 pediatricians in the United Kingdom and Ireland.

There were also nine deaths where delayed presentation was considered a contributing factor, resulting mainly from sepsis and malignancy.

By comparison, over the same 2-week period of the survey there were three child deaths from COVID-19 directly, according to senior study author Shamez Ladhani, MRCPCH, PhD, chair of the British Paediatric Surveillance Unit (BPSU), Royal College of Paediatrics and Child Health, London.

“The unintended consequences of COVID are far greater, in children, than the disease itself. The way we are trying to prevent this is causing more harm than the disease,” he lamented.

One-third of senior U.K. pediatric specialists who responded to the survey reported dealing with so-called emergency delayed presentations in children who they would normally have expected to present much earlier.

After diabetes, the most commonly reported delayed diagnoses were sepsis and child protection issues. Cancer also featured prominently.

“We’ve found that there is great concern that children are not accessing healthcare as they should during lockdown and after,” Dr. Ladhani stressed. “Our emergency departments saw a 50% reduction during the peak, and now it is still 40% less than expected. The problem is improving but it remains.”

The survey findings were recently published online in Archives of Disease in Childhood, by first author Richard M. Lynn, MSc, of the Institute of Child Health, department of epidemiology and public health, University College London Research, and colleagues.
 

New diabetes cases presented very late during lockdown

Over the 2-week reporting period in mid-April 2020, type 1 diabetes was the most frequently reported delayed diagnosis, with 44 cases overall, 23 of which involved diabetic ketoacidosis.

“If you talk to the diabetes specialists, they tell us that generally, most cases of new diabetes arrive late because it has very nonspecific symptoms,” Dr. Ladhani explained.

However, he added, “pediatricians on the frontline know what to expect with diabetes. Those children who would have come in late prior to the pandemic are now arriving very late. Those consultants surveyed were not junior doctors but consultant pediatricians with many years of experience.”

In a recent article looking at pediatric delayed presentations, one patient with diabetes entered intensive care, and the BPSU report recorded one death possibly associated with diabetes, Dr. Ladhani pointed out.

“Pediatricians are worried that children are coming in late. We need to raise awareness that parents need to access healthcare and this message needs to go out now,” he said. “We can’t wait until a second wave. It has to be now because A&E [accident and emergency] attendance is still 40% [lower than] ... expected.”
 

BPSU survey covers over 90% of pediatricians in U.K. and Ireland

After numerous anecdotal reports of delayed presentations in the United Kingdom and abroad, the snapshot survey was conducted as part of routine monthly reports where pediatricians are asked to document any cases of rare conditions seen.

“We had heard stories of delayed presentations, but we wanted to know was this a real problem or just anecdotal?” Dr. Ladhani said.

The regular BPSU survey covers over 90% of U.K.- and Ireland-based pediatric consultants (numbering 4,075). On the back of this established communication, the BPSU decided to gauge the extent of delayed presentations during the peak weeks of the COVID-19 pandemic.

Over the next 7 days, 2,433 pediatricians, representing 60% of BPSU participants, responded.

“This response rate in 7 days highlights the importance given to the survey by pediatricians ... and the widespread professional concern about delayed presentations,” the authors wrote.

Participants were asked whether they had seen any children during the previous 14 days who, in their opinion, presented later than they would have expected prior to the COVID-19 pandemic.

“There’s no one definition for this but these senior clinicians know when something is unusual,” said Dr. Ladhani.

ED attendances were compared with figures for the same period last year. Overall, a total of 32% of 752 pediatricians working in EDs and pediatric assessment units reported witnessing delayed presentations, with 57 (8%) reporting at least three patients with delayed presentation.

“It was clear that those doctors on the frontline were seeing a lot of delayed presentations. Also, neonatologists reported women arriving late for labor, and community physicians said they just weren’t witnessing child protection cases anymore,” added Dr. Ladhani.

Other issues included early discharges following births because of COVID-19 concerns, before feeding had been established, prompting return visits because of feeding problems and dehydration.

The top five delayed diagnoses were diabetes (n = 44), sepsis (n = 21), child protection (n = 14), malignancy (n = 8), and appendicitis (n = 6). There were 10 delayed perinatal presentations.

Of the nine deaths, for which delayed presentation was considered to play a role, three were caused by sepsis, three were caused by new malignancy diagnoses, one was caused by new diagnosis of metabolic disease, and two did not have the cause reported.

The delays in presentation are likely to have been influenced by the U.K. government’s message to “stay at home” during the strict lockdown period, which perhaps was sometimes interpreted too literally, Dr. Ladhani suggested. “It was the right message socially, but not medically.”

Russell Viner, MB, PhD, president of the Royal College of Paediatrics and Child Health, said in a statement: “The impact for children is what we call ‘collateral damage’, including long absences from school and delays or interruptions to vital services. We know that parents adhered very strongly to the ‘stay at home’ [message] and we need to say clearly that this doesn’t apply if your child is very sick. Should we experience a second wave or regional outbreaks, it is vital that we get the message out to parents that we want to see unwell children at the earliest possible stage.”

Dr. Ladhani reported no relevant financial relationships.

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

Diabetes was by far the most common delayed pediatric presentation in emergency care during the COVID-19 pandemic, according to a snapshot survey of nearly 2,500 pediatricians in the United Kingdom and Ireland.

There were also nine deaths where delayed presentation was considered a contributing factor, resulting mainly from sepsis and malignancy.

By comparison, over the same 2-week period of the survey there were three child deaths from COVID-19 directly, according to senior study author Shamez Ladhani, MRCPCH, PhD, chair of the British Paediatric Surveillance Unit (BPSU), Royal College of Paediatrics and Child Health, London.

“The unintended consequences of COVID are far greater, in children, than the disease itself. The way we are trying to prevent this is causing more harm than the disease,” he lamented.

One-third of senior U.K. pediatric specialists who responded to the survey reported dealing with so-called emergency delayed presentations in children who they would normally have expected to present much earlier.

After diabetes, the most commonly reported delayed diagnoses were sepsis and child protection issues. Cancer also featured prominently.

“We’ve found that there is great concern that children are not accessing healthcare as they should during lockdown and after,” Dr. Ladhani stressed. “Our emergency departments saw a 50% reduction during the peak, and now it is still 40% less than expected. The problem is improving but it remains.”

The survey findings were recently published online in Archives of Disease in Childhood, by first author Richard M. Lynn, MSc, of the Institute of Child Health, department of epidemiology and public health, University College London Research, and colleagues.
 

New diabetes cases presented very late during lockdown

Over the 2-week reporting period in mid-April 2020, type 1 diabetes was the most frequently reported delayed diagnosis, with 44 cases overall, 23 of which involved diabetic ketoacidosis.

“If you talk to the diabetes specialists, they tell us that generally, most cases of new diabetes arrive late because it has very nonspecific symptoms,” Dr. Ladhani explained.

However, he added, “pediatricians on the frontline know what to expect with diabetes. Those children who would have come in late prior to the pandemic are now arriving very late. Those consultants surveyed were not junior doctors but consultant pediatricians with many years of experience.”

In a recent article looking at pediatric delayed presentations, one patient with diabetes entered intensive care, and the BPSU report recorded one death possibly associated with diabetes, Dr. Ladhani pointed out.

“Pediatricians are worried that children are coming in late. We need to raise awareness that parents need to access healthcare and this message needs to go out now,” he said. “We can’t wait until a second wave. It has to be now because A&E [accident and emergency] attendance is still 40% [lower than] ... expected.”
 

BPSU survey covers over 90% of pediatricians in U.K. and Ireland

After numerous anecdotal reports of delayed presentations in the United Kingdom and abroad, the snapshot survey was conducted as part of routine monthly reports where pediatricians are asked to document any cases of rare conditions seen.

“We had heard stories of delayed presentations, but we wanted to know was this a real problem or just anecdotal?” Dr. Ladhani said.

The regular BPSU survey covers over 90% of U.K.- and Ireland-based pediatric consultants (numbering 4,075). On the back of this established communication, the BPSU decided to gauge the extent of delayed presentations during the peak weeks of the COVID-19 pandemic.

Over the next 7 days, 2,433 pediatricians, representing 60% of BPSU participants, responded.

“This response rate in 7 days highlights the importance given to the survey by pediatricians ... and the widespread professional concern about delayed presentations,” the authors wrote.

Participants were asked whether they had seen any children during the previous 14 days who, in their opinion, presented later than they would have expected prior to the COVID-19 pandemic.

“There’s no one definition for this but these senior clinicians know when something is unusual,” said Dr. Ladhani.

ED attendances were compared with figures for the same period last year. Overall, a total of 32% of 752 pediatricians working in EDs and pediatric assessment units reported witnessing delayed presentations, with 57 (8%) reporting at least three patients with delayed presentation.

“It was clear that those doctors on the frontline were seeing a lot of delayed presentations. Also, neonatologists reported women arriving late for labor, and community physicians said they just weren’t witnessing child protection cases anymore,” added Dr. Ladhani.

Other issues included early discharges following births because of COVID-19 concerns, before feeding had been established, prompting return visits because of feeding problems and dehydration.

The top five delayed diagnoses were diabetes (n = 44), sepsis (n = 21), child protection (n = 14), malignancy (n = 8), and appendicitis (n = 6). There were 10 delayed perinatal presentations.

Of the nine deaths, for which delayed presentation was considered to play a role, three were caused by sepsis, three were caused by new malignancy diagnoses, one was caused by new diagnosis of metabolic disease, and two did not have the cause reported.

The delays in presentation are likely to have been influenced by the U.K. government’s message to “stay at home” during the strict lockdown period, which perhaps was sometimes interpreted too literally, Dr. Ladhani suggested. “It was the right message socially, but not medically.”

Russell Viner, MB, PhD, president of the Royal College of Paediatrics and Child Health, said in a statement: “The impact for children is what we call ‘collateral damage’, including long absences from school and delays or interruptions to vital services. We know that parents adhered very strongly to the ‘stay at home’ [message] and we need to say clearly that this doesn’t apply if your child is very sick. Should we experience a second wave or regional outbreaks, it is vital that we get the message out to parents that we want to see unwell children at the earliest possible stage.”

Dr. Ladhani reported no relevant financial relationships.

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

Diabetes was by far the most common delayed pediatric presentation in emergency care during the COVID-19 pandemic, according to a snapshot survey of nearly 2,500 pediatricians in the United Kingdom and Ireland.

There were also nine deaths where delayed presentation was considered a contributing factor, resulting mainly from sepsis and malignancy.

By comparison, over the same 2-week period of the survey there were three child deaths from COVID-19 directly, according to senior study author Shamez Ladhani, MRCPCH, PhD, chair of the British Paediatric Surveillance Unit (BPSU), Royal College of Paediatrics and Child Health, London.

“The unintended consequences of COVID are far greater, in children, than the disease itself. The way we are trying to prevent this is causing more harm than the disease,” he lamented.

One-third of senior U.K. pediatric specialists who responded to the survey reported dealing with so-called emergency delayed presentations in children who they would normally have expected to present much earlier.

After diabetes, the most commonly reported delayed diagnoses were sepsis and child protection issues. Cancer also featured prominently.

“We’ve found that there is great concern that children are not accessing healthcare as they should during lockdown and after,” Dr. Ladhani stressed. “Our emergency departments saw a 50% reduction during the peak, and now it is still 40% less than expected. The problem is improving but it remains.”

The survey findings were recently published online in Archives of Disease in Childhood, by first author Richard M. Lynn, MSc, of the Institute of Child Health, department of epidemiology and public health, University College London Research, and colleagues.
 

New diabetes cases presented very late during lockdown

Over the 2-week reporting period in mid-April 2020, type 1 diabetes was the most frequently reported delayed diagnosis, with 44 cases overall, 23 of which involved diabetic ketoacidosis.

“If you talk to the diabetes specialists, they tell us that generally, most cases of new diabetes arrive late because it has very nonspecific symptoms,” Dr. Ladhani explained.

However, he added, “pediatricians on the frontline know what to expect with diabetes. Those children who would have come in late prior to the pandemic are now arriving very late. Those consultants surveyed were not junior doctors but consultant pediatricians with many years of experience.”

In a recent article looking at pediatric delayed presentations, one patient with diabetes entered intensive care, and the BPSU report recorded one death possibly associated with diabetes, Dr. Ladhani pointed out.

“Pediatricians are worried that children are coming in late. We need to raise awareness that parents need to access healthcare and this message needs to go out now,” he said. “We can’t wait until a second wave. It has to be now because A&E [accident and emergency] attendance is still 40% [lower than] ... expected.”
 

BPSU survey covers over 90% of pediatricians in U.K. and Ireland

After numerous anecdotal reports of delayed presentations in the United Kingdom and abroad, the snapshot survey was conducted as part of routine monthly reports where pediatricians are asked to document any cases of rare conditions seen.

“We had heard stories of delayed presentations, but we wanted to know was this a real problem or just anecdotal?” Dr. Ladhani said.

The regular BPSU survey covers over 90% of U.K.- and Ireland-based pediatric consultants (numbering 4,075). On the back of this established communication, the BPSU decided to gauge the extent of delayed presentations during the peak weeks of the COVID-19 pandemic.

Over the next 7 days, 2,433 pediatricians, representing 60% of BPSU participants, responded.

“This response rate in 7 days highlights the importance given to the survey by pediatricians ... and the widespread professional concern about delayed presentations,” the authors wrote.

Participants were asked whether they had seen any children during the previous 14 days who, in their opinion, presented later than they would have expected prior to the COVID-19 pandemic.

“There’s no one definition for this but these senior clinicians know when something is unusual,” said Dr. Ladhani.

ED attendances were compared with figures for the same period last year. Overall, a total of 32% of 752 pediatricians working in EDs and pediatric assessment units reported witnessing delayed presentations, with 57 (8%) reporting at least three patients with delayed presentation.

“It was clear that those doctors on the frontline were seeing a lot of delayed presentations. Also, neonatologists reported women arriving late for labor, and community physicians said they just weren’t witnessing child protection cases anymore,” added Dr. Ladhani.

Other issues included early discharges following births because of COVID-19 concerns, before feeding had been established, prompting return visits because of feeding problems and dehydration.

The top five delayed diagnoses were diabetes (n = 44), sepsis (n = 21), child protection (n = 14), malignancy (n = 8), and appendicitis (n = 6). There were 10 delayed perinatal presentations.

Of the nine deaths, for which delayed presentation was considered to play a role, three were caused by sepsis, three were caused by new malignancy diagnoses, one was caused by new diagnosis of metabolic disease, and two did not have the cause reported.

The delays in presentation are likely to have been influenced by the U.K. government’s message to “stay at home” during the strict lockdown period, which perhaps was sometimes interpreted too literally, Dr. Ladhani suggested. “It was the right message socially, but not medically.”

Russell Viner, MB, PhD, president of the Royal College of Paediatrics and Child Health, said in a statement: “The impact for children is what we call ‘collateral damage’, including long absences from school and delays or interruptions to vital services. We know that parents adhered very strongly to the ‘stay at home’ [message] and we need to say clearly that this doesn’t apply if your child is very sick. Should we experience a second wave or regional outbreaks, it is vital that we get the message out to parents that we want to see unwell children at the earliest possible stage.”

Dr. Ladhani reported no relevant financial relationships.

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

Patients in the Veterans Health Administration (VHA) system 75 years or older, free of cardiovascular (CV) disease and prescribed statins for the first time, had a one-fourth lower risk for death and a 20% lower risk for CV death over an average 7 years than that of comparable patients not prescribed the drugs in an observational study.

The findings, based on more than 320,000 predominantly white male patients, initially without atherosclerotic cardiovascular disease (ASCVD), underscore the notion that “age on its own shouldn’t be a criterion not to use these drugs,” Ariela R. Orkaby, MD, MPH, lead author on the study, published in the July 7 issue of JAMA, said in an interview.

The very elderly are frequently undertreated, particularly in primary prevention, as many physicians consider it unnecessary for them to initiate or continue preventive measures, said Dr. Orkaby, of VA Boston Healthcare System and Harvard Medical School, Boston.

“From available data, we don’t really expect statins to start providing benefit in primary prevention until they’ve been taken for about 2 to 5 years. So for people who have very limited life expectancy, it may not be a great idea to add to their pill burden or increase the possibility that they might decline functionally,” Dr. Orkaby said.

“But what we saw in this study is that there is benefit to prescribing statins even in elderly patients, even within 2 years” of follow-up.

Despite being among the most studied drugs in the world, statins are understudied in older people. Fewer than 2% of the 186,854 participants in 28 statin trials were aged 75 years or older, wrote Dr. Orkaby and associates.

Most of what is known about initiating statin therapy in the 75-and-older age group comes from underpowered subgroup analyses and a few observational studies, Steven J. Nicholls, MBBS, PhD, Monash University, Melbourne, and Adam J. Nelson, MBBS, PhD, Duke Clinical Research Institute, Durham, N.C., wrote in an accompanying editorial. As a result, the evidence is conflicting, with some reports suggesting marked benefit and others possible harm.

The current findings, they wrote, “provide additional support for treatment guidelines that have increasingly advocated for more widespread use of statin therapy for ASCVD prevention in older individuals.”

Of the 326,981 people in the analysis, 57,178 (17.5%) were new statin users or initiated a statin during the study period, usually simvastatin. Their mean age was about 81 years, and 97.3% of the patients were men, 90% were white, and 72% were former smokers.

Using propensity scoring, the authors compared statin users with the other remaining patients who had the same likelihood of being prescribed a statin based on clinical characteristics but did not receive a prescription for a statin.

Michael W. Rich, MD, Washington University, St. Louis, who was not involved in the study but has previously worked with Dr. Orkaby, praised the analysis.

“It’s one of the best studies I’ve seen addressing this particular issue. It’s a large sample size, the analysis was very well done, and I think that it comes to a pretty unequivocal conclusion that, at least in this population, those individuals who were started on statins for the first time, and having no known prior ASCVD, clearly had a lower all-cause mortality and cardiovascular mortality, as well as a lower risk of composite cardiovascular events,” he said in an interview.

But the data have limitations, he added. The findings are still observational and could be confounded by unknown variables, and the select population – mostly white, male veterans – is known to be at somewhat higher risk for events than the general population.

Perhaps even more impressive than the risk reductions seen at a mean 6.8 years of follow-up, Dr. Rich said, are the sensitivity analyses at 2, 4, and 6 years that showed the benefit manifesting early.

The researchers saw a 32% reduction in all-cause mortality risk (P < .05) at 2 years, 21% at 4 years, and 13% at 6 years (P < .05 for all). Risk reductions for CV death followed a similar pattern, they wrote.

Dr. Rich said that the trial, although not a “slam dunk,” has persuaded him to shift from being very conservative about prescribing statins to elderly patients to being much more willing to consider it.

“This doesn’t mean that I will be running to routinely prescribe my 90-plus patients a statin, nor should we should be starting statins in everyone over 75, not even in all male former smokers over 75 – the type of people in this study – but I do think that it provides a stronger basis for talking to these patients about the possibility of starting a statin.”

There are two ongoing trials that may provide greater clarity, the authors observed. The STAREE trial has enrolled adults 70 years and older in Australia and includes serial evaluation of cognitive scores. Also, PREVENTABLE will examine the role of statins for prevention of dementia and disability-free survival in adults 75 years and older.

However, neither trial may fully resolve the question of primary prevention statin use in the elderly, they wrote. “While these trials are necessary to broaden the evidence base for older adults, it is unlikely that any trial will enroll large numbers of individuals at very advanced ages, black individuals, and those with dementia, as were included in this study.”

Dr. Orkaby had no disclosures; potential conflicts for the other authors are in the report. Dr. Rich reported having no conflicts of interest. Dr. Nicholls disclosed receiving research support from AstraZeneca, Amgen, Anthera, Eli Lilly, Novartis, Cerenis, The Medicines Company, Resverlogix, InfraReDx, Roche, Sanofi-Regeneron, and LipoScience; and receiving consulting fees or honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Regeneron, CSL Behring, Esperion, and Boehringer Ingelheim. Dr. Nelson had no disclosures.

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

Patients in the Veterans Health Administration (VHA) system 75 years or older, free of cardiovascular (CV) disease and prescribed statins for the first time, had a one-fourth lower risk for death and a 20% lower risk for CV death over an average 7 years than that of comparable patients not prescribed the drugs in an observational study.

The findings, based on more than 320,000 predominantly white male patients, initially without atherosclerotic cardiovascular disease (ASCVD), underscore the notion that “age on its own shouldn’t be a criterion not to use these drugs,” Ariela R. Orkaby, MD, MPH, lead author on the study, published in the July 7 issue of JAMA, said in an interview.

The very elderly are frequently undertreated, particularly in primary prevention, as many physicians consider it unnecessary for them to initiate or continue preventive measures, said Dr. Orkaby, of VA Boston Healthcare System and Harvard Medical School, Boston.

“From available data, we don’t really expect statins to start providing benefit in primary prevention until they’ve been taken for about 2 to 5 years. So for people who have very limited life expectancy, it may not be a great idea to add to their pill burden or increase the possibility that they might decline functionally,” Dr. Orkaby said.

“But what we saw in this study is that there is benefit to prescribing statins even in elderly patients, even within 2 years” of follow-up.

Despite being among the most studied drugs in the world, statins are understudied in older people. Fewer than 2% of the 186,854 participants in 28 statin trials were aged 75 years or older, wrote Dr. Orkaby and associates.

Most of what is known about initiating statin therapy in the 75-and-older age group comes from underpowered subgroup analyses and a few observational studies, Steven J. Nicholls, MBBS, PhD, Monash University, Melbourne, and Adam J. Nelson, MBBS, PhD, Duke Clinical Research Institute, Durham, N.C., wrote in an accompanying editorial. As a result, the evidence is conflicting, with some reports suggesting marked benefit and others possible harm.

The current findings, they wrote, “provide additional support for treatment guidelines that have increasingly advocated for more widespread use of statin therapy for ASCVD prevention in older individuals.”

Of the 326,981 people in the analysis, 57,178 (17.5%) were new statin users or initiated a statin during the study period, usually simvastatin. Their mean age was about 81 years, and 97.3% of the patients were men, 90% were white, and 72% were former smokers.

Using propensity scoring, the authors compared statin users with the other remaining patients who had the same likelihood of being prescribed a statin based on clinical characteristics but did not receive a prescription for a statin.

Michael W. Rich, MD, Washington University, St. Louis, who was not involved in the study but has previously worked with Dr. Orkaby, praised the analysis.

“It’s one of the best studies I’ve seen addressing this particular issue. It’s a large sample size, the analysis was very well done, and I think that it comes to a pretty unequivocal conclusion that, at least in this population, those individuals who were started on statins for the first time, and having no known prior ASCVD, clearly had a lower all-cause mortality and cardiovascular mortality, as well as a lower risk of composite cardiovascular events,” he said in an interview.

But the data have limitations, he added. The findings are still observational and could be confounded by unknown variables, and the select population – mostly white, male veterans – is known to be at somewhat higher risk for events than the general population.

Perhaps even more impressive than the risk reductions seen at a mean 6.8 years of follow-up, Dr. Rich said, are the sensitivity analyses at 2, 4, and 6 years that showed the benefit manifesting early.

The researchers saw a 32% reduction in all-cause mortality risk (P < .05) at 2 years, 21% at 4 years, and 13% at 6 years (P < .05 for all). Risk reductions for CV death followed a similar pattern, they wrote.

Dr. Rich said that the trial, although not a “slam dunk,” has persuaded him to shift from being very conservative about prescribing statins to elderly patients to being much more willing to consider it.

“This doesn’t mean that I will be running to routinely prescribe my 90-plus patients a statin, nor should we should be starting statins in everyone over 75, not even in all male former smokers over 75 – the type of people in this study – but I do think that it provides a stronger basis for talking to these patients about the possibility of starting a statin.”

There are two ongoing trials that may provide greater clarity, the authors observed. The STAREE trial has enrolled adults 70 years and older in Australia and includes serial evaluation of cognitive scores. Also, PREVENTABLE will examine the role of statins for prevention of dementia and disability-free survival in adults 75 years and older.

However, neither trial may fully resolve the question of primary prevention statin use in the elderly, they wrote. “While these trials are necessary to broaden the evidence base for older adults, it is unlikely that any trial will enroll large numbers of individuals at very advanced ages, black individuals, and those with dementia, as were included in this study.”

Dr. Orkaby had no disclosures; potential conflicts for the other authors are in the report. Dr. Rich reported having no conflicts of interest. Dr. Nicholls disclosed receiving research support from AstraZeneca, Amgen, Anthera, Eli Lilly, Novartis, Cerenis, The Medicines Company, Resverlogix, InfraReDx, Roche, Sanofi-Regeneron, and LipoScience; and receiving consulting fees or honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Regeneron, CSL Behring, Esperion, and Boehringer Ingelheim. Dr. Nelson had no disclosures.

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

Patients in the Veterans Health Administration (VHA) system 75 years or older, free of cardiovascular (CV) disease and prescribed statins for the first time, had a one-fourth lower risk for death and a 20% lower risk for CV death over an average 7 years than that of comparable patients not prescribed the drugs in an observational study.

The findings, based on more than 320,000 predominantly white male patients, initially without atherosclerotic cardiovascular disease (ASCVD), underscore the notion that “age on its own shouldn’t be a criterion not to use these drugs,” Ariela R. Orkaby, MD, MPH, lead author on the study, published in the July 7 issue of JAMA, said in an interview.

The very elderly are frequently undertreated, particularly in primary prevention, as many physicians consider it unnecessary for them to initiate or continue preventive measures, said Dr. Orkaby, of VA Boston Healthcare System and Harvard Medical School, Boston.

“From available data, we don’t really expect statins to start providing benefit in primary prevention until they’ve been taken for about 2 to 5 years. So for people who have very limited life expectancy, it may not be a great idea to add to their pill burden or increase the possibility that they might decline functionally,” Dr. Orkaby said.

“But what we saw in this study is that there is benefit to prescribing statins even in elderly patients, even within 2 years” of follow-up.

Despite being among the most studied drugs in the world, statins are understudied in older people. Fewer than 2% of the 186,854 participants in 28 statin trials were aged 75 years or older, wrote Dr. Orkaby and associates.

Most of what is known about initiating statin therapy in the 75-and-older age group comes from underpowered subgroup analyses and a few observational studies, Steven J. Nicholls, MBBS, PhD, Monash University, Melbourne, and Adam J. Nelson, MBBS, PhD, Duke Clinical Research Institute, Durham, N.C., wrote in an accompanying editorial. As a result, the evidence is conflicting, with some reports suggesting marked benefit and others possible harm.

The current findings, they wrote, “provide additional support for treatment guidelines that have increasingly advocated for more widespread use of statin therapy for ASCVD prevention in older individuals.”

Of the 326,981 people in the analysis, 57,178 (17.5%) were new statin users or initiated a statin during the study period, usually simvastatin. Their mean age was about 81 years, and 97.3% of the patients were men, 90% were white, and 72% were former smokers.

Using propensity scoring, the authors compared statin users with the other remaining patients who had the same likelihood of being prescribed a statin based on clinical characteristics but did not receive a prescription for a statin.

Michael W. Rich, MD, Washington University, St. Louis, who was not involved in the study but has previously worked with Dr. Orkaby, praised the analysis.

“It’s one of the best studies I’ve seen addressing this particular issue. It’s a large sample size, the analysis was very well done, and I think that it comes to a pretty unequivocal conclusion that, at least in this population, those individuals who were started on statins for the first time, and having no known prior ASCVD, clearly had a lower all-cause mortality and cardiovascular mortality, as well as a lower risk of composite cardiovascular events,” he said in an interview.

But the data have limitations, he added. The findings are still observational and could be confounded by unknown variables, and the select population – mostly white, male veterans – is known to be at somewhat higher risk for events than the general population.

Perhaps even more impressive than the risk reductions seen at a mean 6.8 years of follow-up, Dr. Rich said, are the sensitivity analyses at 2, 4, and 6 years that showed the benefit manifesting early.

The researchers saw a 32% reduction in all-cause mortality risk (P < .05) at 2 years, 21% at 4 years, and 13% at 6 years (P < .05 for all). Risk reductions for CV death followed a similar pattern, they wrote.

Dr. Rich said that the trial, although not a “slam dunk,” has persuaded him to shift from being very conservative about prescribing statins to elderly patients to being much more willing to consider it.

“This doesn’t mean that I will be running to routinely prescribe my 90-plus patients a statin, nor should we should be starting statins in everyone over 75, not even in all male former smokers over 75 – the type of people in this study – but I do think that it provides a stronger basis for talking to these patients about the possibility of starting a statin.”

There are two ongoing trials that may provide greater clarity, the authors observed. The STAREE trial has enrolled adults 70 years and older in Australia and includes serial evaluation of cognitive scores. Also, PREVENTABLE will examine the role of statins for prevention of dementia and disability-free survival in adults 75 years and older.

However, neither trial may fully resolve the question of primary prevention statin use in the elderly, they wrote. “While these trials are necessary to broaden the evidence base for older adults, it is unlikely that any trial will enroll large numbers of individuals at very advanced ages, black individuals, and those with dementia, as were included in this study.”

Dr. Orkaby had no disclosures; potential conflicts for the other authors are in the report. Dr. Rich reported having no conflicts of interest. Dr. Nicholls disclosed receiving research support from AstraZeneca, Amgen, Anthera, Eli Lilly, Novartis, Cerenis, The Medicines Company, Resverlogix, InfraReDx, Roche, Sanofi-Regeneron, and LipoScience; and receiving consulting fees or honoraria from AstraZeneca, Eli Lilly, Anthera, Omthera, Merck, Takeda, Resverlogix, Sanofi-Regeneron, CSL Behring, Esperion, and Boehringer Ingelheim. Dr. Nelson had no disclosures.

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

Although the adverse effects of systemic glucocorticoids (GCs) are well known, their association with hypertension in rheumatoid arthritis (RA) has been unclear. Now, a large population-based study shows that the drugs are linked to a 17% overall increased risk for incident hypertension among patients with RA.

Further, when the researchers stratified participants by dose category, they found that doses higher than 7.5 mg were significantly associated with hypertension. Cumulative dosage was not tied to any clear pattern of risk.

The authors, led by Ruth E. Costello, a researcher at the Centre for Epidemiology Versus Arthritis in the Centre for Musculoskeletal Research at the University of Manchester (England) concluded that patients who are taking these drugs for the treatment of RA should be monitored for high blood pressure, which is an important but modifiable cardiovascular risk factor, and treated appropriately.

The results of Ms. Costello and colleagues’ study were published June 27 in Rheumatology.

“While fractures associated with these steroid drugs are well studied, hypertension is a side effect that seems to have been less well studied, and yet it is an important cardiovascular risk factor that can be managed,” Ms. Costello said in an interview.

To better understand the possible association, Ms. Costello and colleagues identified 17,760 patients who were newly diagnosed with RA between 1992 and 2019 and were included in the Clinical Practice Research Datalink, which represents about 7% of the U.K. population. None of the patients had hypertension at initial RA diagnosis. Slightly more than two-thirds were women (68.1%), and the mean age was 56.3 years.

Of those patients, 7,421 (41.8%) were prescribed GCs during postdiagnosis follow-up. Most patients (73%) were followed for at least 2 years.

Patients who used GCs were slightly older than never-users (mean age, 57.7 vs. 55.3 years), were predominantly women, had a history of smoking, and had more comorbidities.

The overall incidence rate (IR) of hypertension was 64.1 per 1,000 person-years (95% confidence interval, 62.5-65.7). There were 6,243 cases of incident hypertension over 97,547 person-years of follow-up.

Among those exposed to GCs, 1,321 patients developed hypertension, for an IR of 87.6 per 1,000 person-years. Among unexposed participants, the IR for hypertension was 59.7 per 1,000 person-years. In Cox proportional hazards modeling, GC use was associated with a 17% increased risk for hypertension (hazard ratio, 1.17; 95% CI, 1.10-1.24).

The researchers noted that 40% of GC users with hypertension were not prescribed an antihypertensive agent at any point during the study. “Whilst some may have been offered lifestyle advice, left untreated this has important implications in terms of addressing modifiable risk factors in an RA population already at increased risk of CV disease,” they wrote.

They noted that cardiovascular disease is a major driver of the elevated mortality risk seen among adults with RA compared with the general population and that recent treatment recommendations address management of cardiovascular risks in these patients.

“There are several routes by which GCs may promote cardiovascular disease, including hypertension, metabolic changes, diabetes, and weight gain. We don’t currently know the extent to which each of these individual mechanisms may be increasing cardiovascular disease,” said Ms. Costello.

“Glucocorticoids increase fluid retention and promote obesity and hypertension,” said Rajat S. Bhatt, MD, a rheumatologist at Prime Rheumatology and Memorial Hermann Katy Hospital in Richmond, Texas, who sees hypertension in GC users in his clinical practice. “So patients need to be monitored for these risk factors,” he said in an interview.

Although hypertension may be a significant factor in the increase in cardiovascular disease in the RA population, Dr. Bhatt said the major driver is likely the intrinsic inflammatory state caused by the disease itself. As to why the GC-hypertension connection has flown under the radar in RA, he added, “That specific link has been difficult to tease out since RA patients are often on multiple medications.”

In regard to the role of dosage, Dr. Bhatt said that hypertension risk increases with higher GC doses, as the U.K. study indicates, and usually subsides when patients stop using GCs.

“Whether the observed dose association is causal or influenced by the underlying disease severity, our results suggest we should be vigilant in patients on all doses of GC, especially higher doses,” Ms. Costello added.

In regard to using drugs that are less cardiotoxic than GCs, Dr. Bhatt said that there are clinical scenarios in which GC therapy is the best choice, so just switching to nonsteroidal drugs is no panacea. “All RA drugs have adverse side effects, and anyway, the goal of rheumatology treatment is always to get patients off corticosteroids as soon as possible,” he said.

Ms. Costello and colleagues noted that their results are consonant with earlier research, including a single-center, cross-sectional study in which less than 6 months’ use of prednisolone at a median dose of 7.5 mg was associated with hypertension. In a German registry study, among patients who received doses of less than 7.5 mg for less than 6 months, there were higher rates of self-reported elevations in blood pressure.

The findings are at odds, however, with a recent matched-cohort study, which also used data from the Clinical Practice Research Datalink. That study found no association between GC use and hypertension.

GCs have come under increasing scrutiny in regard to several diseases. A study published July 7 found that even short-term courses of a few days’ duration entail risks for serious adverse events.

Ms. Costello’s group says that an estimate of GC-related incident hypertension in RA should allow more informed treatment decisions and that their findings highlight the ongoing need to monitor for and address this risk.

The study was supported by the Centre for Epidemiology Versus Arthritis and by the National Institute for Health Research Manchester Biomedical Research Centre. Coauthor William G. Dixon, PhD, has received consultancy fees from Google and Bayer unrelated to this study. Dr. Bhatt has disclosed no relevant financial relationships.

SOURCE: Costello RE et al. Rheumatology. 2020 June 27. doi: 10.1093/rheumatology/keaa209.

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

Although the adverse effects of systemic glucocorticoids (GCs) are well known, their association with hypertension in rheumatoid arthritis (RA) has been unclear. Now, a large population-based study shows that the drugs are linked to a 17% overall increased risk for incident hypertension among patients with RA.

Further, when the researchers stratified participants by dose category, they found that doses higher than 7.5 mg were significantly associated with hypertension. Cumulative dosage was not tied to any clear pattern of risk.

The authors, led by Ruth E. Costello, a researcher at the Centre for Epidemiology Versus Arthritis in the Centre for Musculoskeletal Research at the University of Manchester (England) concluded that patients who are taking these drugs for the treatment of RA should be monitored for high blood pressure, which is an important but modifiable cardiovascular risk factor, and treated appropriately.

The results of Ms. Costello and colleagues’ study were published June 27 in Rheumatology.

“While fractures associated with these steroid drugs are well studied, hypertension is a side effect that seems to have been less well studied, and yet it is an important cardiovascular risk factor that can be managed,” Ms. Costello said in an interview.

To better understand the possible association, Ms. Costello and colleagues identified 17,760 patients who were newly diagnosed with RA between 1992 and 2019 and were included in the Clinical Practice Research Datalink, which represents about 7% of the U.K. population. None of the patients had hypertension at initial RA diagnosis. Slightly more than two-thirds were women (68.1%), and the mean age was 56.3 years.

Of those patients, 7,421 (41.8%) were prescribed GCs during postdiagnosis follow-up. Most patients (73%) were followed for at least 2 years.

Patients who used GCs were slightly older than never-users (mean age, 57.7 vs. 55.3 years), were predominantly women, had a history of smoking, and had more comorbidities.

The overall incidence rate (IR) of hypertension was 64.1 per 1,000 person-years (95% confidence interval, 62.5-65.7). There were 6,243 cases of incident hypertension over 97,547 person-years of follow-up.

Among those exposed to GCs, 1,321 patients developed hypertension, for an IR of 87.6 per 1,000 person-years. Among unexposed participants, the IR for hypertension was 59.7 per 1,000 person-years. In Cox proportional hazards modeling, GC use was associated with a 17% increased risk for hypertension (hazard ratio, 1.17; 95% CI, 1.10-1.24).

The researchers noted that 40% of GC users with hypertension were not prescribed an antihypertensive agent at any point during the study. “Whilst some may have been offered lifestyle advice, left untreated this has important implications in terms of addressing modifiable risk factors in an RA population already at increased risk of CV disease,” they wrote.

They noted that cardiovascular disease is a major driver of the elevated mortality risk seen among adults with RA compared with the general population and that recent treatment recommendations address management of cardiovascular risks in these patients.

“There are several routes by which GCs may promote cardiovascular disease, including hypertension, metabolic changes, diabetes, and weight gain. We don’t currently know the extent to which each of these individual mechanisms may be increasing cardiovascular disease,” said Ms. Costello.

“Glucocorticoids increase fluid retention and promote obesity and hypertension,” said Rajat S. Bhatt, MD, a rheumatologist at Prime Rheumatology and Memorial Hermann Katy Hospital in Richmond, Texas, who sees hypertension in GC users in his clinical practice. “So patients need to be monitored for these risk factors,” he said in an interview.

Although hypertension may be a significant factor in the increase in cardiovascular disease in the RA population, Dr. Bhatt said the major driver is likely the intrinsic inflammatory state caused by the disease itself. As to why the GC-hypertension connection has flown under the radar in RA, he added, “That specific link has been difficult to tease out since RA patients are often on multiple medications.”

In regard to the role of dosage, Dr. Bhatt said that hypertension risk increases with higher GC doses, as the U.K. study indicates, and usually subsides when patients stop using GCs.

“Whether the observed dose association is causal or influenced by the underlying disease severity, our results suggest we should be vigilant in patients on all doses of GC, especially higher doses,” Ms. Costello added.

In regard to using drugs that are less cardiotoxic than GCs, Dr. Bhatt said that there are clinical scenarios in which GC therapy is the best choice, so just switching to nonsteroidal drugs is no panacea. “All RA drugs have adverse side effects, and anyway, the goal of rheumatology treatment is always to get patients off corticosteroids as soon as possible,” he said.

Ms. Costello and colleagues noted that their results are consonant with earlier research, including a single-center, cross-sectional study in which less than 6 months’ use of prednisolone at a median dose of 7.5 mg was associated with hypertension. In a German registry study, among patients who received doses of less than 7.5 mg for less than 6 months, there were higher rates of self-reported elevations in blood pressure.

The findings are at odds, however, with a recent matched-cohort study, which also used data from the Clinical Practice Research Datalink. That study found no association between GC use and hypertension.

GCs have come under increasing scrutiny in regard to several diseases. A study published July 7 found that even short-term courses of a few days’ duration entail risks for serious adverse events.

Ms. Costello’s group says that an estimate of GC-related incident hypertension in RA should allow more informed treatment decisions and that their findings highlight the ongoing need to monitor for and address this risk.

The study was supported by the Centre for Epidemiology Versus Arthritis and by the National Institute for Health Research Manchester Biomedical Research Centre. Coauthor William G. Dixon, PhD, has received consultancy fees from Google and Bayer unrelated to this study. Dr. Bhatt has disclosed no relevant financial relationships.

SOURCE: Costello RE et al. Rheumatology. 2020 June 27. doi: 10.1093/rheumatology/keaa209.

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

Although the adverse effects of systemic glucocorticoids (GCs) are well known, their association with hypertension in rheumatoid arthritis (RA) has been unclear. Now, a large population-based study shows that the drugs are linked to a 17% overall increased risk for incident hypertension among patients with RA.

Further, when the researchers stratified participants by dose category, they found that doses higher than 7.5 mg were significantly associated with hypertension. Cumulative dosage was not tied to any clear pattern of risk.

The authors, led by Ruth E. Costello, a researcher at the Centre for Epidemiology Versus Arthritis in the Centre for Musculoskeletal Research at the University of Manchester (England) concluded that patients who are taking these drugs for the treatment of RA should be monitored for high blood pressure, which is an important but modifiable cardiovascular risk factor, and treated appropriately.

The results of Ms. Costello and colleagues’ study were published June 27 in Rheumatology.

“While fractures associated with these steroid drugs are well studied, hypertension is a side effect that seems to have been less well studied, and yet it is an important cardiovascular risk factor that can be managed,” Ms. Costello said in an interview.

To better understand the possible association, Ms. Costello and colleagues identified 17,760 patients who were newly diagnosed with RA between 1992 and 2019 and were included in the Clinical Practice Research Datalink, which represents about 7% of the U.K. population. None of the patients had hypertension at initial RA diagnosis. Slightly more than two-thirds were women (68.1%), and the mean age was 56.3 years.

Of those patients, 7,421 (41.8%) were prescribed GCs during postdiagnosis follow-up. Most patients (73%) were followed for at least 2 years.

Patients who used GCs were slightly older than never-users (mean age, 57.7 vs. 55.3 years), were predominantly women, had a history of smoking, and had more comorbidities.

The overall incidence rate (IR) of hypertension was 64.1 per 1,000 person-years (95% confidence interval, 62.5-65.7). There were 6,243 cases of incident hypertension over 97,547 person-years of follow-up.

Among those exposed to GCs, 1,321 patients developed hypertension, for an IR of 87.6 per 1,000 person-years. Among unexposed participants, the IR for hypertension was 59.7 per 1,000 person-years. In Cox proportional hazards modeling, GC use was associated with a 17% increased risk for hypertension (hazard ratio, 1.17; 95% CI, 1.10-1.24).

The researchers noted that 40% of GC users with hypertension were not prescribed an antihypertensive agent at any point during the study. “Whilst some may have been offered lifestyle advice, left untreated this has important implications in terms of addressing modifiable risk factors in an RA population already at increased risk of CV disease,” they wrote.

They noted that cardiovascular disease is a major driver of the elevated mortality risk seen among adults with RA compared with the general population and that recent treatment recommendations address management of cardiovascular risks in these patients.

“There are several routes by which GCs may promote cardiovascular disease, including hypertension, metabolic changes, diabetes, and weight gain. We don’t currently know the extent to which each of these individual mechanisms may be increasing cardiovascular disease,” said Ms. Costello.

“Glucocorticoids increase fluid retention and promote obesity and hypertension,” said Rajat S. Bhatt, MD, a rheumatologist at Prime Rheumatology and Memorial Hermann Katy Hospital in Richmond, Texas, who sees hypertension in GC users in his clinical practice. “So patients need to be monitored for these risk factors,” he said in an interview.

Although hypertension may be a significant factor in the increase in cardiovascular disease in the RA population, Dr. Bhatt said the major driver is likely the intrinsic inflammatory state caused by the disease itself. As to why the GC-hypertension connection has flown under the radar in RA, he added, “That specific link has been difficult to tease out since RA patients are often on multiple medications.”

In regard to the role of dosage, Dr. Bhatt said that hypertension risk increases with higher GC doses, as the U.K. study indicates, and usually subsides when patients stop using GCs.

“Whether the observed dose association is causal or influenced by the underlying disease severity, our results suggest we should be vigilant in patients on all doses of GC, especially higher doses,” Ms. Costello added.

In regard to using drugs that are less cardiotoxic than GCs, Dr. Bhatt said that there are clinical scenarios in which GC therapy is the best choice, so just switching to nonsteroidal drugs is no panacea. “All RA drugs have adverse side effects, and anyway, the goal of rheumatology treatment is always to get patients off corticosteroids as soon as possible,” he said.

Ms. Costello and colleagues noted that their results are consonant with earlier research, including a single-center, cross-sectional study in which less than 6 months’ use of prednisolone at a median dose of 7.5 mg was associated with hypertension. In a German registry study, among patients who received doses of less than 7.5 mg for less than 6 months, there were higher rates of self-reported elevations in blood pressure.

The findings are at odds, however, with a recent matched-cohort study, which also used data from the Clinical Practice Research Datalink. That study found no association between GC use and hypertension.

GCs have come under increasing scrutiny in regard to several diseases. A study published July 7 found that even short-term courses of a few days’ duration entail risks for serious adverse events.

Ms. Costello’s group says that an estimate of GC-related incident hypertension in RA should allow more informed treatment decisions and that their findings highlight the ongoing need to monitor for and address this risk.

The study was supported by the Centre for Epidemiology Versus Arthritis and by the National Institute for Health Research Manchester Biomedical Research Centre. Coauthor William G. Dixon, PhD, has received consultancy fees from Google and Bayer unrelated to this study. Dr. Bhatt has disclosed no relevant financial relationships.

SOURCE: Costello RE et al. Rheumatology. 2020 June 27. doi: 10.1093/rheumatology/keaa209.

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

The COVID-19 literature has been peppered with reports about myocarditis accompanying the disease. If true, this could, in part, explain some of the observed cardiac injury and arrhythmias in seriously ill patients, but also have implications for prognosis.

But endomyocardial biopsies and autopsies, the gold-standard confirmation tests, have been few and far between. That has led some cardiologists to question the true rate of myocarditis with SARS-CoV-2, or even if there is definitive proof the virus causes myocarditis.

Predictors of death in COVID-19 are older age, cardiovascular comorbidities, and elevated troponin or NT-proBNP – none of which actually fit well with the epidemiology of myocarditis due to other causes, Alida L.P. Caforio, MD, of Padua (Italy) University said in an interview. Myocarditis is traditionally a disease of the young, and most cases are immune-mediated and do not release troponin.

Moreover, myocarditis is a diagnosis of exclusion. For it to be made with any certainty requires proof, by biopsy or autopsy, of inflammatory infiltrates within the myocardium with myocyte necrosis not typical of myocardial infarction, said Dr. Caforio, who chaired the European Society of Cardiology’s writing committee for its 2013 position statement on myocardial and pericardial diseases.

“We have one biopsy-proven case, and in this case there were no viruses in the myocardium, including COVID-19,” she said. “There’s no proof that we have COVID-19 causing myocarditis because it has not been found in the cardiomyocytes.”
 

Emerging evidence

The virus-negative case from Lombardy, Italy, followed an early case series suggesting fulminant myocarditis was involved in 7% of COVID-related deaths in Wuhan, China.

Other case reports include cardiac magnetic resonance (CMR) findings typical of acute myocarditis in a man with no lung involvement or fever but a massive troponin spike, and myocarditis presenting as reverse takotsubo syndrome in a woman undergoing CMR and endomyocardial biopsy.

A CMR analysis in May said acute myocarditis, by 2018 Lake Louise Criteria, was present in eight of 10 patients with “myocarditis-like syndrome,” and a study just out June 30 said the coronavirus can infect heart cells in a lab dish.

Among the few autopsy series, a preprint on 12 patients with COVID-19 in the Seattle area showed coronavirus in the heart tissue of 1 patient.

“It was a low level, so there’s the possibility that it could be viremia, but the fact we do see actual cardiomyocyte injury associated with inflammation, that’s a myocarditis pattern. So it could be related to the SARS-CoV-2 virus,” said Desiree Marshall, MD, director of autopsy and after-death services, University of Washington Medical Center, Seattle.

The “waters are a little bit muddy,” however, because the patient had a coinfection clinically with influenza and methicillin-susceptible Staphylococcus aureus, which raises the specter that influenza could also have contributed, she said.

Data pending publication from two additional patients show no coronavirus in the heart. Acute respiratory distress syndrome pathology was common in all patients, but there was no evidence of vascular inflammation, such as endotheliitis, Dr. Marshall said.

SARS-CoV-2 cell entry depends on the angiotensin-converting enzyme 2 (ACE2) receptor, which is widely expressed in the heart and on endothelial cells and is linked to inflammatory activation. Autopsy data from three COVID-19 patients showed endothelial cell infection in the heart and diffuse endothelial inflammation, but no sign of lymphocytic myocarditis.
 

Defining myocarditis

“There are some experts who believe we’re likely still dealing with myocarditis but with atypical features, while others suggest there is no myocarditis by strict classic criteria,” said Peter Liu, MD, chief scientific officer/vice president of research, University of Ottawa Heart Institute.

“I don’t think either extreme is accurate,” he said. “The truth is likely somewhere in between, with evidence of both cardiac injury and inflammation. But nothing in COVID-19, as we know today, is classic; it’s a new disease, so we need to be more open minded as new data emerge.”

Part of the divide may indeed stem from the way myocarditis is defined. “Based on traditional Dallas criteria, classic myocarditis requires evidence of myocyte necrosis, which we have, but also inflammatory cell infiltrate, which we don’t consistently have,” he said. “But on the other hand, there is evidence of inflammation-induced cardiac damage, often aggregated around blood vessels.”

The situation is evolving in recent days, and new data under review demonstrated inflammatory infiltrates, which fits the traditional myocarditis criteria, Dr. Liu noted. Yet the viral etiology for the inflammation is still elusive in definitive proof.

In traditional myocarditis, there is an abundance of lymphocytes and foci of inflammation in the myocardium, but COVID-19 is very unusual, in that these lymphocytes are not as exuberant, he said. Lymphopenia or low lymphocyte counts occur in up to 80% of patients. Also, older patients, who initially made up the bulk of the severe COVID-19 cases, are less T-lymphocyte responsive.

“So the lower your lymphocyte count, the worse your outcome is going to be and the more likely you’re going to get cytokine storm,” Dr. Liu said. “And that may be the reason the suspected myocarditis in COVID-19 is atypical because the lymphocytes, in fact, are being suppressed and there is instead more vasculitis.”

Recent data from myocardial gene expression analysis showed that the viral receptor ACE2 is present in the myocardium, and can be upregulated in conditions such as heart failure, he said. However, the highest ACE2 expression is found in pericytes around blood vessels, not myocytes. “This may explain the preferential vascular involvement often observed.”
 

Cardiac damage in the young

Evidence started evolving in early April that young COVID-19 patients without lung disease, generally in their 20s and 30s, can have very high troponin peaks and a form of cardiac damage that does not appear to be related to sepsis, systemic shock, or cytokine storm.

“That’s the group that I do think has some myocarditis, but it’s different. It’s not lymphocytic myocarditis, like enteroviral myocarditis,” Leslie T. Cooper Jr., MD, a myocarditis expert at Mayo Clinic, Jacksonville, Florida, said in an interview.

“The data to date suggest that most SARS cardiac injury is related to stress or high circulating cytokine levels. However, myocarditis probably does affect some patients, he added. “The few published cases suggest a role for macrophages or endothelial cells, which could affect cardiac myocyte function. This type of injury could cause the ST-segment elevation MI-like patterns we have seen in young people with normal epicardial coronary arteries.”

Dr. Cooper, who coauthored a report on the management of COVID-19 cardiovascular syndrome, pointed out that it’s been hard for researchers to isolate genome from autopsy samples because of RNA degradation prior to autopsy and the use of formalin fixation for tissues prior to RNA extraction.

“Most labs are not doing next-generation sequencing, and even with that, RNA protection and fresh tissue may be required to detect viral genome,” he said.
 

No proven therapy

Although up to 50% of acute myocarditis cases undergo spontaneous healing, recognition and multidisciplinary management of clinically suspected myocarditis is important. The optimal treatment remains unclear.

An early case report suggested use of methylprednisolone and intravenous immunoglobulin helped spare the life of a 37-year-old with clinically suspected fulminant myocarditis with cardiogenic shock.

In a related commentary, Dr. Caforio and colleagues pointed out that the World Health Organization considers the use of IV corticosteroids controversial, even in pneumonia due to COVID-19, because it may reduce viral clearance and increase sepsis risk. Intravenous immunoglobulin is also questionable because there is no IgG response to COVID-19 in the plasma donors’ pool.

“Immunosuppression should be reserved for only virus-negative non-COVID myocarditis,” Dr. Caforio said in an interview. “There is no appropriate treatment nowadays for clinically suspected COVID-19 myocarditis. There is no proven therapy for COVID-19, even less for COVID-19 myocarditis.”

Although definitive publication of the RECOVERY trial is still pending, the benefits of dexamethasone – a steroid that works predominantly through its anti-inflammatory effects – appear to be in the sickest patients, such as those requiring ICU admission or respiratory support.

“Many of the same patients would have systemic inflammation and would have also shown elevated cardiac biomarkers,” Dr. Liu observed. “Therefore, it is conceivable that a subset who had cardiac inflammation also benefited from the treatment. Further data, possibly through subgroup analysis and eventually meta-analysis, may help us to understand if dexamethasone also benefited patients with dominant cardiac injury.”

Dr. Caforio, Dr. Marshall, Dr. Liu, and Dr. Cooper reported having no relevant conflicts of interest.

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

The COVID-19 literature has been peppered with reports about myocarditis accompanying the disease. If true, this could, in part, explain some of the observed cardiac injury and arrhythmias in seriously ill patients, but also have implications for prognosis.

But endomyocardial biopsies and autopsies, the gold-standard confirmation tests, have been few and far between. That has led some cardiologists to question the true rate of myocarditis with SARS-CoV-2, or even if there is definitive proof the virus causes myocarditis.

Predictors of death in COVID-19 are older age, cardiovascular comorbidities, and elevated troponin or NT-proBNP – none of which actually fit well with the epidemiology of myocarditis due to other causes, Alida L.P. Caforio, MD, of Padua (Italy) University said in an interview. Myocarditis is traditionally a disease of the young, and most cases are immune-mediated and do not release troponin.

Moreover, myocarditis is a diagnosis of exclusion. For it to be made with any certainty requires proof, by biopsy or autopsy, of inflammatory infiltrates within the myocardium with myocyte necrosis not typical of myocardial infarction, said Dr. Caforio, who chaired the European Society of Cardiology’s writing committee for its 2013 position statement on myocardial and pericardial diseases.

“We have one biopsy-proven case, and in this case there were no viruses in the myocardium, including COVID-19,” she said. “There’s no proof that we have COVID-19 causing myocarditis because it has not been found in the cardiomyocytes.”
 

Emerging evidence

The virus-negative case from Lombardy, Italy, followed an early case series suggesting fulminant myocarditis was involved in 7% of COVID-related deaths in Wuhan, China.

Other case reports include cardiac magnetic resonance (CMR) findings typical of acute myocarditis in a man with no lung involvement or fever but a massive troponin spike, and myocarditis presenting as reverse takotsubo syndrome in a woman undergoing CMR and endomyocardial biopsy.

A CMR analysis in May said acute myocarditis, by 2018 Lake Louise Criteria, was present in eight of 10 patients with “myocarditis-like syndrome,” and a study just out June 30 said the coronavirus can infect heart cells in a lab dish.

Among the few autopsy series, a preprint on 12 patients with COVID-19 in the Seattle area showed coronavirus in the heart tissue of 1 patient.

“It was a low level, so there’s the possibility that it could be viremia, but the fact we do see actual cardiomyocyte injury associated with inflammation, that’s a myocarditis pattern. So it could be related to the SARS-CoV-2 virus,” said Desiree Marshall, MD, director of autopsy and after-death services, University of Washington Medical Center, Seattle.

The “waters are a little bit muddy,” however, because the patient had a coinfection clinically with influenza and methicillin-susceptible Staphylococcus aureus, which raises the specter that influenza could also have contributed, she said.

Data pending publication from two additional patients show no coronavirus in the heart. Acute respiratory distress syndrome pathology was common in all patients, but there was no evidence of vascular inflammation, such as endotheliitis, Dr. Marshall said.

SARS-CoV-2 cell entry depends on the angiotensin-converting enzyme 2 (ACE2) receptor, which is widely expressed in the heart and on endothelial cells and is linked to inflammatory activation. Autopsy data from three COVID-19 patients showed endothelial cell infection in the heart and diffuse endothelial inflammation, but no sign of lymphocytic myocarditis.
 

Defining myocarditis

“There are some experts who believe we’re likely still dealing with myocarditis but with atypical features, while others suggest there is no myocarditis by strict classic criteria,” said Peter Liu, MD, chief scientific officer/vice president of research, University of Ottawa Heart Institute.

“I don’t think either extreme is accurate,” he said. “The truth is likely somewhere in between, with evidence of both cardiac injury and inflammation. But nothing in COVID-19, as we know today, is classic; it’s a new disease, so we need to be more open minded as new data emerge.”

Part of the divide may indeed stem from the way myocarditis is defined. “Based on traditional Dallas criteria, classic myocarditis requires evidence of myocyte necrosis, which we have, but also inflammatory cell infiltrate, which we don’t consistently have,” he said. “But on the other hand, there is evidence of inflammation-induced cardiac damage, often aggregated around blood vessels.”

The situation is evolving in recent days, and new data under review demonstrated inflammatory infiltrates, which fits the traditional myocarditis criteria, Dr. Liu noted. Yet the viral etiology for the inflammation is still elusive in definitive proof.

In traditional myocarditis, there is an abundance of lymphocytes and foci of inflammation in the myocardium, but COVID-19 is very unusual, in that these lymphocytes are not as exuberant, he said. Lymphopenia or low lymphocyte counts occur in up to 80% of patients. Also, older patients, who initially made up the bulk of the severe COVID-19 cases, are less T-lymphocyte responsive.

“So the lower your lymphocyte count, the worse your outcome is going to be and the more likely you’re going to get cytokine storm,” Dr. Liu said. “And that may be the reason the suspected myocarditis in COVID-19 is atypical because the lymphocytes, in fact, are being suppressed and there is instead more vasculitis.”

Recent data from myocardial gene expression analysis showed that the viral receptor ACE2 is present in the myocardium, and can be upregulated in conditions such as heart failure, he said. However, the highest ACE2 expression is found in pericytes around blood vessels, not myocytes. “This may explain the preferential vascular involvement often observed.”
 

Cardiac damage in the young

Evidence started evolving in early April that young COVID-19 patients without lung disease, generally in their 20s and 30s, can have very high troponin peaks and a form of cardiac damage that does not appear to be related to sepsis, systemic shock, or cytokine storm.

“That’s the group that I do think has some myocarditis, but it’s different. It’s not lymphocytic myocarditis, like enteroviral myocarditis,” Leslie T. Cooper Jr., MD, a myocarditis expert at Mayo Clinic, Jacksonville, Florida, said in an interview.

“The data to date suggest that most SARS cardiac injury is related to stress or high circulating cytokine levels. However, myocarditis probably does affect some patients, he added. “The few published cases suggest a role for macrophages or endothelial cells, which could affect cardiac myocyte function. This type of injury could cause the ST-segment elevation MI-like patterns we have seen in young people with normal epicardial coronary arteries.”

Dr. Cooper, who coauthored a report on the management of COVID-19 cardiovascular syndrome, pointed out that it’s been hard for researchers to isolate genome from autopsy samples because of RNA degradation prior to autopsy and the use of formalin fixation for tissues prior to RNA extraction.

“Most labs are not doing next-generation sequencing, and even with that, RNA protection and fresh tissue may be required to detect viral genome,” he said.
 

No proven therapy

Although up to 50% of acute myocarditis cases undergo spontaneous healing, recognition and multidisciplinary management of clinically suspected myocarditis is important. The optimal treatment remains unclear.

An early case report suggested use of methylprednisolone and intravenous immunoglobulin helped spare the life of a 37-year-old with clinically suspected fulminant myocarditis with cardiogenic shock.

In a related commentary, Dr. Caforio and colleagues pointed out that the World Health Organization considers the use of IV corticosteroids controversial, even in pneumonia due to COVID-19, because it may reduce viral clearance and increase sepsis risk. Intravenous immunoglobulin is also questionable because there is no IgG response to COVID-19 in the plasma donors’ pool.

“Immunosuppression should be reserved for only virus-negative non-COVID myocarditis,” Dr. Caforio said in an interview. “There is no appropriate treatment nowadays for clinically suspected COVID-19 myocarditis. There is no proven therapy for COVID-19, even less for COVID-19 myocarditis.”

Although definitive publication of the RECOVERY trial is still pending, the benefits of dexamethasone – a steroid that works predominantly through its anti-inflammatory effects – appear to be in the sickest patients, such as those requiring ICU admission or respiratory support.

“Many of the same patients would have systemic inflammation and would have also shown elevated cardiac biomarkers,” Dr. Liu observed. “Therefore, it is conceivable that a subset who had cardiac inflammation also benefited from the treatment. Further data, possibly through subgroup analysis and eventually meta-analysis, may help us to understand if dexamethasone also benefited patients with dominant cardiac injury.”

Dr. Caforio, Dr. Marshall, Dr. Liu, and Dr. Cooper reported having no relevant conflicts of interest.

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

The COVID-19 literature has been peppered with reports about myocarditis accompanying the disease. If true, this could, in part, explain some of the observed cardiac injury and arrhythmias in seriously ill patients, but also have implications for prognosis.

But endomyocardial biopsies and autopsies, the gold-standard confirmation tests, have been few and far between. That has led some cardiologists to question the true rate of myocarditis with SARS-CoV-2, or even if there is definitive proof the virus causes myocarditis.

Predictors of death in COVID-19 are older age, cardiovascular comorbidities, and elevated troponin or NT-proBNP – none of which actually fit well with the epidemiology of myocarditis due to other causes, Alida L.P. Caforio, MD, of Padua (Italy) University said in an interview. Myocarditis is traditionally a disease of the young, and most cases are immune-mediated and do not release troponin.

Moreover, myocarditis is a diagnosis of exclusion. For it to be made with any certainty requires proof, by biopsy or autopsy, of inflammatory infiltrates within the myocardium with myocyte necrosis not typical of myocardial infarction, said Dr. Caforio, who chaired the European Society of Cardiology’s writing committee for its 2013 position statement on myocardial and pericardial diseases.

“We have one biopsy-proven case, and in this case there were no viruses in the myocardium, including COVID-19,” she said. “There’s no proof that we have COVID-19 causing myocarditis because it has not been found in the cardiomyocytes.”
 

Emerging evidence

The virus-negative case from Lombardy, Italy, followed an early case series suggesting fulminant myocarditis was involved in 7% of COVID-related deaths in Wuhan, China.

Other case reports include cardiac magnetic resonance (CMR) findings typical of acute myocarditis in a man with no lung involvement or fever but a massive troponin spike, and myocarditis presenting as reverse takotsubo syndrome in a woman undergoing CMR and endomyocardial biopsy.

A CMR analysis in May said acute myocarditis, by 2018 Lake Louise Criteria, was present in eight of 10 patients with “myocarditis-like syndrome,” and a study just out June 30 said the coronavirus can infect heart cells in a lab dish.

Among the few autopsy series, a preprint on 12 patients with COVID-19 in the Seattle area showed coronavirus in the heart tissue of 1 patient.

“It was a low level, so there’s the possibility that it could be viremia, but the fact we do see actual cardiomyocyte injury associated with inflammation, that’s a myocarditis pattern. So it could be related to the SARS-CoV-2 virus,” said Desiree Marshall, MD, director of autopsy and after-death services, University of Washington Medical Center, Seattle.

The “waters are a little bit muddy,” however, because the patient had a coinfection clinically with influenza and methicillin-susceptible Staphylococcus aureus, which raises the specter that influenza could also have contributed, she said.

Data pending publication from two additional patients show no coronavirus in the heart. Acute respiratory distress syndrome pathology was common in all patients, but there was no evidence of vascular inflammation, such as endotheliitis, Dr. Marshall said.

SARS-CoV-2 cell entry depends on the angiotensin-converting enzyme 2 (ACE2) receptor, which is widely expressed in the heart and on endothelial cells and is linked to inflammatory activation. Autopsy data from three COVID-19 patients showed endothelial cell infection in the heart and diffuse endothelial inflammation, but no sign of lymphocytic myocarditis.
 

Defining myocarditis

“There are some experts who believe we’re likely still dealing with myocarditis but with atypical features, while others suggest there is no myocarditis by strict classic criteria,” said Peter Liu, MD, chief scientific officer/vice president of research, University of Ottawa Heart Institute.

“I don’t think either extreme is accurate,” he said. “The truth is likely somewhere in between, with evidence of both cardiac injury and inflammation. But nothing in COVID-19, as we know today, is classic; it’s a new disease, so we need to be more open minded as new data emerge.”

Part of the divide may indeed stem from the way myocarditis is defined. “Based on traditional Dallas criteria, classic myocarditis requires evidence of myocyte necrosis, which we have, but also inflammatory cell infiltrate, which we don’t consistently have,” he said. “But on the other hand, there is evidence of inflammation-induced cardiac damage, often aggregated around blood vessels.”

The situation is evolving in recent days, and new data under review demonstrated inflammatory infiltrates, which fits the traditional myocarditis criteria, Dr. Liu noted. Yet the viral etiology for the inflammation is still elusive in definitive proof.

In traditional myocarditis, there is an abundance of lymphocytes and foci of inflammation in the myocardium, but COVID-19 is very unusual, in that these lymphocytes are not as exuberant, he said. Lymphopenia or low lymphocyte counts occur in up to 80% of patients. Also, older patients, who initially made up the bulk of the severe COVID-19 cases, are less T-lymphocyte responsive.

“So the lower your lymphocyte count, the worse your outcome is going to be and the more likely you’re going to get cytokine storm,” Dr. Liu said. “And that may be the reason the suspected myocarditis in COVID-19 is atypical because the lymphocytes, in fact, are being suppressed and there is instead more vasculitis.”

Recent data from myocardial gene expression analysis showed that the viral receptor ACE2 is present in the myocardium, and can be upregulated in conditions such as heart failure, he said. However, the highest ACE2 expression is found in pericytes around blood vessels, not myocytes. “This may explain the preferential vascular involvement often observed.”
 

Cardiac damage in the young

Evidence started evolving in early April that young COVID-19 patients without lung disease, generally in their 20s and 30s, can have very high troponin peaks and a form of cardiac damage that does not appear to be related to sepsis, systemic shock, or cytokine storm.

“That’s the group that I do think has some myocarditis, but it’s different. It’s not lymphocytic myocarditis, like enteroviral myocarditis,” Leslie T. Cooper Jr., MD, a myocarditis expert at Mayo Clinic, Jacksonville, Florida, said in an interview.

“The data to date suggest that most SARS cardiac injury is related to stress or high circulating cytokine levels. However, myocarditis probably does affect some patients, he added. “The few published cases suggest a role for macrophages or endothelial cells, which could affect cardiac myocyte function. This type of injury could cause the ST-segment elevation MI-like patterns we have seen in young people with normal epicardial coronary arteries.”

Dr. Cooper, who coauthored a report on the management of COVID-19 cardiovascular syndrome, pointed out that it’s been hard for researchers to isolate genome from autopsy samples because of RNA degradation prior to autopsy and the use of formalin fixation for tissues prior to RNA extraction.

“Most labs are not doing next-generation sequencing, and even with that, RNA protection and fresh tissue may be required to detect viral genome,” he said.
 

No proven therapy

Although up to 50% of acute myocarditis cases undergo spontaneous healing, recognition and multidisciplinary management of clinically suspected myocarditis is important. The optimal treatment remains unclear.

An early case report suggested use of methylprednisolone and intravenous immunoglobulin helped spare the life of a 37-year-old with clinically suspected fulminant myocarditis with cardiogenic shock.

In a related commentary, Dr. Caforio and colleagues pointed out that the World Health Organization considers the use of IV corticosteroids controversial, even in pneumonia due to COVID-19, because it may reduce viral clearance and increase sepsis risk. Intravenous immunoglobulin is also questionable because there is no IgG response to COVID-19 in the plasma donors’ pool.

“Immunosuppression should be reserved for only virus-negative non-COVID myocarditis,” Dr. Caforio said in an interview. “There is no appropriate treatment nowadays for clinically suspected COVID-19 myocarditis. There is no proven therapy for COVID-19, even less for COVID-19 myocarditis.”

Although definitive publication of the RECOVERY trial is still pending, the benefits of dexamethasone – a steroid that works predominantly through its anti-inflammatory effects – appear to be in the sickest patients, such as those requiring ICU admission or respiratory support.

“Many of the same patients would have systemic inflammation and would have also shown elevated cardiac biomarkers,” Dr. Liu observed. “Therefore, it is conceivable that a subset who had cardiac inflammation also benefited from the treatment. Further data, possibly through subgroup analysis and eventually meta-analysis, may help us to understand if dexamethasone also benefited patients with dominant cardiac injury.”

Dr. Caforio, Dr. Marshall, Dr. Liu, and Dr. Cooper reported having no relevant conflicts of interest.

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

As more jurisdictions mandate facial coverings in public, questions have arisen about whether it’s safe for everyone – including those with lung disease – to wear masks. Stories about people who claim to be unable to wear masks because of breathing problems are appearing in the news with increasing frequency, and patients are starting to call their doctors to request medical exemptions to public mask requirements.

David Fuentes Prieto/Shutterstock

To address these issues, Medscape spoke with the chief medical officer of the American Lung Association, Dr. Albert Rizzo.
 

The CDC recommendations on mask wearing say, “Cloth face coverings should not be placed on young children under age 2, anyone who has trouble breathing, or is unconscious, incapacitated, or otherwise unable to remove the mask without assistance.” Does this language suggest that there indeed is a subset of the adult population with lung disease who shouldn’t wear masks?

It makes sense to say that if it makes you uncomfortable to wear a mask because it affects your breathing, you should think twice about getting in a situation where you would have to wear a mask.

I’ve told many of my high-risk patients, “The best way to avoid getting COVID-19 is to stay home and stay away from sick people, especially if you feel that you are not going to be able to wear a mask or facial covering of some sort.”

The reason that some people have trouble with a mask is that they haven’t tried the right style of mask – by that I mean how tightly it fits and the material it’s made out of. Sometimes it really is just that people with lung disease don’t like to have anything covering their faces. Many of these patients feel better where there is air blowing across their faces – they will have a fan blowing even in the middle of winter because they feel more comfortable.

I won’t say it’s all in their heads, but sometimes it’s a matter of desensitizing themselves to wearing a mask. I liken it to people who have sleep apnea. We often have to desensitize them to wearing a mask for sleeping. We tell them to put it on while they are watching TV — don’t hook it up to anything yet, just get used to having something on your face.

I’ve told my patients the same thing about masks for COVID-19. Put on the mask, see how it feels. If you become uncomfortable breathing with it on, take it off, but maybe you can handle it for a half hour or 45 minutes. Find out how much time you have for a trip to the grocery store based on how comfortable you are wearing it at home.

It’s a matter of training the patient, giving them options of how to get comfortable with it, and then making them realize that they have to weigh the benefits and risks of wearing the mask and feeling out of breath versus going out in public and being potentially exposed to coronavirus. And the bottom line is, anybody who is wearing a mask and starts to feel uncomfortable, they can take the mask off.
 

You mentioned different types of masks. Is there a type of mask that is typically more breathable that clinicians can recommend to patients with lung disease?

First, I remind patients who think they will have trouble breathing with a mask on that they are choosing a mask not so much to protect themselves – that would take an N95 mask to filter out the virus. The mask is worn so that when they cough or drink or speak, they aren’t sending respiratory droplets out into the environment. Even when we speak, respiratory droplets can easily go out as far as 6 feet, or further with coughing or sneezing. With facial coverings, we try to keep those respiratory droplets from getting out and infecting others.

So when choosing a mask, you don’t have to worry as much about a tight-fitting mask. I recommend a loose-fitting mask that covers the nose and mouth and isn’t going to fall off but isn’t so tight around the ears and neck to make them feel uncomfortable. Even though it doesn’t really protect the wearer, it is cutting down on the ability to breathe in droplets – maybe not microscopic particles, but it’s better than nothing.
 

Is a face shield a reasonable alternative for someone who feels they can’t breathe with a mask on?

Yes. I’m surprised that face shields don’t get more attention. I’ve tried them out, and they are actually more comfortable than masks. They do impede the spilling out of droplets into the public, but they are not as close fitting to the face as a mask. If you want to protect others, the face shield should be adequate. It is not as good at preventing you from breathing in viral particles.

Some people have claimed that wearing a mask makes them hyperventilate and feel like they are going to pass out, or the mask causes them to become hypoxic. Are these valid concerns?

We get two questions about masks from patients who feel that they are short of breath or are worried about wearing a mask. One is whether their oxygen level is dropping. It’s usually not that. It’s usually because they feel that the mask is an impediment to getting air in. Their oxygen levels are stable.

The other question is whether the mask causes CO₂ retention. For the mask to trap enough exhaled CO₂ and for us to breathe enough of that CO₂ back in to raise our CO₂ level, it has to be a pretty tight-fitting mask. With the type of masks we are suggesting that people wear, that’s very unlikely to occur.
 

What can clinicians do to reassure patients with some type of lung disease that they can safely wear masks?

There are a few things they can do right in the office. Have them put the mask on for a few minutes and make sure they feel comfortable with it. With an oximeter, patients can see that their oxygen levels don’t change when they are breathing through the mask for a period of time.

You can’t really measure CO₂ retention that easily, but most patients with chronic obstructive pulmonary disease or pulmonary fibrosis don’t have an elevated CO₂ at baseline. A little more education is helpful in those situations. In most cases, they aren’t going to retain enough CO₂ to have problems wearing a mask.

Only a small percentage of patients with lung disease are CO₂ retainers, and many of those patients are being seen by pulmonary specialists. Those are the patients you might want to be more cautious with, to make sure they aren’t wearing anything that is tight fitting or that makes them work harder to breathe. It’s not that the mask is causing CO₂ retention, but the increased work of breathing may make it harder to exhale the CO₂.
 

Does a mask interfere with supplemental oxygen in any way?

Supplemental oxygen is typically supplied through a nasal cannula, so 100% oxygen is still getting to the nasal passages and entrained down into the airway, so it shouldn’t be a problem.

Some of the resistance to wearing masks has come from people with asthma. Is it safe for patients with asthma to wear masks, or should these patients be exempt from wearing masks?

In general, the breathing of people with mild asthma, both young and old, should not be impeded by the wearing of facial coverings. The concerns about oxygen and carbon dioxide among patients with more severe lung disease should not play a role in asthma.

Since younger adults with COVID-19 seem to have fewer or no symptoms and may actually be carrying the virus unknowingly, this should be the main population who should wear masks to prevent transmission to others.

Exemptions for mask wearing for mild asthma should be discouraged and dealt with on a case-by-case basis if there is a particular concern for that individual.
 

How do you respond if a patient asks you for a formal medical exemption to wearing a mask?

We’ve been asked to do a lot of letter writing for patients around going back to work, as well as the issue of wearing masks. The discussion usually revolves around trying to avoid going somewhere where you would have to wear a mask if it makes you feel uncomfortable.

I do not recommend automatically exempting individuals from wearing masks, even many of my pulmonary patients. There needs to be an understanding by the patient regarding the purpose of the mask and the overall advice to stay out of situations where social distancing is not being practiced. If you can take the time to discuss options as mentioned above – mask styles, desensitization, etc – the patient usually understands and will try wearing a mask.

On a case-by-case basis, some individuals may need to be exempted, but I feel this is a small number. I prefer my high-risk (older, chronic disease, etc) patients do everything they can to avoid infection – handwashing, mask wearing, and socially distancing.

They should also realize that even with a note, it is not going to help if they are in the middle of the grocery store and someone confronts them about not wearing a mask. It may help as they enter a store that says “masks required” and they can show it to someone monitoring the door. But I’m not really sure in what situations having that note is going to be helpful if confrontations occur.

Patients are also asking how safe is it for them to go back to work and be out in public. I tell them, nothing is going to be 100% safe. Until we have an effective vaccine, we are all going to have to weigh the potential risks of going to an area where social distancing isn’t maintained, people aren’t wearing face masks, and you can’t wash your hands as much as you’d like to. That’s going to be a struggle for all of us to get back out into situations where people interact socially.

Albert A. Rizzo, MD, is chief medical officer for the American Lung Association, chief of the Section of Pulmonary and Critical Care Medicine at the Christiana Care Health System in Newark, Delaware, and a member of Christiana Care Pulmonary Associates. He is board certified in internal medicine, pulmonary medicine, critical care medicine, and sleep medicine and is a clinical assistant professor of medicine at Thomas Jefferson University Medical School, Philadelphia.

This article first appeared on Medscape.com.

As more jurisdictions mandate facial coverings in public, questions have arisen about whether it’s safe for everyone – including those with lung disease – to wear masks. Stories about people who claim to be unable to wear masks because of breathing problems are appearing in the news with increasing frequency, and patients are starting to call their doctors to request medical exemptions to public mask requirements.

David Fuentes Prieto/Shutterstock

To address these issues, Medscape spoke with the chief medical officer of the American Lung Association, Dr. Albert Rizzo.
 

The CDC recommendations on mask wearing say, “Cloth face coverings should not be placed on young children under age 2, anyone who has trouble breathing, or is unconscious, incapacitated, or otherwise unable to remove the mask without assistance.” Does this language suggest that there indeed is a subset of the adult population with lung disease who shouldn’t wear masks?

It makes sense to say that if it makes you uncomfortable to wear a mask because it affects your breathing, you should think twice about getting in a situation where you would have to wear a mask.

I’ve told many of my high-risk patients, “The best way to avoid getting COVID-19 is to stay home and stay away from sick people, especially if you feel that you are not going to be able to wear a mask or facial covering of some sort.”

The reason that some people have trouble with a mask is that they haven’t tried the right style of mask – by that I mean how tightly it fits and the material it’s made out of. Sometimes it really is just that people with lung disease don’t like to have anything covering their faces. Many of these patients feel better where there is air blowing across their faces – they will have a fan blowing even in the middle of winter because they feel more comfortable.

I won’t say it’s all in their heads, but sometimes it’s a matter of desensitizing themselves to wearing a mask. I liken it to people who have sleep apnea. We often have to desensitize them to wearing a mask for sleeping. We tell them to put it on while they are watching TV — don’t hook it up to anything yet, just get used to having something on your face.

I’ve told my patients the same thing about masks for COVID-19. Put on the mask, see how it feels. If you become uncomfortable breathing with it on, take it off, but maybe you can handle it for a half hour or 45 minutes. Find out how much time you have for a trip to the grocery store based on how comfortable you are wearing it at home.

It’s a matter of training the patient, giving them options of how to get comfortable with it, and then making them realize that they have to weigh the benefits and risks of wearing the mask and feeling out of breath versus going out in public and being potentially exposed to coronavirus. And the bottom line is, anybody who is wearing a mask and starts to feel uncomfortable, they can take the mask off.
 

You mentioned different types of masks. Is there a type of mask that is typically more breathable that clinicians can recommend to patients with lung disease?

First, I remind patients who think they will have trouble breathing with a mask on that they are choosing a mask not so much to protect themselves – that would take an N95 mask to filter out the virus. The mask is worn so that when they cough or drink or speak, they aren’t sending respiratory droplets out into the environment. Even when we speak, respiratory droplets can easily go out as far as 6 feet, or further with coughing or sneezing. With facial coverings, we try to keep those respiratory droplets from getting out and infecting others.

So when choosing a mask, you don’t have to worry as much about a tight-fitting mask. I recommend a loose-fitting mask that covers the nose and mouth and isn’t going to fall off but isn’t so tight around the ears and neck to make them feel uncomfortable. Even though it doesn’t really protect the wearer, it is cutting down on the ability to breathe in droplets – maybe not microscopic particles, but it’s better than nothing.
 

Is a face shield a reasonable alternative for someone who feels they can’t breathe with a mask on?

Yes. I’m surprised that face shields don’t get more attention. I’ve tried them out, and they are actually more comfortable than masks. They do impede the spilling out of droplets into the public, but they are not as close fitting to the face as a mask. If you want to protect others, the face shield should be adequate. It is not as good at preventing you from breathing in viral particles.

Some people have claimed that wearing a mask makes them hyperventilate and feel like they are going to pass out, or the mask causes them to become hypoxic. Are these valid concerns?

We get two questions about masks from patients who feel that they are short of breath or are worried about wearing a mask. One is whether their oxygen level is dropping. It’s usually not that. It’s usually because they feel that the mask is an impediment to getting air in. Their oxygen levels are stable.

The other question is whether the mask causes CO₂ retention. For the mask to trap enough exhaled CO₂ and for us to breathe enough of that CO₂ back in to raise our CO₂ level, it has to be a pretty tight-fitting mask. With the type of masks we are suggesting that people wear, that’s very unlikely to occur.
 

What can clinicians do to reassure patients with some type of lung disease that they can safely wear masks?

There are a few things they can do right in the office. Have them put the mask on for a few minutes and make sure they feel comfortable with it. With an oximeter, patients can see that their oxygen levels don’t change when they are breathing through the mask for a period of time.

You can’t really measure CO₂ retention that easily, but most patients with chronic obstructive pulmonary disease or pulmonary fibrosis don’t have an elevated CO₂ at baseline. A little more education is helpful in those situations. In most cases, they aren’t going to retain enough CO₂ to have problems wearing a mask.

Only a small percentage of patients with lung disease are CO₂ retainers, and many of those patients are being seen by pulmonary specialists. Those are the patients you might want to be more cautious with, to make sure they aren’t wearing anything that is tight fitting or that makes them work harder to breathe. It’s not that the mask is causing CO₂ retention, but the increased work of breathing may make it harder to exhale the CO₂.
 

Does a mask interfere with supplemental oxygen in any way?

Supplemental oxygen is typically supplied through a nasal cannula, so 100% oxygen is still getting to the nasal passages and entrained down into the airway, so it shouldn’t be a problem.

Some of the resistance to wearing masks has come from people with asthma. Is it safe for patients with asthma to wear masks, or should these patients be exempt from wearing masks?

In general, the breathing of people with mild asthma, both young and old, should not be impeded by the wearing of facial coverings. The concerns about oxygen and carbon dioxide among patients with more severe lung disease should not play a role in asthma.

Since younger adults with COVID-19 seem to have fewer or no symptoms and may actually be carrying the virus unknowingly, this should be the main population who should wear masks to prevent transmission to others.

Exemptions for mask wearing for mild asthma should be discouraged and dealt with on a case-by-case basis if there is a particular concern for that individual.
 

How do you respond if a patient asks you for a formal medical exemption to wearing a mask?

We’ve been asked to do a lot of letter writing for patients around going back to work, as well as the issue of wearing masks. The discussion usually revolves around trying to avoid going somewhere where you would have to wear a mask if it makes you feel uncomfortable.

I do not recommend automatically exempting individuals from wearing masks, even many of my pulmonary patients. There needs to be an understanding by the patient regarding the purpose of the mask and the overall advice to stay out of situations where social distancing is not being practiced. If you can take the time to discuss options as mentioned above – mask styles, desensitization, etc – the patient usually understands and will try wearing a mask.

On a case-by-case basis, some individuals may need to be exempted, but I feel this is a small number. I prefer my high-risk (older, chronic disease, etc) patients do everything they can to avoid infection – handwashing, mask wearing, and socially distancing.

They should also realize that even with a note, it is not going to help if they are in the middle of the grocery store and someone confronts them about not wearing a mask. It may help as they enter a store that says “masks required” and they can show it to someone monitoring the door. But I’m not really sure in what situations having that note is going to be helpful if confrontations occur.

Patients are also asking how safe is it for them to go back to work and be out in public. I tell them, nothing is going to be 100% safe. Until we have an effective vaccine, we are all going to have to weigh the potential risks of going to an area where social distancing isn’t maintained, people aren’t wearing face masks, and you can’t wash your hands as much as you’d like to. That’s going to be a struggle for all of us to get back out into situations where people interact socially.

Albert A. Rizzo, MD, is chief medical officer for the American Lung Association, chief of the Section of Pulmonary and Critical Care Medicine at the Christiana Care Health System in Newark, Delaware, and a member of Christiana Care Pulmonary Associates. He is board certified in internal medicine, pulmonary medicine, critical care medicine, and sleep medicine and is a clinical assistant professor of medicine at Thomas Jefferson University Medical School, Philadelphia.

This article first appeared on Medscape.com.

As more jurisdictions mandate facial coverings in public, questions have arisen about whether it’s safe for everyone – including those with lung disease – to wear masks. Stories about people who claim to be unable to wear masks because of breathing problems are appearing in the news with increasing frequency, and patients are starting to call their doctors to request medical exemptions to public mask requirements.

David Fuentes Prieto/Shutterstock

To address these issues, Medscape spoke with the chief medical officer of the American Lung Association, Dr. Albert Rizzo.
 

The CDC recommendations on mask wearing say, “Cloth face coverings should not be placed on young children under age 2, anyone who has trouble breathing, or is unconscious, incapacitated, or otherwise unable to remove the mask without assistance.” Does this language suggest that there indeed is a subset of the adult population with lung disease who shouldn’t wear masks?

It makes sense to say that if it makes you uncomfortable to wear a mask because it affects your breathing, you should think twice about getting in a situation where you would have to wear a mask.

I’ve told many of my high-risk patients, “The best way to avoid getting COVID-19 is to stay home and stay away from sick people, especially if you feel that you are not going to be able to wear a mask or facial covering of some sort.”

The reason that some people have trouble with a mask is that they haven’t tried the right style of mask – by that I mean how tightly it fits and the material it’s made out of. Sometimes it really is just that people with lung disease don’t like to have anything covering their faces. Many of these patients feel better where there is air blowing across their faces – they will have a fan blowing even in the middle of winter because they feel more comfortable.

I won’t say it’s all in their heads, but sometimes it’s a matter of desensitizing themselves to wearing a mask. I liken it to people who have sleep apnea. We often have to desensitize them to wearing a mask for sleeping. We tell them to put it on while they are watching TV — don’t hook it up to anything yet, just get used to having something on your face.

I’ve told my patients the same thing about masks for COVID-19. Put on the mask, see how it feels. If you become uncomfortable breathing with it on, take it off, but maybe you can handle it for a half hour or 45 minutes. Find out how much time you have for a trip to the grocery store based on how comfortable you are wearing it at home.

It’s a matter of training the patient, giving them options of how to get comfortable with it, and then making them realize that they have to weigh the benefits and risks of wearing the mask and feeling out of breath versus going out in public and being potentially exposed to coronavirus. And the bottom line is, anybody who is wearing a mask and starts to feel uncomfortable, they can take the mask off.
 

You mentioned different types of masks. Is there a type of mask that is typically more breathable that clinicians can recommend to patients with lung disease?

First, I remind patients who think they will have trouble breathing with a mask on that they are choosing a mask not so much to protect themselves – that would take an N95 mask to filter out the virus. The mask is worn so that when they cough or drink or speak, they aren’t sending respiratory droplets out into the environment. Even when we speak, respiratory droplets can easily go out as far as 6 feet, or further with coughing or sneezing. With facial coverings, we try to keep those respiratory droplets from getting out and infecting others.

So when choosing a mask, you don’t have to worry as much about a tight-fitting mask. I recommend a loose-fitting mask that covers the nose and mouth and isn’t going to fall off but isn’t so tight around the ears and neck to make them feel uncomfortable. Even though it doesn’t really protect the wearer, it is cutting down on the ability to breathe in droplets – maybe not microscopic particles, but it’s better than nothing.
 

Is a face shield a reasonable alternative for someone who feels they can’t breathe with a mask on?

Yes. I’m surprised that face shields don’t get more attention. I’ve tried them out, and they are actually more comfortable than masks. They do impede the spilling out of droplets into the public, but they are not as close fitting to the face as a mask. If you want to protect others, the face shield should be adequate. It is not as good at preventing you from breathing in viral particles.

Some people have claimed that wearing a mask makes them hyperventilate and feel like they are going to pass out, or the mask causes them to become hypoxic. Are these valid concerns?

We get two questions about masks from patients who feel that they are short of breath or are worried about wearing a mask. One is whether their oxygen level is dropping. It’s usually not that. It’s usually because they feel that the mask is an impediment to getting air in. Their oxygen levels are stable.

The other question is whether the mask causes CO₂ retention. For the mask to trap enough exhaled CO₂ and for us to breathe enough of that CO₂ back in to raise our CO₂ level, it has to be a pretty tight-fitting mask. With the type of masks we are suggesting that people wear, that’s very unlikely to occur.
 

What can clinicians do to reassure patients with some type of lung disease that they can safely wear masks?

There are a few things they can do right in the office. Have them put the mask on for a few minutes and make sure they feel comfortable with it. With an oximeter, patients can see that their oxygen levels don’t change when they are breathing through the mask for a period of time.

You can’t really measure CO₂ retention that easily, but most patients with chronic obstructive pulmonary disease or pulmonary fibrosis don’t have an elevated CO₂ at baseline. A little more education is helpful in those situations. In most cases, they aren’t going to retain enough CO₂ to have problems wearing a mask.

Only a small percentage of patients with lung disease are CO₂ retainers, and many of those patients are being seen by pulmonary specialists. Those are the patients you might want to be more cautious with, to make sure they aren’t wearing anything that is tight fitting or that makes them work harder to breathe. It’s not that the mask is causing CO₂ retention, but the increased work of breathing may make it harder to exhale the CO₂.
 

Does a mask interfere with supplemental oxygen in any way?

Supplemental oxygen is typically supplied through a nasal cannula, so 100% oxygen is still getting to the nasal passages and entrained down into the airway, so it shouldn’t be a problem.

Some of the resistance to wearing masks has come from people with asthma. Is it safe for patients with asthma to wear masks, or should these patients be exempt from wearing masks?

In general, the breathing of people with mild asthma, both young and old, should not be impeded by the wearing of facial coverings. The concerns about oxygen and carbon dioxide among patients with more severe lung disease should not play a role in asthma.

Since younger adults with COVID-19 seem to have fewer or no symptoms and may actually be carrying the virus unknowingly, this should be the main population who should wear masks to prevent transmission to others.

Exemptions for mask wearing for mild asthma should be discouraged and dealt with on a case-by-case basis if there is a particular concern for that individual.
 

How do you respond if a patient asks you for a formal medical exemption to wearing a mask?

We’ve been asked to do a lot of letter writing for patients around going back to work, as well as the issue of wearing masks. The discussion usually revolves around trying to avoid going somewhere where you would have to wear a mask if it makes you feel uncomfortable.

I do not recommend automatically exempting individuals from wearing masks, even many of my pulmonary patients. There needs to be an understanding by the patient regarding the purpose of the mask and the overall advice to stay out of situations where social distancing is not being practiced. If you can take the time to discuss options as mentioned above – mask styles, desensitization, etc – the patient usually understands and will try wearing a mask.

On a case-by-case basis, some individuals may need to be exempted, but I feel this is a small number. I prefer my high-risk (older, chronic disease, etc) patients do everything they can to avoid infection – handwashing, mask wearing, and socially distancing.

They should also realize that even with a note, it is not going to help if they are in the middle of the grocery store and someone confronts them about not wearing a mask. It may help as they enter a store that says “masks required” and they can show it to someone monitoring the door. But I’m not really sure in what situations having that note is going to be helpful if confrontations occur.

Patients are also asking how safe is it for them to go back to work and be out in public. I tell them, nothing is going to be 100% safe. Until we have an effective vaccine, we are all going to have to weigh the potential risks of going to an area where social distancing isn’t maintained, people aren’t wearing face masks, and you can’t wash your hands as much as you’d like to. That’s going to be a struggle for all of us to get back out into situations where people interact socially.

Albert A. Rizzo, MD, is chief medical officer for the American Lung Association, chief of the Section of Pulmonary and Critical Care Medicine at the Christiana Care Health System in Newark, Delaware, and a member of Christiana Care Pulmonary Associates. He is board certified in internal medicine, pulmonary medicine, critical care medicine, and sleep medicine and is a clinical assistant professor of medicine at Thomas Jefferson University Medical School, Philadelphia.

This article first appeared on Medscape.com.

A small number of U.S. health systems, as well as some individual physicians, have begun dropping the African American–specific modifier when recording estimated glomerular filtration rate (eGFR), a measure of renal function.

The move aims to correct a race-based health access inequity that’s been in place for more than 2 decades, say advocates, while others voice concern that the change threatens over-diagnosis of both chronic and end-stage kidney disease in some patients.

In late June, the Boston-based Massachusetts General Brigham health system stopped noting the race-based modifier when its laboratories reported eGFR, and the leadership sent its staff a message discouraging them from applying the modifier. A similar change in eGFR reporting started on June 1 at the University of Washington health system, UW Medicine, Seattle.

These steps followed what is widely regarded as the first institutional change away from race-based adjustment of eGFR, which began in March 2017 at Beth Israel Deaconess Medical Center in Boston, and they have come amid a growing movement by some individual U.S. physicians to drop the modifier from their practice.

“Momentum is clearly building,” said Nwamaka D. Eneanya, MD, a nephrologist at the University of Pennsylvania in Philadelphia and lead author of a commentary published a little more than a year ago that laid out the case for reconsidering how to calculate eGFR in African Americans.

“Many discussions are happening at other [US] academic medical centers,” Dr. Eneanya added, including the system where she works.
 

Why was the decision taken to modify eGFR in African Americans?

The concept is that the formula used to calculate eGFR systematically underestimates the value in African Americans. Hence, it requires a small but meaningful up-adjustment, which can be traced back to the introduction of the Modification of Diet in Renal Disease (MDRD) study equation in 1999.

The idea was perpetuated in an improved calculation formula, the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), that came out a decade later.

These are the most widely used U.S. approaches to eGFR calculation, with the newer CKD-EPI formula predominating.

The rationale for including a modifier for Blacks in the 2009 formula was for improved accuracy relative to the standard reference measure based on iothalamate clearance.

The data used to develop the CKD-EPI formula showed that Black individuals in the dataset had, on average, GFR levels that were 16% higher than people of other races with the same age, sex, and serum creatinine level, according to a recent commentary. The first author, Andrew S. Levey, MD, was also lead author of the reports that introduced both the MDRD and CKD-EPI equations.

But the argument withers in the light of both its flimsy underpinning – race assessment – and the medical and social consequences of its application, say those who have sought change.
 

Reporting eGFR by race might do more harm than good

“Race is a social, not a biological, construct and the kidney-function race multiplier ignores the substantial genetic diversity within self-identified Black patients,” said Thomas D. Sequist, MD, professor of medicine at Harvard Medical School in Boston and chief patient experience and equity officer for Mass General Brigham, who spearheaded the policy change for that system.

“Do we really believe that the population breaks down into just ‘Black’ and ‘not Black,’ as the CKD-EPI equation asks us to believe?” he said in an interview. “The equation was developed from a few thousand patients, and we now apply it to millions of people using a very imprecise measure – race.”

“Reporting eGFR by race perpetuates a notion that race is a biologic construct when it’s not,” agreed Rajnish Mehrotra, MD, a professor and chief of nephrology at the University of Washington in Seattle and leader of the eGFR change within his medical system.

Equally compelling, said Dr. Mehrotra, Dr. Sequist, and others, are the health inequities that have resulted from routinely raising the eGFR in African Americans.

This has led to “withholding treatment from people longer than needed. We arrived at the conclusion that reporting eGFR by race does more harm than good,” Dr. Mehrotra said in an interview.

Dr. Sequist added: “Researchers across Mass General Brigham have demonstrated that use of these race multipliers can lead to important delays in care for Black patients, such as timely evaluation for kidney transplantation.”

“Our main concern is that race correction is creating harm.”

Dr. Eneanya concurs: “It was never designed to oppress patients, but that’s where we are. No one ever thought about the repercussions of using race.”

And while the movement to eliminate the race modifier is clearly gaining steam, it’s also receiving pushback from those who see benefit from the modification and have concern that its abolition could lead to overestimates of kidney disease severity.

Some clinicians “have a hard time letting the race modifier go,” Dr. Eneanya noted.
 

“In the nephrology community, it’s pretty controversial”

In their 2020 commentary, Levey and coauthors wrote: “We propose a more cautious approach that maintains and improves accuracy of GFR estimates and avoids disadvantaging any racial group.”

Their suggested remedies included full disclosure of use of race, accommodation of people who decline to self-identify themselves that way, shared decision-making, and “mindful” use of cystatin C, an alternative to serum creatinine for calculating eGFR.

The latter is regarded as more precise and accurate than serum creatinine across populations but is often not as readily available to many clinicians. Their article also supported looking for even better and more accessible ways to calculate eGFR.

“In the nephrology community, it’s pretty controversial,” said Mallika L. Mendu, MD, a nephrologist at Brigham and Women’s Hospital in Boston, Massachusetts, who has studied the effects of using the modifier on patient assessment.

Her recent review of Mass General Brigham patients found that close to a third of African Americans would have been reclassified with a more severe form of kidney disease if their eGFR had remained unmodified.

“That raised concerns that, by using race adjustment we’re potentially leading to less equitable outcomes for African American patients,” she said. “I’d rather over diagnose than not diagnose in a timely way.”

The research that led to development of the MDRD and CKD-EPI equations “are gold-standard studies” that “saw a real difference,” Dr. Mendu acknowledged in an interview. “But the way those studies were run and the way they defined the patients was problematic.” Despite that, “many nephrologists” agree with the position taken by Dr. Levey and coauthors in their recent commentary, she said.

She added that she stopped using the modifier about a year ago in her own practice, well before the system where she works adopted the same approach.
 

Consensus takes time

In one sign of the controversy, a quartet of clinicians affiliated with San Francisco General Hospital (SFGH) recently posted an online petition in which they noted that the race modifier had been eliminated in eGFR reports from the hospital’s laboratory in October 2019, but more recently had been slated for reinstitution. “We were deeply distressed to recently discover the intended plan to revert back to race-based eGFR reporting at SFGH,” they noted.

The same four clinicians also wrote an opinion piece calling for elimination of the modifier in November 2019 in the San Francisco Examiner.

Controversy will likely linger as the movement to withdraw the race modifier spreads without clear agreement on what to do instead.

Dr. Mehrotra said he’s received inquiries about his system’s experience from clinicians at several U.S. medical centers and systems, and he remains comfortable applying the unadjusted CKD-EPI formula to all adults, an approach he called “sufficient.”

Other physicians, like nephrologist Vanessa Grubbs, MD, call for a rapid shift to a cystatin C–based, fully race-neutral method for calculating eGFR, a position she detailed in a recent editorial.

And at the University of Pennsylvania, where the health system continues to issue eGFR reports with the race modifier, Dr. Eneanya says that she stopped using the modifier “some time” ago.

“People have a hard time letting it go because it is so important in clinical care. Getting everyone to come to a consensus takes time,” she said.

Dr. Eneanya, Dr. Sequist, and Dr. Mendu have reported no relevant financial relationships. Dr. Mehrotra has been a consultant for Baxter Healthcare.

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

A small number of U.S. health systems, as well as some individual physicians, have begun dropping the African American–specific modifier when recording estimated glomerular filtration rate (eGFR), a measure of renal function.

The move aims to correct a race-based health access inequity that’s been in place for more than 2 decades, say advocates, while others voice concern that the change threatens over-diagnosis of both chronic and end-stage kidney disease in some patients.

In late June, the Boston-based Massachusetts General Brigham health system stopped noting the race-based modifier when its laboratories reported eGFR, and the leadership sent its staff a message discouraging them from applying the modifier. A similar change in eGFR reporting started on June 1 at the University of Washington health system, UW Medicine, Seattle.

These steps followed what is widely regarded as the first institutional change away from race-based adjustment of eGFR, which began in March 2017 at Beth Israel Deaconess Medical Center in Boston, and they have come amid a growing movement by some individual U.S. physicians to drop the modifier from their practice.

“Momentum is clearly building,” said Nwamaka D. Eneanya, MD, a nephrologist at the University of Pennsylvania in Philadelphia and lead author of a commentary published a little more than a year ago that laid out the case for reconsidering how to calculate eGFR in African Americans.

“Many discussions are happening at other [US] academic medical centers,” Dr. Eneanya added, including the system where she works.
 

Why was the decision taken to modify eGFR in African Americans?

The concept is that the formula used to calculate eGFR systematically underestimates the value in African Americans. Hence, it requires a small but meaningful up-adjustment, which can be traced back to the introduction of the Modification of Diet in Renal Disease (MDRD) study equation in 1999.

The idea was perpetuated in an improved calculation formula, the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), that came out a decade later.

These are the most widely used U.S. approaches to eGFR calculation, with the newer CKD-EPI formula predominating.

The rationale for including a modifier for Blacks in the 2009 formula was for improved accuracy relative to the standard reference measure based on iothalamate clearance.

The data used to develop the CKD-EPI formula showed that Black individuals in the dataset had, on average, GFR levels that were 16% higher than people of other races with the same age, sex, and serum creatinine level, according to a recent commentary. The first author, Andrew S. Levey, MD, was also lead author of the reports that introduced both the MDRD and CKD-EPI equations.

But the argument withers in the light of both its flimsy underpinning – race assessment – and the medical and social consequences of its application, say those who have sought change.
 

Reporting eGFR by race might do more harm than good

“Race is a social, not a biological, construct and the kidney-function race multiplier ignores the substantial genetic diversity within self-identified Black patients,” said Thomas D. Sequist, MD, professor of medicine at Harvard Medical School in Boston and chief patient experience and equity officer for Mass General Brigham, who spearheaded the policy change for that system.

“Do we really believe that the population breaks down into just ‘Black’ and ‘not Black,’ as the CKD-EPI equation asks us to believe?” he said in an interview. “The equation was developed from a few thousand patients, and we now apply it to millions of people using a very imprecise measure – race.”

“Reporting eGFR by race perpetuates a notion that race is a biologic construct when it’s not,” agreed Rajnish Mehrotra, MD, a professor and chief of nephrology at the University of Washington in Seattle and leader of the eGFR change within his medical system.

Equally compelling, said Dr. Mehrotra, Dr. Sequist, and others, are the health inequities that have resulted from routinely raising the eGFR in African Americans.

This has led to “withholding treatment from people longer than needed. We arrived at the conclusion that reporting eGFR by race does more harm than good,” Dr. Mehrotra said in an interview.

Dr. Sequist added: “Researchers across Mass General Brigham have demonstrated that use of these race multipliers can lead to important delays in care for Black patients, such as timely evaluation for kidney transplantation.”

“Our main concern is that race correction is creating harm.”

Dr. Eneanya concurs: “It was never designed to oppress patients, but that’s where we are. No one ever thought about the repercussions of using race.”

And while the movement to eliminate the race modifier is clearly gaining steam, it’s also receiving pushback from those who see benefit from the modification and have concern that its abolition could lead to overestimates of kidney disease severity.

Some clinicians “have a hard time letting the race modifier go,” Dr. Eneanya noted.
 

“In the nephrology community, it’s pretty controversial”

In their 2020 commentary, Levey and coauthors wrote: “We propose a more cautious approach that maintains and improves accuracy of GFR estimates and avoids disadvantaging any racial group.”

Their suggested remedies included full disclosure of use of race, accommodation of people who decline to self-identify themselves that way, shared decision-making, and “mindful” use of cystatin C, an alternative to serum creatinine for calculating eGFR.

The latter is regarded as more precise and accurate than serum creatinine across populations but is often not as readily available to many clinicians. Their article also supported looking for even better and more accessible ways to calculate eGFR.

“In the nephrology community, it’s pretty controversial,” said Mallika L. Mendu, MD, a nephrologist at Brigham and Women’s Hospital in Boston, Massachusetts, who has studied the effects of using the modifier on patient assessment.

Her recent review of Mass General Brigham patients found that close to a third of African Americans would have been reclassified with a more severe form of kidney disease if their eGFR had remained unmodified.

“That raised concerns that, by using race adjustment we’re potentially leading to less equitable outcomes for African American patients,” she said. “I’d rather over diagnose than not diagnose in a timely way.”

The research that led to development of the MDRD and CKD-EPI equations “are gold-standard studies” that “saw a real difference,” Dr. Mendu acknowledged in an interview. “But the way those studies were run and the way they defined the patients was problematic.” Despite that, “many nephrologists” agree with the position taken by Dr. Levey and coauthors in their recent commentary, she said.

She added that she stopped using the modifier about a year ago in her own practice, well before the system where she works adopted the same approach.
 

Consensus takes time

In one sign of the controversy, a quartet of clinicians affiliated with San Francisco General Hospital (SFGH) recently posted an online petition in which they noted that the race modifier had been eliminated in eGFR reports from the hospital’s laboratory in October 2019, but more recently had been slated for reinstitution. “We were deeply distressed to recently discover the intended plan to revert back to race-based eGFR reporting at SFGH,” they noted.

The same four clinicians also wrote an opinion piece calling for elimination of the modifier in November 2019 in the San Francisco Examiner.

Controversy will likely linger as the movement to withdraw the race modifier spreads without clear agreement on what to do instead.

Dr. Mehrotra said he’s received inquiries about his system’s experience from clinicians at several U.S. medical centers and systems, and he remains comfortable applying the unadjusted CKD-EPI formula to all adults, an approach he called “sufficient.”

Other physicians, like nephrologist Vanessa Grubbs, MD, call for a rapid shift to a cystatin C–based, fully race-neutral method for calculating eGFR, a position she detailed in a recent editorial.

And at the University of Pennsylvania, where the health system continues to issue eGFR reports with the race modifier, Dr. Eneanya says that she stopped using the modifier “some time” ago.

“People have a hard time letting it go because it is so important in clinical care. Getting everyone to come to a consensus takes time,” she said.

Dr. Eneanya, Dr. Sequist, and Dr. Mendu have reported no relevant financial relationships. Dr. Mehrotra has been a consultant for Baxter Healthcare.

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

A small number of U.S. health systems, as well as some individual physicians, have begun dropping the African American–specific modifier when recording estimated glomerular filtration rate (eGFR), a measure of renal function.

The move aims to correct a race-based health access inequity that’s been in place for more than 2 decades, say advocates, while others voice concern that the change threatens over-diagnosis of both chronic and end-stage kidney disease in some patients.

In late June, the Boston-based Massachusetts General Brigham health system stopped noting the race-based modifier when its laboratories reported eGFR, and the leadership sent its staff a message discouraging them from applying the modifier. A similar change in eGFR reporting started on June 1 at the University of Washington health system, UW Medicine, Seattle.

These steps followed what is widely regarded as the first institutional change away from race-based adjustment of eGFR, which began in March 2017 at Beth Israel Deaconess Medical Center in Boston, and they have come amid a growing movement by some individual U.S. physicians to drop the modifier from their practice.

“Momentum is clearly building,” said Nwamaka D. Eneanya, MD, a nephrologist at the University of Pennsylvania in Philadelphia and lead author of a commentary published a little more than a year ago that laid out the case for reconsidering how to calculate eGFR in African Americans.

“Many discussions are happening at other [US] academic medical centers,” Dr. Eneanya added, including the system where she works.
 

Why was the decision taken to modify eGFR in African Americans?

The concept is that the formula used to calculate eGFR systematically underestimates the value in African Americans. Hence, it requires a small but meaningful up-adjustment, which can be traced back to the introduction of the Modification of Diet in Renal Disease (MDRD) study equation in 1999.

The idea was perpetuated in an improved calculation formula, the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), that came out a decade later.

These are the most widely used U.S. approaches to eGFR calculation, with the newer CKD-EPI formula predominating.

The rationale for including a modifier for Blacks in the 2009 formula was for improved accuracy relative to the standard reference measure based on iothalamate clearance.

The data used to develop the CKD-EPI formula showed that Black individuals in the dataset had, on average, GFR levels that were 16% higher than people of other races with the same age, sex, and serum creatinine level, according to a recent commentary. The first author, Andrew S. Levey, MD, was also lead author of the reports that introduced both the MDRD and CKD-EPI equations.

But the argument withers in the light of both its flimsy underpinning – race assessment – and the medical and social consequences of its application, say those who have sought change.
 

Reporting eGFR by race might do more harm than good

“Race is a social, not a biological, construct and the kidney-function race multiplier ignores the substantial genetic diversity within self-identified Black patients,” said Thomas D. Sequist, MD, professor of medicine at Harvard Medical School in Boston and chief patient experience and equity officer for Mass General Brigham, who spearheaded the policy change for that system.

“Do we really believe that the population breaks down into just ‘Black’ and ‘not Black,’ as the CKD-EPI equation asks us to believe?” he said in an interview. “The equation was developed from a few thousand patients, and we now apply it to millions of people using a very imprecise measure – race.”

“Reporting eGFR by race perpetuates a notion that race is a biologic construct when it’s not,” agreed Rajnish Mehrotra, MD, a professor and chief of nephrology at the University of Washington in Seattle and leader of the eGFR change within his medical system.

Equally compelling, said Dr. Mehrotra, Dr. Sequist, and others, are the health inequities that have resulted from routinely raising the eGFR in African Americans.

This has led to “withholding treatment from people longer than needed. We arrived at the conclusion that reporting eGFR by race does more harm than good,” Dr. Mehrotra said in an interview.

Dr. Sequist added: “Researchers across Mass General Brigham have demonstrated that use of these race multipliers can lead to important delays in care for Black patients, such as timely evaluation for kidney transplantation.”

“Our main concern is that race correction is creating harm.”

Dr. Eneanya concurs: “It was never designed to oppress patients, but that’s where we are. No one ever thought about the repercussions of using race.”

And while the movement to eliminate the race modifier is clearly gaining steam, it’s also receiving pushback from those who see benefit from the modification and have concern that its abolition could lead to overestimates of kidney disease severity.

Some clinicians “have a hard time letting the race modifier go,” Dr. Eneanya noted.
 

“In the nephrology community, it’s pretty controversial”

In their 2020 commentary, Levey and coauthors wrote: “We propose a more cautious approach that maintains and improves accuracy of GFR estimates and avoids disadvantaging any racial group.”

Their suggested remedies included full disclosure of use of race, accommodation of people who decline to self-identify themselves that way, shared decision-making, and “mindful” use of cystatin C, an alternative to serum creatinine for calculating eGFR.

The latter is regarded as more precise and accurate than serum creatinine across populations but is often not as readily available to many clinicians. Their article also supported looking for even better and more accessible ways to calculate eGFR.

“In the nephrology community, it’s pretty controversial,” said Mallika L. Mendu, MD, a nephrologist at Brigham and Women’s Hospital in Boston, Massachusetts, who has studied the effects of using the modifier on patient assessment.

Her recent review of Mass General Brigham patients found that close to a third of African Americans would have been reclassified with a more severe form of kidney disease if their eGFR had remained unmodified.

“That raised concerns that, by using race adjustment we’re potentially leading to less equitable outcomes for African American patients,” she said. “I’d rather over diagnose than not diagnose in a timely way.”

The research that led to development of the MDRD and CKD-EPI equations “are gold-standard studies” that “saw a real difference,” Dr. Mendu acknowledged in an interview. “But the way those studies were run and the way they defined the patients was problematic.” Despite that, “many nephrologists” agree with the position taken by Dr. Levey and coauthors in their recent commentary, she said.

She added that she stopped using the modifier about a year ago in her own practice, well before the system where she works adopted the same approach.
 

Consensus takes time

In one sign of the controversy, a quartet of clinicians affiliated with San Francisco General Hospital (SFGH) recently posted an online petition in which they noted that the race modifier had been eliminated in eGFR reports from the hospital’s laboratory in October 2019, but more recently had been slated for reinstitution. “We were deeply distressed to recently discover the intended plan to revert back to race-based eGFR reporting at SFGH,” they noted.

The same four clinicians also wrote an opinion piece calling for elimination of the modifier in November 2019 in the San Francisco Examiner.

Controversy will likely linger as the movement to withdraw the race modifier spreads without clear agreement on what to do instead.

Dr. Mehrotra said he’s received inquiries about his system’s experience from clinicians at several U.S. medical centers and systems, and he remains comfortable applying the unadjusted CKD-EPI formula to all adults, an approach he called “sufficient.”

Other physicians, like nephrologist Vanessa Grubbs, MD, call for a rapid shift to a cystatin C–based, fully race-neutral method for calculating eGFR, a position she detailed in a recent editorial.

And at the University of Pennsylvania, where the health system continues to issue eGFR reports with the race modifier, Dr. Eneanya says that she stopped using the modifier “some time” ago.

“People have a hard time letting it go because it is so important in clinical care. Getting everyone to come to a consensus takes time,” she said.

Dr. Eneanya, Dr. Sequist, and Dr. Mendu have reported no relevant financial relationships. Dr. Mehrotra has been a consultant for Baxter Healthcare.

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

During a family medicine rotation at Oregon Health & Sciences University, Portland, third-year medical students are preparing for a patient visit. Only, instead of entering a clinic room, students sit down at a computer. The patient they’re virtually examining – a 42-year-old male cattle rancher with knee problems – is an actor.

He asks for an MRI. A student explains that kneecap pain calls for rehab rather than a scan. The patient pushes back. “It would ease my mind,” he says. “I really need to make sure I can keep the ranch running.” The student must now try to digitally maintain rapport while explaining why imaging isn’t necessary.

When COVID-19 hit, telehealth training and remote learning became major parts of medical education, seemingly overnight. Since the start of the pandemic, students have contended with canceled classes, missed rotations, and revised training timelines, even as the demand for new doctors grows ever more pressing.

Institutions have been forced to rethink how to best establish solid, long-term foundations to ensure that young doctors are adequately trained. “They may find themselves the only doctors to be practicing in a small town,” said Stephen G. Post, PhD, bioethicist and professor at Stony Brook (N.Y.) University. “They have to be ready.”

With limited hands-on access to patients, students must learn in ways most never have before. Medical schools are now test-driving a mix of new and reimagined teaching strategies that aim to produce doctors who will enter medicine just as prepared as their more seasoned peers.

Hands-off education

Soon after starting her pediatrics rotation in March, recent Stanford (Calif.) University graduate Paloma Marin-Nevarez, MD, heard that children were being admitted to her hospital for evaluation to rule out COVID-19. Dr. Marin-Nevarez was assigned to help care for them but never physically met any – an approach called “virtual rounding.”

In virtual rounding, a provider typically goes in, examines a patient, and uses a portable device such as an iPad to send video or take notes about the encounter. Students or others in another room then give input on the patient’s care. “It was bizarre doing rounds on patients I had not met yet, discussing their treatment plans in one of the team rooms,” Dr. Marin-Nevarez said. “There was something very eerie about passing that particular unit that said: ‘Do not enter,’ and never being able to go inside.”

Within weeks, the Association of American Medical Colleges advised medical schools to suspend any activities – including clinical rotations – that involved direct student contact with patients, even those who weren’t COVID-19 positive.

Many schools hope to have students back and participating in some degree of patient care at non–COVID-19 hospital wards as early as July 1, said Michael Gisondi, MD, vice chair of education at Stanford’s department of emergency medicine. Returning students must now adapt to a restricted training environment, often while scrambling to make up training time. “This is uncharted territory for medical schools. Elective cases are down, surgical cases are down. That’s potentially going to decrease exposure to training opportunities.”

When students come back, lectures are still likely to remain on hold at most schools, replaced by Zoom conferences and virtual presentations. That’s not completely new: A trend away from large, traditional classes predated the pandemic. In a 2017-2018 AAMC survey, one in four second-year medical students said they almost never went to in-person lectures. COVID-19 has accelerated this shift.

For faculty who have long emphasized hands-on, in-person learning, the shift presents “a whole pedagogical issue – you don’t necessarily know how to adjust your practices to an online format,” Dr. Gisondi said. Instructors have to be even more flexible in order to engage students. “Every week I ask the students: ‘What’s working? What’s not working?’ ” Dr. Gisondi said about his online classes. “We have to solicit feedback.”

Changes to lectures are the easy part, says Elisabeth Fassas, a second-year student at the University of Maryland, Baltimore County. Before the pandemic, she was taking a clinical medicine course that involved time in the hospital, something that helped link the academic with the practical. “You really get to see the stuff you’re learning being relevant: ‘Here’s a patient who has a cardiology problem,’ ” she said. “[Capturing] that piece of connection to what you’re working toward is going to be tricky, I think.”

Some students who graduated this past spring worry about that clinical time they lost. Many remain acutely conscious of specific knowledge gaps. “I did not get a ton of experience examining crying children or holding babies,” said Dr. Marin-Nevarez, who starts an emergency medicine residency this year. “I am going to have to be transparent with my future instructors and let them know I missed out because of the pandemic.”

Such knowledge gaps mean new doctors will have to make up ground, said Jeremiah Tao, MD, who trains ophthalmology residents at the University of California, Irvine. But Dr. Tao doesn’t see these setbacks as a major long-term problem. His residents are already starting to make up the patient hours they missed in the spring and are refining the skills that got short shrift earlier on. For eligibility, “most boards require a certain number of days of experience. But most of the message from our board is [that] they’re understanding, and they’re going to leave it to the program directors to declare someone competent.”

Robert Johnson, MD, dean of New Jersey Medical School, Newark, said short-term setbacks in training likely won’t translate into longer-term skill deficits. “What most schools have done is overprepare students. We’re sure they have acquired all the skills they need to practice.”

Closing the gaps

To fill existing knowledge gaps and prevent future deficits, institutions hope to strike a balance between keeping trainees safe and providing necessary on-site learning. In line with ongoing AAMC recommendations, which suggest schools curtail student involvement in direct patient care in areas with significant COVID-19 spread, virtual rounding will likely continue.

Many schools may use a hybrid approach, in which students take turns entering patient rooms to perform checkups or observations while other students and instructors watch a video broadcast. “It’s not that different from when I go into the room and supervise a trainee,” Dr. Gisondi said.

Some schools are going even further, transforming education in ways that reflect the demands of a COVID-19–era medical marketplace. Institutions such as Weill Cornell Medicine, New York, and OHSU have invested in telemedicine training for years, but COVID-19 has given telehealth education an additional boost. These types of visits have surged dramatically, underscoring the importance of preparing new doctors to practice in a virtual setting – something that wasn’t common previously. In a 2019 survey, only about a quarter of sampled medical schools offered a telemedicine curriculum.

Simulated telehealth consults such as OHSU’s knee-pain scenario serve several purposes, says Ryan Palmer, EdD, associate dean of education at Northeast Ohio Universities, Rootstown. They virtually teach skills that students need – such as clearly explaining to patients why a care plan is called for – while allowing the trainees to practice forging an emotional connection with patients they are treating remotely.

“It’s less about how you use a specific system,” said Dr. Palmer, who developed OHSU’s TeleOSCE, a telehealth training system that has interested other schools. He sees this as an opportunity, inasmuch as telemedicine is likely to remain an important part of practice for the foreseeable future.

To that end, the AAMC recently hosted an online seminar to help faculty with telehealth instruction. But training such as this can only go so far, said Dr. Johnson. “There are techniques you do have to learn at the patient’s side.”

Dr. Johnson says that a traditional part of medical school at Rutgers has been having students spend time in general practitioners’ offices early on to see what the experience is like. “That’s going to be a problem – I expect many primary care practices will go out of business. Those types of shadowing experiences will probably go away. They may be replaced by experiences at larger clinics.”

Some learning in clinics may soon resume. Although fears about COVID-19 still loom large, Dr. Tao’s ophthalmology residents have started taking on something closer to a normal workload, thanks to patients returning for regular office visits. As people return to medical facilities in larger numbers, hospitals around the country have started separating patients with COVID-19 from others. Dr. Gisondi suggested that this means medical students may be able to circulate in non–COVID-19 wards, provided the institution has enough personal protective equipment. “The inpatient wards are really safe – there’s a low risk of transmission. That’s where core rotations occur.”

The road ahead

In settings where patients’ viral status remains uncertain, such as emergency wards and off-site clinics without rapid testing, in-person learning may be slower to resume. That’s where longer-term changes may come into play. Some schools are preparing digital learning platforms that have the potential to transform medical education.

For example, Haru Okuda, MD, an emergency medicine doctor and director of the Center for Advanced Medical Learning and Simulation at the University of South Florida, Tampa, is testing a new virtual-reality platform called Immertec. Dr. Okuda said that, unlike older teaching tools, the system is not a stale, static virtual environment that will become obsolete. Instead, it uses a live camera to visually teleport students into the space of a real clinic or operating room.

“Let’s say you have students learning gross anatomy, how to dissect the chest. You’d have a cadaver on the table, demonstrating anatomy. The student has a headset – you can see like you’re in the room.” The wraparound visual device allows students to watch surgical maneuvers close up or view additional input from devices such as laparoscopes.

Dr. Okuda acknowledges that educators don’t yet know whether this works as well as older, hands-on methods. As yet, no virtual reality system has touch-based sensors sophisticated enough to simulate even skills such as tying a basic surgical knot, Dr. Gisondi said. And immersive platforms are expensive, which means a gap may occur between schools that can afford them and those that can’t.

The long-term consequences of COVID-19 go beyond costs that institutions may have to bear. Some students are concerned that the pandemic is affecting their mental well-being in ways that may make training a tougher slog. A few students graduated early to serve on the COVID-19 front lines. Others, rather than planning trips to celebrate the gap between medical school and residency, watched from home as young doctors they knew worked under abusive and unsafe conditions.

“Many of us felt powerless, given what we saw happening around us,” said recent University of Michigan, Ann Arbor, graduate Marina Haque, MD. She thinks those feelings, along with the rigors of practicing medicine during a pandemic, may leave her and her colleagues more prone to burnout.

The pandemic has also had a galvanizing effect on students – some excited new doctors are eager to line up for duty on COVID-19 wards. But supervisors say they must weigh young doctors’ desire to serve against the possible risks. “You don’t want people who have a big future ahead of them rushing into these situations and getting severely ill,” said Dr. Post. “There is a balance.”

All these changes, temporary or lasting, have led many to question whether doctors who complete their training under the cloud of the pandemic will be more – or less – prepared than those who came before them. But it’s not really a question of better or worse, says Dr. Johnson, who stresses that medical education has always required flexibility.

“You come into medicine with a plan in mind, but things happen,” he said. He reflected on the HIV pandemic of the late 1980s and early 1990s that influenced his medical career. He hopes young doctors come through the COVID-19 crucible more seasoned, resilient, and confident in crisis situations. “This is a pivotal event in their lives, and it will shape many careers.”

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

During a family medicine rotation at Oregon Health & Sciences University, Portland, third-year medical students are preparing for a patient visit. Only, instead of entering a clinic room, students sit down at a computer. The patient they’re virtually examining – a 42-year-old male cattle rancher with knee problems – is an actor.

He asks for an MRI. A student explains that kneecap pain calls for rehab rather than a scan. The patient pushes back. “It would ease my mind,” he says. “I really need to make sure I can keep the ranch running.” The student must now try to digitally maintain rapport while explaining why imaging isn’t necessary.

When COVID-19 hit, telehealth training and remote learning became major parts of medical education, seemingly overnight. Since the start of the pandemic, students have contended with canceled classes, missed rotations, and revised training timelines, even as the demand for new doctors grows ever more pressing.

Institutions have been forced to rethink how to best establish solid, long-term foundations to ensure that young doctors are adequately trained. “They may find themselves the only doctors to be practicing in a small town,” said Stephen G. Post, PhD, bioethicist and professor at Stony Brook (N.Y.) University. “They have to be ready.”

With limited hands-on access to patients, students must learn in ways most never have before. Medical schools are now test-driving a mix of new and reimagined teaching strategies that aim to produce doctors who will enter medicine just as prepared as their more seasoned peers.

Hands-off education

Soon after starting her pediatrics rotation in March, recent Stanford (Calif.) University graduate Paloma Marin-Nevarez, MD, heard that children were being admitted to her hospital for evaluation to rule out COVID-19. Dr. Marin-Nevarez was assigned to help care for them but never physically met any – an approach called “virtual rounding.”

In virtual rounding, a provider typically goes in, examines a patient, and uses a portable device such as an iPad to send video or take notes about the encounter. Students or others in another room then give input on the patient’s care. “It was bizarre doing rounds on patients I had not met yet, discussing their treatment plans in one of the team rooms,” Dr. Marin-Nevarez said. “There was something very eerie about passing that particular unit that said: ‘Do not enter,’ and never being able to go inside.”

Within weeks, the Association of American Medical Colleges advised medical schools to suspend any activities – including clinical rotations – that involved direct student contact with patients, even those who weren’t COVID-19 positive.

Many schools hope to have students back and participating in some degree of patient care at non–COVID-19 hospital wards as early as July 1, said Michael Gisondi, MD, vice chair of education at Stanford’s department of emergency medicine. Returning students must now adapt to a restricted training environment, often while scrambling to make up training time. “This is uncharted territory for medical schools. Elective cases are down, surgical cases are down. That’s potentially going to decrease exposure to training opportunities.”

When students come back, lectures are still likely to remain on hold at most schools, replaced by Zoom conferences and virtual presentations. That’s not completely new: A trend away from large, traditional classes predated the pandemic. In a 2017-2018 AAMC survey, one in four second-year medical students said they almost never went to in-person lectures. COVID-19 has accelerated this shift.

For faculty who have long emphasized hands-on, in-person learning, the shift presents “a whole pedagogical issue – you don’t necessarily know how to adjust your practices to an online format,” Dr. Gisondi said. Instructors have to be even more flexible in order to engage students. “Every week I ask the students: ‘What’s working? What’s not working?’ ” Dr. Gisondi said about his online classes. “We have to solicit feedback.”

Changes to lectures are the easy part, says Elisabeth Fassas, a second-year student at the University of Maryland, Baltimore County. Before the pandemic, she was taking a clinical medicine course that involved time in the hospital, something that helped link the academic with the practical. “You really get to see the stuff you’re learning being relevant: ‘Here’s a patient who has a cardiology problem,’ ” she said. “[Capturing] that piece of connection to what you’re working toward is going to be tricky, I think.”

Some students who graduated this past spring worry about that clinical time they lost. Many remain acutely conscious of specific knowledge gaps. “I did not get a ton of experience examining crying children or holding babies,” said Dr. Marin-Nevarez, who starts an emergency medicine residency this year. “I am going to have to be transparent with my future instructors and let them know I missed out because of the pandemic.”

Such knowledge gaps mean new doctors will have to make up ground, said Jeremiah Tao, MD, who trains ophthalmology residents at the University of California, Irvine. But Dr. Tao doesn’t see these setbacks as a major long-term problem. His residents are already starting to make up the patient hours they missed in the spring and are refining the skills that got short shrift earlier on. For eligibility, “most boards require a certain number of days of experience. But most of the message from our board is [that] they’re understanding, and they’re going to leave it to the program directors to declare someone competent.”

Robert Johnson, MD, dean of New Jersey Medical School, Newark, said short-term setbacks in training likely won’t translate into longer-term skill deficits. “What most schools have done is overprepare students. We’re sure they have acquired all the skills they need to practice.”

Closing the gaps

To fill existing knowledge gaps and prevent future deficits, institutions hope to strike a balance between keeping trainees safe and providing necessary on-site learning. In line with ongoing AAMC recommendations, which suggest schools curtail student involvement in direct patient care in areas with significant COVID-19 spread, virtual rounding will likely continue.

Many schools may use a hybrid approach, in which students take turns entering patient rooms to perform checkups or observations while other students and instructors watch a video broadcast. “It’s not that different from when I go into the room and supervise a trainee,” Dr. Gisondi said.

Some schools are going even further, transforming education in ways that reflect the demands of a COVID-19–era medical marketplace. Institutions such as Weill Cornell Medicine, New York, and OHSU have invested in telemedicine training for years, but COVID-19 has given telehealth education an additional boost. These types of visits have surged dramatically, underscoring the importance of preparing new doctors to practice in a virtual setting – something that wasn’t common previously. In a 2019 survey, only about a quarter of sampled medical schools offered a telemedicine curriculum.

Simulated telehealth consults such as OHSU’s knee-pain scenario serve several purposes, says Ryan Palmer, EdD, associate dean of education at Northeast Ohio Universities, Rootstown. They virtually teach skills that students need – such as clearly explaining to patients why a care plan is called for – while allowing the trainees to practice forging an emotional connection with patients they are treating remotely.

“It’s less about how you use a specific system,” said Dr. Palmer, who developed OHSU’s TeleOSCE, a telehealth training system that has interested other schools. He sees this as an opportunity, inasmuch as telemedicine is likely to remain an important part of practice for the foreseeable future.

To that end, the AAMC recently hosted an online seminar to help faculty with telehealth instruction. But training such as this can only go so far, said Dr. Johnson. “There are techniques you do have to learn at the patient’s side.”

Dr. Johnson says that a traditional part of medical school at Rutgers has been having students spend time in general practitioners’ offices early on to see what the experience is like. “That’s going to be a problem – I expect many primary care practices will go out of business. Those types of shadowing experiences will probably go away. They may be replaced by experiences at larger clinics.”

Some learning in clinics may soon resume. Although fears about COVID-19 still loom large, Dr. Tao’s ophthalmology residents have started taking on something closer to a normal workload, thanks to patients returning for regular office visits. As people return to medical facilities in larger numbers, hospitals around the country have started separating patients with COVID-19 from others. Dr. Gisondi suggested that this means medical students may be able to circulate in non–COVID-19 wards, provided the institution has enough personal protective equipment. “The inpatient wards are really safe – there’s a low risk of transmission. That’s where core rotations occur.”

The road ahead

In settings where patients’ viral status remains uncertain, such as emergency wards and off-site clinics without rapid testing, in-person learning may be slower to resume. That’s where longer-term changes may come into play. Some schools are preparing digital learning platforms that have the potential to transform medical education.

For example, Haru Okuda, MD, an emergency medicine doctor and director of the Center for Advanced Medical Learning and Simulation at the University of South Florida, Tampa, is testing a new virtual-reality platform called Immertec. Dr. Okuda said that, unlike older teaching tools, the system is not a stale, static virtual environment that will become obsolete. Instead, it uses a live camera to visually teleport students into the space of a real clinic or operating room.

“Let’s say you have students learning gross anatomy, how to dissect the chest. You’d have a cadaver on the table, demonstrating anatomy. The student has a headset – you can see like you’re in the room.” The wraparound visual device allows students to watch surgical maneuvers close up or view additional input from devices such as laparoscopes.

Dr. Okuda acknowledges that educators don’t yet know whether this works as well as older, hands-on methods. As yet, no virtual reality system has touch-based sensors sophisticated enough to simulate even skills such as tying a basic surgical knot, Dr. Gisondi said. And immersive platforms are expensive, which means a gap may occur between schools that can afford them and those that can’t.

The long-term consequences of COVID-19 go beyond costs that institutions may have to bear. Some students are concerned that the pandemic is affecting their mental well-being in ways that may make training a tougher slog. A few students graduated early to serve on the COVID-19 front lines. Others, rather than planning trips to celebrate the gap between medical school and residency, watched from home as young doctors they knew worked under abusive and unsafe conditions.

“Many of us felt powerless, given what we saw happening around us,” said recent University of Michigan, Ann Arbor, graduate Marina Haque, MD. She thinks those feelings, along with the rigors of practicing medicine during a pandemic, may leave her and her colleagues more prone to burnout.

The pandemic has also had a galvanizing effect on students – some excited new doctors are eager to line up for duty on COVID-19 wards. But supervisors say they must weigh young doctors’ desire to serve against the possible risks. “You don’t want people who have a big future ahead of them rushing into these situations and getting severely ill,” said Dr. Post. “There is a balance.”

All these changes, temporary or lasting, have led many to question whether doctors who complete their training under the cloud of the pandemic will be more – or less – prepared than those who came before them. But it’s not really a question of better or worse, says Dr. Johnson, who stresses that medical education has always required flexibility.

“You come into medicine with a plan in mind, but things happen,” he said. He reflected on the HIV pandemic of the late 1980s and early 1990s that influenced his medical career. He hopes young doctors come through the COVID-19 crucible more seasoned, resilient, and confident in crisis situations. “This is a pivotal event in their lives, and it will shape many careers.”

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

During a family medicine rotation at Oregon Health & Sciences University, Portland, third-year medical students are preparing for a patient visit. Only, instead of entering a clinic room, students sit down at a computer. The patient they’re virtually examining – a 42-year-old male cattle rancher with knee problems – is an actor.

He asks for an MRI. A student explains that kneecap pain calls for rehab rather than a scan. The patient pushes back. “It would ease my mind,” he says. “I really need to make sure I can keep the ranch running.” The student must now try to digitally maintain rapport while explaining why imaging isn’t necessary.

When COVID-19 hit, telehealth training and remote learning became major parts of medical education, seemingly overnight. Since the start of the pandemic, students have contended with canceled classes, missed rotations, and revised training timelines, even as the demand for new doctors grows ever more pressing.

Institutions have been forced to rethink how to best establish solid, long-term foundations to ensure that young doctors are adequately trained. “They may find themselves the only doctors to be practicing in a small town,” said Stephen G. Post, PhD, bioethicist and professor at Stony Brook (N.Y.) University. “They have to be ready.”

With limited hands-on access to patients, students must learn in ways most never have before. Medical schools are now test-driving a mix of new and reimagined teaching strategies that aim to produce doctors who will enter medicine just as prepared as their more seasoned peers.

Hands-off education

Soon after starting her pediatrics rotation in March, recent Stanford (Calif.) University graduate Paloma Marin-Nevarez, MD, heard that children were being admitted to her hospital for evaluation to rule out COVID-19. Dr. Marin-Nevarez was assigned to help care for them but never physically met any – an approach called “virtual rounding.”

In virtual rounding, a provider typically goes in, examines a patient, and uses a portable device such as an iPad to send video or take notes about the encounter. Students or others in another room then give input on the patient’s care. “It was bizarre doing rounds on patients I had not met yet, discussing their treatment plans in one of the team rooms,” Dr. Marin-Nevarez said. “There was something very eerie about passing that particular unit that said: ‘Do not enter,’ and never being able to go inside.”

Within weeks, the Association of American Medical Colleges advised medical schools to suspend any activities – including clinical rotations – that involved direct student contact with patients, even those who weren’t COVID-19 positive.

Many schools hope to have students back and participating in some degree of patient care at non–COVID-19 hospital wards as early as July 1, said Michael Gisondi, MD, vice chair of education at Stanford’s department of emergency medicine. Returning students must now adapt to a restricted training environment, often while scrambling to make up training time. “This is uncharted territory for medical schools. Elective cases are down, surgical cases are down. That’s potentially going to decrease exposure to training opportunities.”

When students come back, lectures are still likely to remain on hold at most schools, replaced by Zoom conferences and virtual presentations. That’s not completely new: A trend away from large, traditional classes predated the pandemic. In a 2017-2018 AAMC survey, one in four second-year medical students said they almost never went to in-person lectures. COVID-19 has accelerated this shift.

For faculty who have long emphasized hands-on, in-person learning, the shift presents “a whole pedagogical issue – you don’t necessarily know how to adjust your practices to an online format,” Dr. Gisondi said. Instructors have to be even more flexible in order to engage students. “Every week I ask the students: ‘What’s working? What’s not working?’ ” Dr. Gisondi said about his online classes. “We have to solicit feedback.”

Changes to lectures are the easy part, says Elisabeth Fassas, a second-year student at the University of Maryland, Baltimore County. Before the pandemic, she was taking a clinical medicine course that involved time in the hospital, something that helped link the academic with the practical. “You really get to see the stuff you’re learning being relevant: ‘Here’s a patient who has a cardiology problem,’ ” she said. “[Capturing] that piece of connection to what you’re working toward is going to be tricky, I think.”

Some students who graduated this past spring worry about that clinical time they lost. Many remain acutely conscious of specific knowledge gaps. “I did not get a ton of experience examining crying children or holding babies,” said Dr. Marin-Nevarez, who starts an emergency medicine residency this year. “I am going to have to be transparent with my future instructors and let them know I missed out because of the pandemic.”

Such knowledge gaps mean new doctors will have to make up ground, said Jeremiah Tao, MD, who trains ophthalmology residents at the University of California, Irvine. But Dr. Tao doesn’t see these setbacks as a major long-term problem. His residents are already starting to make up the patient hours they missed in the spring and are refining the skills that got short shrift earlier on. For eligibility, “most boards require a certain number of days of experience. But most of the message from our board is [that] they’re understanding, and they’re going to leave it to the program directors to declare someone competent.”

Robert Johnson, MD, dean of New Jersey Medical School, Newark, said short-term setbacks in training likely won’t translate into longer-term skill deficits. “What most schools have done is overprepare students. We’re sure they have acquired all the skills they need to practice.”

Closing the gaps

To fill existing knowledge gaps and prevent future deficits, institutions hope to strike a balance between keeping trainees safe and providing necessary on-site learning. In line with ongoing AAMC recommendations, which suggest schools curtail student involvement in direct patient care in areas with significant COVID-19 spread, virtual rounding will likely continue.

Many schools may use a hybrid approach, in which students take turns entering patient rooms to perform checkups or observations while other students and instructors watch a video broadcast. “It’s not that different from when I go into the room and supervise a trainee,” Dr. Gisondi said.

Some schools are going even further, transforming education in ways that reflect the demands of a COVID-19–era medical marketplace. Institutions such as Weill Cornell Medicine, New York, and OHSU have invested in telemedicine training for years, but COVID-19 has given telehealth education an additional boost. These types of visits have surged dramatically, underscoring the importance of preparing new doctors to practice in a virtual setting – something that wasn’t common previously. In a 2019 survey, only about a quarter of sampled medical schools offered a telemedicine curriculum.

Simulated telehealth consults such as OHSU’s knee-pain scenario serve several purposes, says Ryan Palmer, EdD, associate dean of education at Northeast Ohio Universities, Rootstown. They virtually teach skills that students need – such as clearly explaining to patients why a care plan is called for – while allowing the trainees to practice forging an emotional connection with patients they are treating remotely.

“It’s less about how you use a specific system,” said Dr. Palmer, who developed OHSU’s TeleOSCE, a telehealth training system that has interested other schools. He sees this as an opportunity, inasmuch as telemedicine is likely to remain an important part of practice for the foreseeable future.

To that end, the AAMC recently hosted an online seminar to help faculty with telehealth instruction. But training such as this can only go so far, said Dr. Johnson. “There are techniques you do have to learn at the patient’s side.”

Dr. Johnson says that a traditional part of medical school at Rutgers has been having students spend time in general practitioners’ offices early on to see what the experience is like. “That’s going to be a problem – I expect many primary care practices will go out of business. Those types of shadowing experiences will probably go away. They may be replaced by experiences at larger clinics.”

Some learning in clinics may soon resume. Although fears about COVID-19 still loom large, Dr. Tao’s ophthalmology residents have started taking on something closer to a normal workload, thanks to patients returning for regular office visits. As people return to medical facilities in larger numbers, hospitals around the country have started separating patients with COVID-19 from others. Dr. Gisondi suggested that this means medical students may be able to circulate in non–COVID-19 wards, provided the institution has enough personal protective equipment. “The inpatient wards are really safe – there’s a low risk of transmission. That’s where core rotations occur.”

The road ahead

In settings where patients’ viral status remains uncertain, such as emergency wards and off-site clinics without rapid testing, in-person learning may be slower to resume. That’s where longer-term changes may come into play. Some schools are preparing digital learning platforms that have the potential to transform medical education.

For example, Haru Okuda, MD, an emergency medicine doctor and director of the Center for Advanced Medical Learning and Simulation at the University of South Florida, Tampa, is testing a new virtual-reality platform called Immertec. Dr. Okuda said that, unlike older teaching tools, the system is not a stale, static virtual environment that will become obsolete. Instead, it uses a live camera to visually teleport students into the space of a real clinic or operating room.

“Let’s say you have students learning gross anatomy, how to dissect the chest. You’d have a cadaver on the table, demonstrating anatomy. The student has a headset – you can see like you’re in the room.” The wraparound visual device allows students to watch surgical maneuvers close up or view additional input from devices such as laparoscopes.

Dr. Okuda acknowledges that educators don’t yet know whether this works as well as older, hands-on methods. As yet, no virtual reality system has touch-based sensors sophisticated enough to simulate even skills such as tying a basic surgical knot, Dr. Gisondi said. And immersive platforms are expensive, which means a gap may occur between schools that can afford them and those that can’t.

The long-term consequences of COVID-19 go beyond costs that institutions may have to bear. Some students are concerned that the pandemic is affecting their mental well-being in ways that may make training a tougher slog. A few students graduated early to serve on the COVID-19 front lines. Others, rather than planning trips to celebrate the gap between medical school and residency, watched from home as young doctors they knew worked under abusive and unsafe conditions.

“Many of us felt powerless, given what we saw happening around us,” said recent University of Michigan, Ann Arbor, graduate Marina Haque, MD. She thinks those feelings, along with the rigors of practicing medicine during a pandemic, may leave her and her colleagues more prone to burnout.

The pandemic has also had a galvanizing effect on students – some excited new doctors are eager to line up for duty on COVID-19 wards. But supervisors say they must weigh young doctors’ desire to serve against the possible risks. “You don’t want people who have a big future ahead of them rushing into these situations and getting severely ill,” said Dr. Post. “There is a balance.”

All these changes, temporary or lasting, have led many to question whether doctors who complete their training under the cloud of the pandemic will be more – or less – prepared than those who came before them. But it’s not really a question of better or worse, says Dr. Johnson, who stresses that medical education has always required flexibility.

“You come into medicine with a plan in mind, but things happen,” he said. He reflected on the HIV pandemic of the late 1980s and early 1990s that influenced his medical career. He hopes young doctors come through the COVID-19 crucible more seasoned, resilient, and confident in crisis situations. “This is a pivotal event in their lives, and it will shape many careers.”

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

The World Health Organization is preparing a scientific brief to address the continually emerging evidence on transmission of COVID-19 and plans to release its guidance “in the coming days.”

WHO will likely address airborne transmission of the virus after a commentary from almost 240 multidisciplinary scientists raised the alarm that virus particles could remain airborne longer that previously appreciated, particularly in poorly ventilated indoor spaces.

“Airborne route of infection transmission is significant, but so far completely undermined, and not recognized by the decision makers and bodies responsible for infection control,” lead commentary author Lidia Morawska, PhD, told Medscape Medical News.

“This means that no control measures are taken to mitigate airborne transmission and, as a consequence, people are infected and can die,” said Morawska, director of the International Laboratory for Air Quality and Health at Queensland University of Technology in Brisbane, Australia. “We wanted to bring this to the attention of the world to prevent this from happening.”

The commentary was published July 6 in Clinical Infectious Diseases.

WHO leaders defended their progress in announcing any changes regarding how COVID-19 can be transmitted during a virtual press briefing today. They have collaborated since April with some of the scientists who coauthored the commentary, for example, said Maria Van Kerkhove, PhD, WHO technical lead on COVID-19.

“We have been working on a scientific brief ... to consolidate knowledge around transmission,” she added.

One focus will be on how masks protect healthcare workers. “We are also looking at the possible role of airborne transmission in other settings,” Van Kerkhove said. “We will be releasing our brief in the coming days.”

“We acknowledge there is emerging evidence in this field,” Benedetta Allegranzi, MD, WHO technical lead on COVID-19, said during the briefing from Geneva. “Therefore, we believe we have to be open to this evidence and its implications.”

WHO participated in an international research meeting last week that addressed means for controlling modes of COVID-19 transmission, Allegranzi said. “Our group and others really highlighted importance of research on different modes of transmission, including droplets of different sizes and their relative importance,” she said. Another aim was determining the dose of the virus required for airborne transmission.

“These fields of research are really growing but not definitive. More evidence needs to be gathered and evaluated,” she explained.

In the meantime, Allegranzi said, “the possibility of airborne transmission in public settings – especially closed, poorly ventilated settings – cannot be ruled out.”

Morawska said the evidence already exists. “A continuous surprise is that it takes the world such a long time to accept this, while this has such solid scientific foundation.” As an example, she cited an April report she coauthored in the journal Environment International. She and colleagues call for “national authorities to acknowledge the reality that the virus spreads through air and recommend that adequate control measures be implemented to prevent further spread of the SARS-CoV-2 virus, in particularly removal of the virus-laden droplets from indoor air by ventilation.”

The take-home message from the commentary, Morawska said, is a call to action. The authors state there is a need “to provide sufficient and effective ventilation (supply clean outdoor air, minimize recirculating air) particularly in public buildings, workplace environments, schools, hospitals, and aged care homes.”

WHO Chief Scientist Soumya Swaminathan, MD, explained why the organization remains cautious about making premature pronouncements regarding airborne transmission. “Any guidance we put out has implications for billions of people around the world, so we want to be as careful as possible,” she said during the press briefing. “We have to consider the weight of the evidence.”

“We are constantly looking for information on how we can do better,” Swaminathan added. WHO officials are reviewing hundreds of scientific reports every day, she said, and not all are of good quality. For this reason, she and other scientists at WHO perform a “living systematic review” – updating the consensus of evidence on a weekly basis.  

“This process on COVID-19 will, I am sure, continue for the weeks and months to come,” she added.

This article first appeared on Medscape.com.

The World Health Organization is preparing a scientific brief to address the continually emerging evidence on transmission of COVID-19 and plans to release its guidance “in the coming days.”

WHO will likely address airborne transmission of the virus after a commentary from almost 240 multidisciplinary scientists raised the alarm that virus particles could remain airborne longer that previously appreciated, particularly in poorly ventilated indoor spaces.

“Airborne route of infection transmission is significant, but so far completely undermined, and not recognized by the decision makers and bodies responsible for infection control,” lead commentary author Lidia Morawska, PhD, told Medscape Medical News.

“This means that no control measures are taken to mitigate airborne transmission and, as a consequence, people are infected and can die,” said Morawska, director of the International Laboratory for Air Quality and Health at Queensland University of Technology in Brisbane, Australia. “We wanted to bring this to the attention of the world to prevent this from happening.”

The commentary was published July 6 in Clinical Infectious Diseases.

WHO leaders defended their progress in announcing any changes regarding how COVID-19 can be transmitted during a virtual press briefing today. They have collaborated since April with some of the scientists who coauthored the commentary, for example, said Maria Van Kerkhove, PhD, WHO technical lead on COVID-19.

“We have been working on a scientific brief ... to consolidate knowledge around transmission,” she added.

One focus will be on how masks protect healthcare workers. “We are also looking at the possible role of airborne transmission in other settings,” Van Kerkhove said. “We will be releasing our brief in the coming days.”

“We acknowledge there is emerging evidence in this field,” Benedetta Allegranzi, MD, WHO technical lead on COVID-19, said during the briefing from Geneva. “Therefore, we believe we have to be open to this evidence and its implications.”

WHO participated in an international research meeting last week that addressed means for controlling modes of COVID-19 transmission, Allegranzi said. “Our group and others really highlighted importance of research on different modes of transmission, including droplets of different sizes and their relative importance,” she said. Another aim was determining the dose of the virus required for airborne transmission.

“These fields of research are really growing but not definitive. More evidence needs to be gathered and evaluated,” she explained.

In the meantime, Allegranzi said, “the possibility of airborne transmission in public settings – especially closed, poorly ventilated settings – cannot be ruled out.”

Morawska said the evidence already exists. “A continuous surprise is that it takes the world such a long time to accept this, while this has such solid scientific foundation.” As an example, she cited an April report she coauthored in the journal Environment International. She and colleagues call for “national authorities to acknowledge the reality that the virus spreads through air and recommend that adequate control measures be implemented to prevent further spread of the SARS-CoV-2 virus, in particularly removal of the virus-laden droplets from indoor air by ventilation.”

The take-home message from the commentary, Morawska said, is a call to action. The authors state there is a need “to provide sufficient and effective ventilation (supply clean outdoor air, minimize recirculating air) particularly in public buildings, workplace environments, schools, hospitals, and aged care homes.”

WHO Chief Scientist Soumya Swaminathan, MD, explained why the organization remains cautious about making premature pronouncements regarding airborne transmission. “Any guidance we put out has implications for billions of people around the world, so we want to be as careful as possible,” she said during the press briefing. “We have to consider the weight of the evidence.”

“We are constantly looking for information on how we can do better,” Swaminathan added. WHO officials are reviewing hundreds of scientific reports every day, she said, and not all are of good quality. For this reason, she and other scientists at WHO perform a “living systematic review” – updating the consensus of evidence on a weekly basis.  

“This process on COVID-19 will, I am sure, continue for the weeks and months to come,” she added.

This article first appeared on Medscape.com.

The World Health Organization is preparing a scientific brief to address the continually emerging evidence on transmission of COVID-19 and plans to release its guidance “in the coming days.”

WHO will likely address airborne transmission of the virus after a commentary from almost 240 multidisciplinary scientists raised the alarm that virus particles could remain airborne longer that previously appreciated, particularly in poorly ventilated indoor spaces.

“Airborne route of infection transmission is significant, but so far completely undermined, and not recognized by the decision makers and bodies responsible for infection control,” lead commentary author Lidia Morawska, PhD, told Medscape Medical News.

“This means that no control measures are taken to mitigate airborne transmission and, as a consequence, people are infected and can die,” said Morawska, director of the International Laboratory for Air Quality and Health at Queensland University of Technology in Brisbane, Australia. “We wanted to bring this to the attention of the world to prevent this from happening.”

The commentary was published July 6 in Clinical Infectious Diseases.

WHO leaders defended their progress in announcing any changes regarding how COVID-19 can be transmitted during a virtual press briefing today. They have collaborated since April with some of the scientists who coauthored the commentary, for example, said Maria Van Kerkhove, PhD, WHO technical lead on COVID-19.

“We have been working on a scientific brief ... to consolidate knowledge around transmission,” she added.

One focus will be on how masks protect healthcare workers. “We are also looking at the possible role of airborne transmission in other settings,” Van Kerkhove said. “We will be releasing our brief in the coming days.”

“We acknowledge there is emerging evidence in this field,” Benedetta Allegranzi, MD, WHO technical lead on COVID-19, said during the briefing from Geneva. “Therefore, we believe we have to be open to this evidence and its implications.”

WHO participated in an international research meeting last week that addressed means for controlling modes of COVID-19 transmission, Allegranzi said. “Our group and others really highlighted importance of research on different modes of transmission, including droplets of different sizes and their relative importance,” she said. Another aim was determining the dose of the virus required for airborne transmission.

“These fields of research are really growing but not definitive. More evidence needs to be gathered and evaluated,” she explained.

In the meantime, Allegranzi said, “the possibility of airborne transmission in public settings – especially closed, poorly ventilated settings – cannot be ruled out.”

Morawska said the evidence already exists. “A continuous surprise is that it takes the world such a long time to accept this, while this has such solid scientific foundation.” As an example, she cited an April report she coauthored in the journal Environment International. She and colleagues call for “national authorities to acknowledge the reality that the virus spreads through air and recommend that adequate control measures be implemented to prevent further spread of the SARS-CoV-2 virus, in particularly removal of the virus-laden droplets from indoor air by ventilation.”

The take-home message from the commentary, Morawska said, is a call to action. The authors state there is a need “to provide sufficient and effective ventilation (supply clean outdoor air, minimize recirculating air) particularly in public buildings, workplace environments, schools, hospitals, and aged care homes.”

WHO Chief Scientist Soumya Swaminathan, MD, explained why the organization remains cautious about making premature pronouncements regarding airborne transmission. “Any guidance we put out has implications for billions of people around the world, so we want to be as careful as possible,” she said during the press briefing. “We have to consider the weight of the evidence.”

“We are constantly looking for information on how we can do better,” Swaminathan added. WHO officials are reviewing hundreds of scientific reports every day, she said, and not all are of good quality. For this reason, she and other scientists at WHO perform a “living systematic review” – updating the consensus of evidence on a weekly basis.  

“This process on COVID-19 will, I am sure, continue for the weeks and months to come,” she added.

This article first appeared on Medscape.com.

“Patients with type 2 diabetes should consider intermittent fasting carefully” and “not undertake it without the involvement of their physician,” stress the authors of a new viewpoint published online July 2 in JAMA.

This is because intermittent fasting in patients with type 2 diabetes has only been studied in seven small, short published trials of very different regimens, with limited evidence of benefit. In addition, some concerns arose from these studies.

Weight loss with intermittent fasting appears to be similar to that attained with caloric restriction, but in the case of those with diabetes, the best way to adjust glucose-lowering medicines to reduce the risk of hypoglycemia while practicing intermittent fasting has not been established, and there is potential for such fasting to cause glycemic variability.

The viewpoint’s lead author Benjamin D. Horne, PhD, MStat, MPH, from Intermountain Medical Center, Salt Lake City, and Stanford (Calif.) University, expanded on the issues in a podcast interview with JAMA editor in chief Howard C. Bauchner, MD.

Asked if he would advise intermittent fasting for patients with type 2 diabetes, Dr. Horne replied that he would recommend it, with caveats, “because of the safety issues – some of which are fairly benign for people who are apparently healthy but may be not quite as benign for people with type 2 diabetes.

“Things such as low blood pressure, weakness, headaches, [and] dizziness are considerations,” he continued, but “the big issue” is hypoglycemia, so caloric restriction may be a better choice for some patients with diabetes.

Dr. Horne said he likes to give patients options. “I’ve met quite a number of people who are very behind time-restricted feeding – eating during a 6- to 8-hour window,” he said. “If they are able to stay on it, they tend to really love it.”

The most popular regimen that results in some weight loss is fasting for 24 hours – with or without a 500-calorie meal – on 2 nonconsecutive days a week, the so-called 5:2 diet. And “as someone who’s in cardiovascular research,” Dr. Horne added, “the one that I’m thinking for long term is once-a-week fasting for a 24-hour period.”
 

Intermittent fasting: Less safe than calorie restriction in diabetes?

Patients who already have diabetes and lose weight benefit from improved glucose, blood pressure, and lipid levels, Dr. Horne and colleagues wrote.

Currently, intermittent fasting is popular in the lay press and on social media with claims of potential benefits for diabetes “that are as yet untested or unproven,” they added. In fact, “whether a patient with type 2 diabetes should engage in intermittent fasting involves a variety of concerns over safety and efficacy.”

Thus, they examined the existing evidence for the health effects and safety of intermittent fasting – defined as time-restricted feeding, or fasting on alternate days or during 1-4 days a week, with only water or also juice and bone broth, or no more than 700 calories allowed on fasting days – in patients with type 2 diabetes.

They found seven published studies of intermittent fasting in patients with type 2 diabetes, including five randomized clinical trials, of which only one study had more than 63 patients.

Intermittent fasting regimens in the studies included five fasting frequencies and most follow-up durations were 4 months or less, including 18-20 hours a day for 2 weeks; 2 days a week for 12 weeks (two studies) or for 12 months (one study); 3-4 days a week for 7-11 months; 4 days a week for 12 weeks; and 17 days in 4 months.

They all reported that intermittent fasting was tied to weight loss, and most (but not all) of the studies also found that it was associated with decreases in A1c and improved glucose levels, quality of life, and blood pressure, but not insulin resistance.

But this “heterogeneity of designs and regimens and the variance in results make it difficult to draw clinically meaningful direction,” Dr. Horne and colleagues observed.

Moreover, only one study addressed the relative safety of two intermittent fasting regimens, and it found that both regimens increased hypoglycemic events despite the use of a medication dose-change protocol.

Only one study explicitly compared intermittent fasting with caloric restriction, which found “that a twice-weekly intermittent fasting regimen improved [A1c] levels is promising,” the authors wrote.

However, that study showed only noninferiority for change in A1c level (–0.3% for intermittent fasting vs. –0.5% for caloric restriction).

The major implication, according to the viewpoint authors, is that “intermittent fasting may be less safe than caloric restriction although approximately equivalently effective.”

“Therefore,” they summarized, “until intermittent fasting is shown to be more effective than caloric restriction for reducing [A1c] or otherwise controlling diabetes, that study – and the limited other high-quality data – suggest that intermittent fasting regimens for patients with type 2 diabetes recommended by health professionals or promoted to the public should be limited to individuals for whom the risk of hypoglycemia is closely monitored and medications are carefully adjusted to ensure safety.”

Should continuous glucose monitoring to detect glycemic variability be considered?

Intermittent fasting may also bring wider fluctuations of glycemic control than simple calorie restriction, with hypoglycemia during fasting times and hyperglycemia during feeding times, which would not be reflected in A1c levels, Dr. Horne and colleagues pointed out.

“Studies have raised concern that glycemic variability leads to both microvascular (e.g., retinopathy) and macrovascular (e.g., coronary disease) complications in patients with type 2 diabetes,” they cautioned.

Therefore, “continuous glucose monitoring should be considered for studies of ... clinical interventions using intermittent fasting in patients with type 2 diabetes,” they concluded.

Dr. Horne has reported serving as principal investigator of grants for studies on intermittent fasting from the Intermountain Research and Medical Foundation. Disclosures of the other two authors are listed with the viewpoint.

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

“Patients with type 2 diabetes should consider intermittent fasting carefully” and “not undertake it without the involvement of their physician,” stress the authors of a new viewpoint published online July 2 in JAMA.

This is because intermittent fasting in patients with type 2 diabetes has only been studied in seven small, short published trials of very different regimens, with limited evidence of benefit. In addition, some concerns arose from these studies.

Weight loss with intermittent fasting appears to be similar to that attained with caloric restriction, but in the case of those with diabetes, the best way to adjust glucose-lowering medicines to reduce the risk of hypoglycemia while practicing intermittent fasting has not been established, and there is potential for such fasting to cause glycemic variability.

The viewpoint’s lead author Benjamin D. Horne, PhD, MStat, MPH, from Intermountain Medical Center, Salt Lake City, and Stanford (Calif.) University, expanded on the issues in a podcast interview with JAMA editor in chief Howard C. Bauchner, MD.

Asked if he would advise intermittent fasting for patients with type 2 diabetes, Dr. Horne replied that he would recommend it, with caveats, “because of the safety issues – some of which are fairly benign for people who are apparently healthy but may be not quite as benign for people with type 2 diabetes.

“Things such as low blood pressure, weakness, headaches, [and] dizziness are considerations,” he continued, but “the big issue” is hypoglycemia, so caloric restriction may be a better choice for some patients with diabetes.

Dr. Horne said he likes to give patients options. “I’ve met quite a number of people who are very behind time-restricted feeding – eating during a 6- to 8-hour window,” he said. “If they are able to stay on it, they tend to really love it.”

The most popular regimen that results in some weight loss is fasting for 24 hours – with or without a 500-calorie meal – on 2 nonconsecutive days a week, the so-called 5:2 diet. And “as someone who’s in cardiovascular research,” Dr. Horne added, “the one that I’m thinking for long term is once-a-week fasting for a 24-hour period.”
 

Intermittent fasting: Less safe than calorie restriction in diabetes?

Patients who already have diabetes and lose weight benefit from improved glucose, blood pressure, and lipid levels, Dr. Horne and colleagues wrote.

Currently, intermittent fasting is popular in the lay press and on social media with claims of potential benefits for diabetes “that are as yet untested or unproven,” they added. In fact, “whether a patient with type 2 diabetes should engage in intermittent fasting involves a variety of concerns over safety and efficacy.”

Thus, they examined the existing evidence for the health effects and safety of intermittent fasting – defined as time-restricted feeding, or fasting on alternate days or during 1-4 days a week, with only water or also juice and bone broth, or no more than 700 calories allowed on fasting days – in patients with type 2 diabetes.

They found seven published studies of intermittent fasting in patients with type 2 diabetes, including five randomized clinical trials, of which only one study had more than 63 patients.

Intermittent fasting regimens in the studies included five fasting frequencies and most follow-up durations were 4 months or less, including 18-20 hours a day for 2 weeks; 2 days a week for 12 weeks (two studies) or for 12 months (one study); 3-4 days a week for 7-11 months; 4 days a week for 12 weeks; and 17 days in 4 months.

They all reported that intermittent fasting was tied to weight loss, and most (but not all) of the studies also found that it was associated with decreases in A1c and improved glucose levels, quality of life, and blood pressure, but not insulin resistance.

But this “heterogeneity of designs and regimens and the variance in results make it difficult to draw clinically meaningful direction,” Dr. Horne and colleagues observed.

Moreover, only one study addressed the relative safety of two intermittent fasting regimens, and it found that both regimens increased hypoglycemic events despite the use of a medication dose-change protocol.

Only one study explicitly compared intermittent fasting with caloric restriction, which found “that a twice-weekly intermittent fasting regimen improved [A1c] levels is promising,” the authors wrote.

However, that study showed only noninferiority for change in A1c level (–0.3% for intermittent fasting vs. –0.5% for caloric restriction).

The major implication, according to the viewpoint authors, is that “intermittent fasting may be less safe than caloric restriction although approximately equivalently effective.”

“Therefore,” they summarized, “until intermittent fasting is shown to be more effective than caloric restriction for reducing [A1c] or otherwise controlling diabetes, that study – and the limited other high-quality data – suggest that intermittent fasting regimens for patients with type 2 diabetes recommended by health professionals or promoted to the public should be limited to individuals for whom the risk of hypoglycemia is closely monitored and medications are carefully adjusted to ensure safety.”

Should continuous glucose monitoring to detect glycemic variability be considered?

Intermittent fasting may also bring wider fluctuations of glycemic control than simple calorie restriction, with hypoglycemia during fasting times and hyperglycemia during feeding times, which would not be reflected in A1c levels, Dr. Horne and colleagues pointed out.

“Studies have raised concern that glycemic variability leads to both microvascular (e.g., retinopathy) and macrovascular (e.g., coronary disease) complications in patients with type 2 diabetes,” they cautioned.

Therefore, “continuous glucose monitoring should be considered for studies of ... clinical interventions using intermittent fasting in patients with type 2 diabetes,” they concluded.

Dr. Horne has reported serving as principal investigator of grants for studies on intermittent fasting from the Intermountain Research and Medical Foundation. Disclosures of the other two authors are listed with the viewpoint.

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

“Patients with type 2 diabetes should consider intermittent fasting carefully” and “not undertake it without the involvement of their physician,” stress the authors of a new viewpoint published online July 2 in JAMA.

This is because intermittent fasting in patients with type 2 diabetes has only been studied in seven small, short published trials of very different regimens, with limited evidence of benefit. In addition, some concerns arose from these studies.

Weight loss with intermittent fasting appears to be similar to that attained with caloric restriction, but in the case of those with diabetes, the best way to adjust glucose-lowering medicines to reduce the risk of hypoglycemia while practicing intermittent fasting has not been established, and there is potential for such fasting to cause glycemic variability.

The viewpoint’s lead author Benjamin D. Horne, PhD, MStat, MPH, from Intermountain Medical Center, Salt Lake City, and Stanford (Calif.) University, expanded on the issues in a podcast interview with JAMA editor in chief Howard C. Bauchner, MD.

Asked if he would advise intermittent fasting for patients with type 2 diabetes, Dr. Horne replied that he would recommend it, with caveats, “because of the safety issues – some of which are fairly benign for people who are apparently healthy but may be not quite as benign for people with type 2 diabetes.

“Things such as low blood pressure, weakness, headaches, [and] dizziness are considerations,” he continued, but “the big issue” is hypoglycemia, so caloric restriction may be a better choice for some patients with diabetes.

Dr. Horne said he likes to give patients options. “I’ve met quite a number of people who are very behind time-restricted feeding – eating during a 6- to 8-hour window,” he said. “If they are able to stay on it, they tend to really love it.”

The most popular regimen that results in some weight loss is fasting for 24 hours – with or without a 500-calorie meal – on 2 nonconsecutive days a week, the so-called 5:2 diet. And “as someone who’s in cardiovascular research,” Dr. Horne added, “the one that I’m thinking for long term is once-a-week fasting for a 24-hour period.”
 

Intermittent fasting: Less safe than calorie restriction in diabetes?

Patients who already have diabetes and lose weight benefit from improved glucose, blood pressure, and lipid levels, Dr. Horne and colleagues wrote.

Currently, intermittent fasting is popular in the lay press and on social media with claims of potential benefits for diabetes “that are as yet untested or unproven,” they added. In fact, “whether a patient with type 2 diabetes should engage in intermittent fasting involves a variety of concerns over safety and efficacy.”

Thus, they examined the existing evidence for the health effects and safety of intermittent fasting – defined as time-restricted feeding, or fasting on alternate days or during 1-4 days a week, with only water or also juice and bone broth, or no more than 700 calories allowed on fasting days – in patients with type 2 diabetes.

They found seven published studies of intermittent fasting in patients with type 2 diabetes, including five randomized clinical trials, of which only one study had more than 63 patients.

Intermittent fasting regimens in the studies included five fasting frequencies and most follow-up durations were 4 months or less, including 18-20 hours a day for 2 weeks; 2 days a week for 12 weeks (two studies) or for 12 months (one study); 3-4 days a week for 7-11 months; 4 days a week for 12 weeks; and 17 days in 4 months.

They all reported that intermittent fasting was tied to weight loss, and most (but not all) of the studies also found that it was associated with decreases in A1c and improved glucose levels, quality of life, and blood pressure, but not insulin resistance.

But this “heterogeneity of designs and regimens and the variance in results make it difficult to draw clinically meaningful direction,” Dr. Horne and colleagues observed.

Moreover, only one study addressed the relative safety of two intermittent fasting regimens, and it found that both regimens increased hypoglycemic events despite the use of a medication dose-change protocol.

Only one study explicitly compared intermittent fasting with caloric restriction, which found “that a twice-weekly intermittent fasting regimen improved [A1c] levels is promising,” the authors wrote.

However, that study showed only noninferiority for change in A1c level (–0.3% for intermittent fasting vs. –0.5% for caloric restriction).

The major implication, according to the viewpoint authors, is that “intermittent fasting may be less safe than caloric restriction although approximately equivalently effective.”

“Therefore,” they summarized, “until intermittent fasting is shown to be more effective than caloric restriction for reducing [A1c] or otherwise controlling diabetes, that study – and the limited other high-quality data – suggest that intermittent fasting regimens for patients with type 2 diabetes recommended by health professionals or promoted to the public should be limited to individuals for whom the risk of hypoglycemia is closely monitored and medications are carefully adjusted to ensure safety.”

Should continuous glucose monitoring to detect glycemic variability be considered?

Intermittent fasting may also bring wider fluctuations of glycemic control than simple calorie restriction, with hypoglycemia during fasting times and hyperglycemia during feeding times, which would not be reflected in A1c levels, Dr. Horne and colleagues pointed out.

“Studies have raised concern that glycemic variability leads to both microvascular (e.g., retinopathy) and macrovascular (e.g., coronary disease) complications in patients with type 2 diabetes,” they cautioned.

Therefore, “continuous glucose monitoring should be considered for studies of ... clinical interventions using intermittent fasting in patients with type 2 diabetes,” they concluded.

Dr. Horne has reported serving as principal investigator of grants for studies on intermittent fasting from the Intermountain Research and Medical Foundation. Disclosures of the other two authors are listed with the viewpoint.

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