Clinical Endocrinology News

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.

The Pharmaceutical Research and Manufacturers Association (PhRMA) is suing the state of Minnesota in an attempt to overturn a law that requires insulin makers to provide an emergency supply to individuals free of charge.

PhRMA filed the complaint in the U.S. District Court in Minnesota on July 1, the day the Alec Smith Insulin Affordability Act went into effect. The law created the Minnesota Insulin Safety Net Program, which is continuing to operate in the meantime.

Advocates said they were appalled by the PhRMA action.
 

PhRMA says law is unconstitutional

In the filing, PhRMA’s attorneys said the law is unconstitutional. It “order[s] pharmaceutical manufacturers to give insulin to state residents, on the state’s prescribed terms, at no charge to the recipients and without compensating the manufacturers in any way.”

“A state cannot simply commandeer private property to achieve its public policy goals,” the PhRMA lawyers argued.

The suit said the three leading insulin makers already provide discounts, copayment assistance, and free insulin to “a great number of patients.”

The state has estimated that as many as 30,000 Minnesotans would be eligible for free insulin in the first year of the program. The drugmakers strenuously objected, noting that would mean they would “be compelled to provide 173,800 monthly supplies of free insulin” just in the first year.

“No one living with diabetes should be forced to ration or go without their life-saving insulin because they can’t afford it,” said PhRMA executive vice president and general counsel James C. Stansel in a statement.

The law, said Mr. Stansel, “overlooks common sense solutions to help patients afford their insulin and, despite its claims, still allows for patients to be charged at the pharmacy for the insulin that manufacturers are required to provide for free.”
 

Advocates decry suit

Advocates had worked for several years to secure passage of the legislation, named in honor of a young man who died in 2017 after rationing his insulin. Minnesota Gov. Tim Walz of the Democratic-Farmer-Labor Party signed the bill into law on April 15.

It requires manufacturers to make at least a 30-day supply of insulin available to those who are in urgent need and cannot afford the medication. Manufacturers can be fined $200,000 per month for not complying.

Mayo Clinic hematologist S. Vincent Rajkumar, MD, who called for action on the cost of insulin in an article published in the January 2020 issue of the Mayo Clinic Proceedings, as reported by Medscape Medical News, said the lawsuit was a “bad move.”

Dr. Rajkumar, the Edward W. and Betty Knight Scripps professor of medicine at the Mayo Clinic, noted that it has strict limits and is aimed to help patients in emergent need.

“There is nothing in the US constitution that prevents states from saving the lives of its citizens who are in imminent danger,” Dr. Rajkumar said. “The only motives for this lawsuit in my opinion are greed and the worry that other states may also choose to put lives of patients ahead of pharma profits.”

Alec Smith’s mother, Nicole Smith-Holt, who is active with T1International’s #insulin4all campaign, took to Twitter to express her anger.

“Throwing up road blocks to securing affordable insulin for the people of MN, haven’t they taken enough innocent lives? How many more bodies are they looking for?” she tweeted. “When are they going to realize we are not going to stop fighting?”

T1International said in a statement: “It is clear that the pharmaceutical industry can see only one thing – their bottom line,” and promised that patients would not give up.

“We will not stop showing them the real price we pay for their greed,” said the organization.

Abigail Hansmeyer, a Minnesota-based #insulin4all advocate, also talked about her frustration at what appeared to be disingenuous behavior by the insulin makers.

“I guess the endless opportunities insulin manufacturer reps had as stakeholders during numerous discussions and negotiations in the making of this law, wasn’t what they wanted,” she tweeted. “They were buying time to protect their profits. Yeah, we’re not done here.”

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

The Pharmaceutical Research and Manufacturers Association (PhRMA) is suing the state of Minnesota in an attempt to overturn a law that requires insulin makers to provide an emergency supply to individuals free of charge.

PhRMA filed the complaint in the U.S. District Court in Minnesota on July 1, the day the Alec Smith Insulin Affordability Act went into effect. The law created the Minnesota Insulin Safety Net Program, which is continuing to operate in the meantime.

Advocates said they were appalled by the PhRMA action.
 

PhRMA says law is unconstitutional

In the filing, PhRMA’s attorneys said the law is unconstitutional. It “order[s] pharmaceutical manufacturers to give insulin to state residents, on the state’s prescribed terms, at no charge to the recipients and without compensating the manufacturers in any way.”

“A state cannot simply commandeer private property to achieve its public policy goals,” the PhRMA lawyers argued.

The suit said the three leading insulin makers already provide discounts, copayment assistance, and free insulin to “a great number of patients.”

The state has estimated that as many as 30,000 Minnesotans would be eligible for free insulin in the first year of the program. The drugmakers strenuously objected, noting that would mean they would “be compelled to provide 173,800 monthly supplies of free insulin” just in the first year.

“No one living with diabetes should be forced to ration or go without their life-saving insulin because they can’t afford it,” said PhRMA executive vice president and general counsel James C. Stansel in a statement.

The law, said Mr. Stansel, “overlooks common sense solutions to help patients afford their insulin and, despite its claims, still allows for patients to be charged at the pharmacy for the insulin that manufacturers are required to provide for free.”
 

Advocates decry suit

Advocates had worked for several years to secure passage of the legislation, named in honor of a young man who died in 2017 after rationing his insulin. Minnesota Gov. Tim Walz of the Democratic-Farmer-Labor Party signed the bill into law on April 15.

It requires manufacturers to make at least a 30-day supply of insulin available to those who are in urgent need and cannot afford the medication. Manufacturers can be fined $200,000 per month for not complying.

Mayo Clinic hematologist S. Vincent Rajkumar, MD, who called for action on the cost of insulin in an article published in the January 2020 issue of the Mayo Clinic Proceedings, as reported by Medscape Medical News, said the lawsuit was a “bad move.”

Dr. Rajkumar, the Edward W. and Betty Knight Scripps professor of medicine at the Mayo Clinic, noted that it has strict limits and is aimed to help patients in emergent need.

“There is nothing in the US constitution that prevents states from saving the lives of its citizens who are in imminent danger,” Dr. Rajkumar said. “The only motives for this lawsuit in my opinion are greed and the worry that other states may also choose to put lives of patients ahead of pharma profits.”

Alec Smith’s mother, Nicole Smith-Holt, who is active with T1International’s #insulin4all campaign, took to Twitter to express her anger.

“Throwing up road blocks to securing affordable insulin for the people of MN, haven’t they taken enough innocent lives? How many more bodies are they looking for?” she tweeted. “When are they going to realize we are not going to stop fighting?”

T1International said in a statement: “It is clear that the pharmaceutical industry can see only one thing – their bottom line,” and promised that patients would not give up.

“We will not stop showing them the real price we pay for their greed,” said the organization.

Abigail Hansmeyer, a Minnesota-based #insulin4all advocate, also talked about her frustration at what appeared to be disingenuous behavior by the insulin makers.

“I guess the endless opportunities insulin manufacturer reps had as stakeholders during numerous discussions and negotiations in the making of this law, wasn’t what they wanted,” she tweeted. “They were buying time to protect their profits. Yeah, we’re not done here.”

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

The Pharmaceutical Research and Manufacturers Association (PhRMA) is suing the state of Minnesota in an attempt to overturn a law that requires insulin makers to provide an emergency supply to individuals free of charge.

PhRMA filed the complaint in the U.S. District Court in Minnesota on July 1, the day the Alec Smith Insulin Affordability Act went into effect. The law created the Minnesota Insulin Safety Net Program, which is continuing to operate in the meantime.

Advocates said they were appalled by the PhRMA action.
 

PhRMA says law is unconstitutional

In the filing, PhRMA’s attorneys said the law is unconstitutional. It “order[s] pharmaceutical manufacturers to give insulin to state residents, on the state’s prescribed terms, at no charge to the recipients and without compensating the manufacturers in any way.”

“A state cannot simply commandeer private property to achieve its public policy goals,” the PhRMA lawyers argued.

The suit said the three leading insulin makers already provide discounts, copayment assistance, and free insulin to “a great number of patients.”

The state has estimated that as many as 30,000 Minnesotans would be eligible for free insulin in the first year of the program. The drugmakers strenuously objected, noting that would mean they would “be compelled to provide 173,800 monthly supplies of free insulin” just in the first year.

“No one living with diabetes should be forced to ration or go without their life-saving insulin because they can’t afford it,” said PhRMA executive vice president and general counsel James C. Stansel in a statement.

The law, said Mr. Stansel, “overlooks common sense solutions to help patients afford their insulin and, despite its claims, still allows for patients to be charged at the pharmacy for the insulin that manufacturers are required to provide for free.”
 

Advocates decry suit

Advocates had worked for several years to secure passage of the legislation, named in honor of a young man who died in 2017 after rationing his insulin. Minnesota Gov. Tim Walz of the Democratic-Farmer-Labor Party signed the bill into law on April 15.

It requires manufacturers to make at least a 30-day supply of insulin available to those who are in urgent need and cannot afford the medication. Manufacturers can be fined $200,000 per month for not complying.

Mayo Clinic hematologist S. Vincent Rajkumar, MD, who called for action on the cost of insulin in an article published in the January 2020 issue of the Mayo Clinic Proceedings, as reported by Medscape Medical News, said the lawsuit was a “bad move.”

Dr. Rajkumar, the Edward W. and Betty Knight Scripps professor of medicine at the Mayo Clinic, noted that it has strict limits and is aimed to help patients in emergent need.

“There is nothing in the US constitution that prevents states from saving the lives of its citizens who are in imminent danger,” Dr. Rajkumar said. “The only motives for this lawsuit in my opinion are greed and the worry that other states may also choose to put lives of patients ahead of pharma profits.”

Alec Smith’s mother, Nicole Smith-Holt, who is active with T1International’s #insulin4all campaign, took to Twitter to express her anger.

“Throwing up road blocks to securing affordable insulin for the people of MN, haven’t they taken enough innocent lives? How many more bodies are they looking for?” she tweeted. “When are they going to realize we are not going to stop fighting?”

T1International said in a statement: “It is clear that the pharmaceutical industry can see only one thing – their bottom line,” and promised that patients would not give up.

“We will not stop showing them the real price we pay for their greed,” said the organization.

Abigail Hansmeyer, a Minnesota-based #insulin4all advocate, also talked about her frustration at what appeared to be disingenuous behavior by the insulin makers.

“I guess the endless opportunities insulin manufacturer reps had as stakeholders during numerous discussions and negotiations in the making of this law, wasn’t what they wanted,” she tweeted. “They were buying time to protect their profits. Yeah, we’re not done here.”

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

Transcatheter bariatric embolotherapy (TBE) provides sustained weight loss without serious adverse effects among obese patients, results of a pilot sham-controlled study suggest.

At 6-month follow-up, the patients receiving the intervention had lost 7.4 kg (16.3 lbs), compared with 3.0 kg (6.6 lbs) in those randomized to a sham procedure in an intention-to-treat analysis (P = .034).

Results were similar in a per-protocol analysis (9.4 kg/20.7 lbs vs. 1.9 kg/4.1 lbs; P = .0002).

Weight loss after embolotherapy was sustained over 12 months, falling 7.8 kg (17.1 lbs) from baseline in the intention-to-treat population (P = .0011) and 9.3 kg (20.5 lbs) in the per-protocol population (P = .0005).

Safety events after TBE were mild nausea or vomiting, reported Vivek Reddy, MD, Mount Sinai Hospital, New York City. Five participants had minor, asymptomatic ulcers that required no additional treatment.

“In this randomized pilot trial, we established the proof of principle that transcatheter bariatric embolotherapy of the left gastric artery is safe and it promotes clinically significant weight loss,” he concluded at PCR e-Course, the virtual meeting of the Congress of European Association of Percutaneous Cardiovascular Interventions 2020.

Although bariatric surgery is highly effective, he noted that the associated morbidity and mortality limit its use to the severely obese with a body mass index (BMI) typically over 40 kg/m².

TBE is a minimally invasive approach that uses a custom occlusion balloon microcatheter and robotic manifold to inject 300- to 500-mcm beads to the left gastric artery. Preclinical and case studies suggest it promotes weight loss by reducing ghrelin, an appetite-stimulating hormone secreted from the gastric fundus, Dr. Reddy said.

The study enrolled 44 patients (aged 21-60 years) with a BMI of 35-55, excluding those with prior bariatric surgery and a history of ulcers, type 2 diabetes, chronic aspirin or nonsteroidal inflammatory use, and active Helicobacter pylori infection.

A total of 40 patients were randomly assigned to TBE or a sham procedure, in which lidocaine was applied to the femoral area and propofol infused for 1 hour. The two groups were well matched, with a mean age of 45 vs. 46 years, weight of 110 kg vs. 119 kg, and BMI of 39 vs. 40, Dr. Reddy noted.

Embolotherapy was performed at a single center in Prague, and, on average, took 82.3 minutes and used 127 mL of contrast, 163 Gy/cm² radiation, and 4.2 mL of microspheres. A single vessel was injected in 80% of cases.

The intention-to-treat population comprised 19 TBE and 18 control subjects, and the per-protocol population comprised 15 TBE and 16 control subjects, after the exclusion of patients in whom embolotherapy was unsuccessful or incomplete or who withdrew consent.

All patients received endoscopy at baseline and 1 week, as well as an intensive 19-session lifestyle and dietary education intervention out to 6 months.

Patients who underwent TBE had significant improvement in hunger scores at 6 and 12 months, compared with baseline. Similarly, quality of life improved across all six domains, including significant gains in physical function, self-esteem, and overall quality of life at both time points, Dr. Reddy reported.

Dr. Reddy disclosed receiving research support from Endobar Solutions.

This article first appeared on Medscape.com.

Transcatheter bariatric embolotherapy (TBE) provides sustained weight loss without serious adverse effects among obese patients, results of a pilot sham-controlled study suggest.

At 6-month follow-up, the patients receiving the intervention had lost 7.4 kg (16.3 lbs), compared with 3.0 kg (6.6 lbs) in those randomized to a sham procedure in an intention-to-treat analysis (P = .034).

Results were similar in a per-protocol analysis (9.4 kg/20.7 lbs vs. 1.9 kg/4.1 lbs; P = .0002).

Weight loss after embolotherapy was sustained over 12 months, falling 7.8 kg (17.1 lbs) from baseline in the intention-to-treat population (P = .0011) and 9.3 kg (20.5 lbs) in the per-protocol population (P = .0005).

Safety events after TBE were mild nausea or vomiting, reported Vivek Reddy, MD, Mount Sinai Hospital, New York City. Five participants had minor, asymptomatic ulcers that required no additional treatment.

“In this randomized pilot trial, we established the proof of principle that transcatheter bariatric embolotherapy of the left gastric artery is safe and it promotes clinically significant weight loss,” he concluded at PCR e-Course, the virtual meeting of the Congress of European Association of Percutaneous Cardiovascular Interventions 2020.

Although bariatric surgery is highly effective, he noted that the associated morbidity and mortality limit its use to the severely obese with a body mass index (BMI) typically over 40 kg/m².

TBE is a minimally invasive approach that uses a custom occlusion balloon microcatheter and robotic manifold to inject 300- to 500-mcm beads to the left gastric artery. Preclinical and case studies suggest it promotes weight loss by reducing ghrelin, an appetite-stimulating hormone secreted from the gastric fundus, Dr. Reddy said.

The study enrolled 44 patients (aged 21-60 years) with a BMI of 35-55, excluding those with prior bariatric surgery and a history of ulcers, type 2 diabetes, chronic aspirin or nonsteroidal inflammatory use, and active Helicobacter pylori infection.

A total of 40 patients were randomly assigned to TBE or a sham procedure, in which lidocaine was applied to the femoral area and propofol infused for 1 hour. The two groups were well matched, with a mean age of 45 vs. 46 years, weight of 110 kg vs. 119 kg, and BMI of 39 vs. 40, Dr. Reddy noted.

Embolotherapy was performed at a single center in Prague, and, on average, took 82.3 minutes and used 127 mL of contrast, 163 Gy/cm² radiation, and 4.2 mL of microspheres. A single vessel was injected in 80% of cases.

The intention-to-treat population comprised 19 TBE and 18 control subjects, and the per-protocol population comprised 15 TBE and 16 control subjects, after the exclusion of patients in whom embolotherapy was unsuccessful or incomplete or who withdrew consent.

All patients received endoscopy at baseline and 1 week, as well as an intensive 19-session lifestyle and dietary education intervention out to 6 months.

Patients who underwent TBE had significant improvement in hunger scores at 6 and 12 months, compared with baseline. Similarly, quality of life improved across all six domains, including significant gains in physical function, self-esteem, and overall quality of life at both time points, Dr. Reddy reported.

Dr. Reddy disclosed receiving research support from Endobar Solutions.

This article first appeared on Medscape.com.

Transcatheter bariatric embolotherapy (TBE) provides sustained weight loss without serious adverse effects among obese patients, results of a pilot sham-controlled study suggest.

At 6-month follow-up, the patients receiving the intervention had lost 7.4 kg (16.3 lbs), compared with 3.0 kg (6.6 lbs) in those randomized to a sham procedure in an intention-to-treat analysis (P = .034).

Results were similar in a per-protocol analysis (9.4 kg/20.7 lbs vs. 1.9 kg/4.1 lbs; P = .0002).

Weight loss after embolotherapy was sustained over 12 months, falling 7.8 kg (17.1 lbs) from baseline in the intention-to-treat population (P = .0011) and 9.3 kg (20.5 lbs) in the per-protocol population (P = .0005).

Safety events after TBE were mild nausea or vomiting, reported Vivek Reddy, MD, Mount Sinai Hospital, New York City. Five participants had minor, asymptomatic ulcers that required no additional treatment.

“In this randomized pilot trial, we established the proof of principle that transcatheter bariatric embolotherapy of the left gastric artery is safe and it promotes clinically significant weight loss,” he concluded at PCR e-Course, the virtual meeting of the Congress of European Association of Percutaneous Cardiovascular Interventions 2020.

Although bariatric surgery is highly effective, he noted that the associated morbidity and mortality limit its use to the severely obese with a body mass index (BMI) typically over 40 kg/m².

TBE is a minimally invasive approach that uses a custom occlusion balloon microcatheter and robotic manifold to inject 300- to 500-mcm beads to the left gastric artery. Preclinical and case studies suggest it promotes weight loss by reducing ghrelin, an appetite-stimulating hormone secreted from the gastric fundus, Dr. Reddy said.

The study enrolled 44 patients (aged 21-60 years) with a BMI of 35-55, excluding those with prior bariatric surgery and a history of ulcers, type 2 diabetes, chronic aspirin or nonsteroidal inflammatory use, and active Helicobacter pylori infection.

A total of 40 patients were randomly assigned to TBE or a sham procedure, in which lidocaine was applied to the femoral area and propofol infused for 1 hour. The two groups were well matched, with a mean age of 45 vs. 46 years, weight of 110 kg vs. 119 kg, and BMI of 39 vs. 40, Dr. Reddy noted.

Embolotherapy was performed at a single center in Prague, and, on average, took 82.3 minutes and used 127 mL of contrast, 163 Gy/cm² radiation, and 4.2 mL of microspheres. A single vessel was injected in 80% of cases.

The intention-to-treat population comprised 19 TBE and 18 control subjects, and the per-protocol population comprised 15 TBE and 16 control subjects, after the exclusion of patients in whom embolotherapy was unsuccessful or incomplete or who withdrew consent.

All patients received endoscopy at baseline and 1 week, as well as an intensive 19-session lifestyle and dietary education intervention out to 6 months.

Patients who underwent TBE had significant improvement in hunger scores at 6 and 12 months, compared with baseline. Similarly, quality of life improved across all six domains, including significant gains in physical function, self-esteem, and overall quality of life at both time points, Dr. Reddy reported.

Dr. Reddy disclosed receiving research support from Endobar Solutions.

This article first appeared on Medscape.com.

Fifteen-year projections for the shortage of primary care and specialty physicians in the United States grew to between 54,000 and 139,000 in the latest annual report by the Association of American Medical Colleges.

Those estimates are up from last year’s projections of a shortfall of 46,900-121,900 by 2032.

The Complexities of Physician Supply and Demand: Projections from 2018 to 2033, was the sixth annual study conducted for the AAMC by the Life Science division of global analytics firm IHS Markit.

This analysis, conducted in 2019, includes supply and demand scenarios but predates the COVID-19 pandemic.

In a telephone press briefing this morning, David J. Skorton, MD, AAMC’s president and CEO, told reporters that the pandemic has highlighted the acute effects of physician shortages.

“We’ve seen in stark detail how fragile and quickly overwhelmed America’s health care system truly is, and we’re nowhere near out of the woods with this public health emergency yet,” he said.

The persistent shortages mean people “will have ongoing difficulty accessing the care that they need, especially as we all age.”

Some of the biggest shortages will be seen in non–primary care specialists. Dr. Skorton notes that, during the pandemic, shortages of specialists in hospital settings, including critical care, emergency medicine, pulmonology, and infectious disease, are an urgent concern.

Population trends continue to be the biggest drivers of the shortage. Report authors found that by 2033, the U.S. population is expected to grow by 10.4% from 327 million to 361 million, with wide differences by age.

The under-18 population is expected to grow by 3.9%, whereas the numbers of those aged 65 and older is expected to balloon by 45.1% in that time, thus stoking demand for specialties focused on care for older Americans.

Physician age is also a large factor in the projections. More than two in five currently active physicians will be 65 or older in the next 10 years, according to the report. A wave of retirements will have a large impact on the supply of physicians.

The report explains that the projected shortages remain under predictable scenarios: an increase in the use of advanced practice nurses (APRNs) and physician assistants (PAs), more care in alternate settings such as retail clinics, and changes in payment and delivery.

According to the report, the supply of APRNs and PAs is on track to double over the next 15 years (with growth rates varying by APRN and PA specialty).

“At current rates of production, by 2033 APRN supply will grow by 276,000 [full-time equivalents (FTEs)] and PA supply by nearly 138,000 FTEs,” the report states.

However, authors acknowledge there is scant evidence on what effect these numbers will have on demand for physicians.

The report points out that if underserved communities were able to access health care in numbers similar to those without barriers imposed by where they live or what insurance they have, demand could rise beyond the projections in this report by an additional 74,000 to 145,000 physicians.
 

Stemming the shortages

The first step in addressing the shortage, Dr. Skorton said, is assuring a healthy physician pipeline to meet the demand for generations.

“One essential step that we believe Congress must take is to end the freeze that has been in place since 1997 that limits federal support for residency training of new physicians,” Skorton said.

He noted that AAMC supports the bipartisan Resident Physician Shortage Reduction Act, introduced to Congress in 2019, which calls for an increase in Medicare support for 3000 new residency positions each year over the next 5 years.

However, additional steps are needed, including enabling advanced practice providers to play a greater role in increasing the health care workforce, Dr. Skorton said.

Pointing out some of the effects of physician shortages, Janis M. Orlowski, MD, chief health care officer for the AAMC, noted that high rates of maternal morbidity are partially linked to lack of adequate numbers of physicians in the United States, and a lack of behavioral health specialists has exacerbated effects of the opioid epidemic.

Shortages are already evident in the current pandemic, she added, saying, “Today we see governors calling for retired physicians or physicians from other states to come and help battle the pandemic within their states.”

The report explains that long-term effects on physician numbers from the pandemic likely will include workforce exits because of COVID-19 deaths, early retirements from burnout, or a shift in interest in certain specialties.

Karen Fisher, JD, chief public policy officer for AAMC, said telehealth will also play an important role in bridging gaps in access to care, and its importance has already been seen in this first wave of the pandemic.

She noted that temporary federal waivers have made it easier for those enrolled in Medicare, Medicaid, and the Children’s Health Insurance Program to receive telehealth services during the pandemic.

Expanding the access to telehealth permanently will be important in helping to fill gaps, Ms. Fisher said.

Dr. Skorton, Dr. Orlowski, and Ms. Fisher have disclosed no relevant financial relationships.

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

Fifteen-year projections for the shortage of primary care and specialty physicians in the United States grew to between 54,000 and 139,000 in the latest annual report by the Association of American Medical Colleges.

Those estimates are up from last year’s projections of a shortfall of 46,900-121,900 by 2032.

The Complexities of Physician Supply and Demand: Projections from 2018 to 2033, was the sixth annual study conducted for the AAMC by the Life Science division of global analytics firm IHS Markit.

This analysis, conducted in 2019, includes supply and demand scenarios but predates the COVID-19 pandemic.

In a telephone press briefing this morning, David J. Skorton, MD, AAMC’s president and CEO, told reporters that the pandemic has highlighted the acute effects of physician shortages.

“We’ve seen in stark detail how fragile and quickly overwhelmed America’s health care system truly is, and we’re nowhere near out of the woods with this public health emergency yet,” he said.

The persistent shortages mean people “will have ongoing difficulty accessing the care that they need, especially as we all age.”

Some of the biggest shortages will be seen in non–primary care specialists. Dr. Skorton notes that, during the pandemic, shortages of specialists in hospital settings, including critical care, emergency medicine, pulmonology, and infectious disease, are an urgent concern.

Population trends continue to be the biggest drivers of the shortage. Report authors found that by 2033, the U.S. population is expected to grow by 10.4% from 327 million to 361 million, with wide differences by age.

The under-18 population is expected to grow by 3.9%, whereas the numbers of those aged 65 and older is expected to balloon by 45.1% in that time, thus stoking demand for specialties focused on care for older Americans.

Physician age is also a large factor in the projections. More than two in five currently active physicians will be 65 or older in the next 10 years, according to the report. A wave of retirements will have a large impact on the supply of physicians.

The report explains that the projected shortages remain under predictable scenarios: an increase in the use of advanced practice nurses (APRNs) and physician assistants (PAs), more care in alternate settings such as retail clinics, and changes in payment and delivery.

According to the report, the supply of APRNs and PAs is on track to double over the next 15 years (with growth rates varying by APRN and PA specialty).

“At current rates of production, by 2033 APRN supply will grow by 276,000 [full-time equivalents (FTEs)] and PA supply by nearly 138,000 FTEs,” the report states.

However, authors acknowledge there is scant evidence on what effect these numbers will have on demand for physicians.

The report points out that if underserved communities were able to access health care in numbers similar to those without barriers imposed by where they live or what insurance they have, demand could rise beyond the projections in this report by an additional 74,000 to 145,000 physicians.
 

Stemming the shortages

The first step in addressing the shortage, Dr. Skorton said, is assuring a healthy physician pipeline to meet the demand for generations.

“One essential step that we believe Congress must take is to end the freeze that has been in place since 1997 that limits federal support for residency training of new physicians,” Skorton said.

He noted that AAMC supports the bipartisan Resident Physician Shortage Reduction Act, introduced to Congress in 2019, which calls for an increase in Medicare support for 3000 new residency positions each year over the next 5 years.

However, additional steps are needed, including enabling advanced practice providers to play a greater role in increasing the health care workforce, Dr. Skorton said.

Pointing out some of the effects of physician shortages, Janis M. Orlowski, MD, chief health care officer for the AAMC, noted that high rates of maternal morbidity are partially linked to lack of adequate numbers of physicians in the United States, and a lack of behavioral health specialists has exacerbated effects of the opioid epidemic.

Shortages are already evident in the current pandemic, she added, saying, “Today we see governors calling for retired physicians or physicians from other states to come and help battle the pandemic within their states.”

The report explains that long-term effects on physician numbers from the pandemic likely will include workforce exits because of COVID-19 deaths, early retirements from burnout, or a shift in interest in certain specialties.

Karen Fisher, JD, chief public policy officer for AAMC, said telehealth will also play an important role in bridging gaps in access to care, and its importance has already been seen in this first wave of the pandemic.

She noted that temporary federal waivers have made it easier for those enrolled in Medicare, Medicaid, and the Children’s Health Insurance Program to receive telehealth services during the pandemic.

Expanding the access to telehealth permanently will be important in helping to fill gaps, Ms. Fisher said.

Dr. Skorton, Dr. Orlowski, and Ms. Fisher have disclosed no relevant financial relationships.

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

Fifteen-year projections for the shortage of primary care and specialty physicians in the United States grew to between 54,000 and 139,000 in the latest annual report by the Association of American Medical Colleges.

Those estimates are up from last year’s projections of a shortfall of 46,900-121,900 by 2032.

The Complexities of Physician Supply and Demand: Projections from 2018 to 2033, was the sixth annual study conducted for the AAMC by the Life Science division of global analytics firm IHS Markit.

This analysis, conducted in 2019, includes supply and demand scenarios but predates the COVID-19 pandemic.

In a telephone press briefing this morning, David J. Skorton, MD, AAMC’s president and CEO, told reporters that the pandemic has highlighted the acute effects of physician shortages.

“We’ve seen in stark detail how fragile and quickly overwhelmed America’s health care system truly is, and we’re nowhere near out of the woods with this public health emergency yet,” he said.

The persistent shortages mean people “will have ongoing difficulty accessing the care that they need, especially as we all age.”

Some of the biggest shortages will be seen in non–primary care specialists. Dr. Skorton notes that, during the pandemic, shortages of specialists in hospital settings, including critical care, emergency medicine, pulmonology, and infectious disease, are an urgent concern.

Population trends continue to be the biggest drivers of the shortage. Report authors found that by 2033, the U.S. population is expected to grow by 10.4% from 327 million to 361 million, with wide differences by age.

The under-18 population is expected to grow by 3.9%, whereas the numbers of those aged 65 and older is expected to balloon by 45.1% in that time, thus stoking demand for specialties focused on care for older Americans.

Physician age is also a large factor in the projections. More than two in five currently active physicians will be 65 or older in the next 10 years, according to the report. A wave of retirements will have a large impact on the supply of physicians.

The report explains that the projected shortages remain under predictable scenarios: an increase in the use of advanced practice nurses (APRNs) and physician assistants (PAs), more care in alternate settings such as retail clinics, and changes in payment and delivery.

According to the report, the supply of APRNs and PAs is on track to double over the next 15 years (with growth rates varying by APRN and PA specialty).

“At current rates of production, by 2033 APRN supply will grow by 276,000 [full-time equivalents (FTEs)] and PA supply by nearly 138,000 FTEs,” the report states.

However, authors acknowledge there is scant evidence on what effect these numbers will have on demand for physicians.

The report points out that if underserved communities were able to access health care in numbers similar to those without barriers imposed by where they live or what insurance they have, demand could rise beyond the projections in this report by an additional 74,000 to 145,000 physicians.
 

Stemming the shortages

The first step in addressing the shortage, Dr. Skorton said, is assuring a healthy physician pipeline to meet the demand for generations.

“One essential step that we believe Congress must take is to end the freeze that has been in place since 1997 that limits federal support for residency training of new physicians,” Skorton said.

He noted that AAMC supports the bipartisan Resident Physician Shortage Reduction Act, introduced to Congress in 2019, which calls for an increase in Medicare support for 3000 new residency positions each year over the next 5 years.

However, additional steps are needed, including enabling advanced practice providers to play a greater role in increasing the health care workforce, Dr. Skorton said.

Pointing out some of the effects of physician shortages, Janis M. Orlowski, MD, chief health care officer for the AAMC, noted that high rates of maternal morbidity are partially linked to lack of adequate numbers of physicians in the United States, and a lack of behavioral health specialists has exacerbated effects of the opioid epidemic.

Shortages are already evident in the current pandemic, she added, saying, “Today we see governors calling for retired physicians or physicians from other states to come and help battle the pandemic within their states.”

The report explains that long-term effects on physician numbers from the pandemic likely will include workforce exits because of COVID-19 deaths, early retirements from burnout, or a shift in interest in certain specialties.

Karen Fisher, JD, chief public policy officer for AAMC, said telehealth will also play an important role in bridging gaps in access to care, and its importance has already been seen in this first wave of the pandemic.

She noted that temporary federal waivers have made it easier for those enrolled in Medicare, Medicaid, and the Children’s Health Insurance Program to receive telehealth services during the pandemic.

Expanding the access to telehealth permanently will be important in helping to fill gaps, Ms. Fisher said.

Dr. Skorton, Dr. Orlowski, and Ms. Fisher have disclosed no relevant financial relationships.

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

New data from active surveillance of the severe inflammatory condition associated with COVID-19 in previously healthy children provide further insight into the prevalence and course of the rare syndrome, but experts are concerned that current diagnostic criteria may not capture the true scope of the problem.

In separate reports published online June 29 in the New England Journal of Medicine, researchers from the New York State Department of Health and the Centers for Disease Control and Prevention (CDC) describe the epidemiology and clinical features of multisystem inflammatory syndrome in children (MIS-C) on the basis of information derived from targeted surveillance programs in New York State and across the country.

For the New York study, Elizabeth M. Dufort, MD, from the New York Department of Health in Albany and colleagues analyzed MIS-C surveillance data from 106 hospitals across the state. Of 191 suspected MIS-C cases reported to the Department of Health from March 1 through May 10, 99 met the state’s interim case definition of the condition and were included in the analysis.

The incidence rate for MIS-C was two cases per 100,000 individuals younger than 21 years, whereas the incidence rate of confirmed COVID-19 cases in this age group was 322 per 100,000. Most cases occurred approximately 1 month after the state’s COVID-19 peak.

“Among our patients, predominantly from the New York Metropolitan Region, 40% were black and 36% were Hispanic. This may be a reflection of the well-documented elevated incidence of SARS-CoV-2 infection among black and Hispanic communities,” the authors report.

All children presented with fever or chills, and most had tachycardia (97%) and gastrointestinal symptoms (80%). Rash (60%), conjunctival infection (56%), hypotension (32%), and mucosal changes (27%) were reported. Among all of the children, levels of inflammatory markers were elevated, including levels of C-reactive protein (100%), D-dimer (91%), and troponin (71%). More than one third of the patients (36%) were diagnosed with myocarditis, and an additional 16% had clinical myocarditis.

Of the full cohort, 80% of the children required intensive care, 62% received vasopressor support, and two children died.

The high prevalence of cardiac dysfunction or depression, coagulopathy, gastrointestinal symptoms, mild respiratory symptoms, and indications for supplemental oxygen in patients with MIS-C stands in contrast to the clinical picture observed in most acute cases of COVID-19 in hospitalized children, the authors write.

“Although most children have mild or no illness from SARS-CoV-2 infection, MIS-C may follow Covid-19 or asymptomatic SARS-CoV-2 infection. Recognition of the syndrome and early identification of children with MIS-C, including early monitoring of blood pressure and electrocardiographic and echocardiographic evaluation, could inform appropriate supportive care and other potential therapeutic options,” they continue.

The incidence of MIS-C among children infected with SARS-CoV-2 is unclear because children with COVID-19 often have mild or no symptoms and because children are not tested as frequently, the authors state. For this reason, “[i]t is crucial to establish surveillance for MIS-C cases, particularly in communities with higher levels of SARS-CoV-2 transmission.”

Important Differences From Kawasaki Disease

In a separate study, Leora R. Feldstein, MD, of the CDC, and colleagues report 186 cases of MIS-C collected through targeted surveillance of pediatric health centers in 26 US states from March 15 to May 20, 2020. As with the New York cohort, a disproportionate number of children in this cohort were black (25%) and Hispanic or Latino (31%).

Similar to the New York cohort, 80% of the children in this group required intensive care, 48% received vasoactive support, 20% required invasive mechanical ventilation, and four children died. Skin rashes, gastrointestinal symptoms, cardiovascular and hematologic effects, mucous changes, and elevations of inflammatory biomarkers were also similarly observed.

The researchers note that, although many of the features of MIS-C overlap with Kawasaki disease, there are some important differences, particularly with respect to the nature of cardiovascular involvement. “Approximately 5% of children with Kawasaki’s disease in the United States present with cardiovascular shock leading to vasopressor or inotropic support, as compared with 50% of the patients in our series,” the authors write.

In addition, coronary-artery aneurysms affect approximately one quarter of Kawasaki disease patients within 21 days of disease onset. “In our series, a maximum z score of 2.5 or higher in the left anterior descending or right coronary artery was reported in 8% of the patients overall and in 9% of patients with echocardiograms,” they report.

Additional differentiating features include patient age and race/ethnicity. Kawasaki disease occurs most commonly in children younger than 5 years. The median age in the multistate study was 8.3 years, and nearly half of the children in the New York cohort were in the 6- to 12-year age group. Further, Kawasaki disease is disproportionately prevalent in children of Asian descent.

Despite the differences, “until more is known about long-term cardiac sequelae of MIS-C, providers could consider following Kawasaki’s disease guidelines for follow-up, which recommend repeat echocardiographic imaging at 1 to 2 weeks.”

As was the case in the New York series, treatment in the multistate cohort most commonly included intravenous immunoglobulin and systemic glucocorticoids. Optimal management, however, will require a better understanding of the pathogenesis of MIS-C, Feldstein and colleagues write.

Questions Remain

With the accumulating data on this syndrome, the MIS-C picture seems to be getting incrementally clearer, but there is still much uncertainty, according to Michael Levin, FMedSci, PhD, from the Department of Infectious Disease, Imperial College London, United Kingdom.

“The recognition and description of new diseases often resemble the parable of the blind men and the elephant, with each declaring that the part of the beast they have touched fully defines it,” he writes in an accompanying editorial.

“As the coronavirus disease 2019 (Covid-19) pandemic has evolved, case reports have appeared describing children with unusual febrile illnesses that have features of Kawasaki’s disease, toxic shock syndrome, acute abdominal conditions, and encephalopathy, along with other reports of children with fever, elevated inflammatory markers, and multisystem involvement. It is now apparent that these reports were describing different clinical presentations of a new childhood inflammatory disorder.”

Although a consistent clinical picture is emerging, “[t]he published reports have used a variety of hastily developed case definitions based on the most severe cases, possibly missing less serious cases,” Levin writes. In particular, both the CDC and World Health Organization definitions require evidence of SARS-CoV-2 infection or exposure, which might contribute to underrecognition and underreporting because asymptomatic infections are common and antibody testing is not universally available.

“There is concern that children meeting current diagnostic criteria for MIS-C are the ‘tip of the iceberg,’ and a bigger problem may be lurking below the waterline,” Levin states. With approximately 1000 cases of the syndrome reported worldwide, “do we now have a clear picture of the new disorder, or as in the story of the blind men and the elephant, has only part of the beast been described?”

Adrienne Randolph, MD, of Boston Children’s Hospital, who is a coauthor of the multistate report, agrees that there is still much to learn about MIS-C before the whole beast can be understood. In an interview with Medscape Medical News, she listed the following key questions that have yet to be answered:

• Why do some children get MIS-C and not others?
• What is the long-term outcome of children with MIS-C?
• How can we differentiate MIS-C from acute COVID-19 infection in children with respiratory failure?
• Does MIS-C occur in young adults?

Randolph said her team is taking the best path forward toward answering these questions, including conducting a second study to identify risk factors for MIS-C and longer-term follow-up studies with the National Institutes of Health. “We are also getting consent to collect blood samples and look at other tests to help distinguish MIS-C from acute COVID-19 infection,” she said. She encouraged heightened awareness among physicians who care for young adults to consider MIS-C in patients aged 21 years and older who present with similar signs and symptoms.

On the basis of the answers to these and additional questions, the case definitions for MIS-C may need refinement to capture the wider spectrum of illness, Levin writes in his editorial. “The challenges of this new condition will now be to understand its pathophysiological mechanisms, to develop diagnostics, and to define the best treatment.”

Kleinman has received grants from the Health Services Resources Administration outside the submitted work. Maddux has received grants from the NIH/NICHD and the Francis Family Foundation outside the submitted work. Randolph has received grants from Genentech and personal fees from La Jolla Pharma outside the submitted work and others from the CDC during the conduct of the study.

This article first appeared on Medscape.com.

New data from active surveillance of the severe inflammatory condition associated with COVID-19 in previously healthy children provide further insight into the prevalence and course of the rare syndrome, but experts are concerned that current diagnostic criteria may not capture the true scope of the problem.

In separate reports published online June 29 in the New England Journal of Medicine, researchers from the New York State Department of Health and the Centers for Disease Control and Prevention (CDC) describe the epidemiology and clinical features of multisystem inflammatory syndrome in children (MIS-C) on the basis of information derived from targeted surveillance programs in New York State and across the country.

For the New York study, Elizabeth M. Dufort, MD, from the New York Department of Health in Albany and colleagues analyzed MIS-C surveillance data from 106 hospitals across the state. Of 191 suspected MIS-C cases reported to the Department of Health from March 1 through May 10, 99 met the state’s interim case definition of the condition and were included in the analysis.

The incidence rate for MIS-C was two cases per 100,000 individuals younger than 21 years, whereas the incidence rate of confirmed COVID-19 cases in this age group was 322 per 100,000. Most cases occurred approximately 1 month after the state’s COVID-19 peak.

“Among our patients, predominantly from the New York Metropolitan Region, 40% were black and 36% were Hispanic. This may be a reflection of the well-documented elevated incidence of SARS-CoV-2 infection among black and Hispanic communities,” the authors report.

All children presented with fever or chills, and most had tachycardia (97%) and gastrointestinal symptoms (80%). Rash (60%), conjunctival infection (56%), hypotension (32%), and mucosal changes (27%) were reported. Among all of the children, levels of inflammatory markers were elevated, including levels of C-reactive protein (100%), D-dimer (91%), and troponin (71%). More than one third of the patients (36%) were diagnosed with myocarditis, and an additional 16% had clinical myocarditis.

Of the full cohort, 80% of the children required intensive care, 62% received vasopressor support, and two children died.

The high prevalence of cardiac dysfunction or depression, coagulopathy, gastrointestinal symptoms, mild respiratory symptoms, and indications for supplemental oxygen in patients with MIS-C stands in contrast to the clinical picture observed in most acute cases of COVID-19 in hospitalized children, the authors write.

“Although most children have mild or no illness from SARS-CoV-2 infection, MIS-C may follow Covid-19 or asymptomatic SARS-CoV-2 infection. Recognition of the syndrome and early identification of children with MIS-C, including early monitoring of blood pressure and electrocardiographic and echocardiographic evaluation, could inform appropriate supportive care and other potential therapeutic options,” they continue.

The incidence of MIS-C among children infected with SARS-CoV-2 is unclear because children with COVID-19 often have mild or no symptoms and because children are not tested as frequently, the authors state. For this reason, “[i]t is crucial to establish surveillance for MIS-C cases, particularly in communities with higher levels of SARS-CoV-2 transmission.”

Important Differences From Kawasaki Disease

In a separate study, Leora R. Feldstein, MD, of the CDC, and colleagues report 186 cases of MIS-C collected through targeted surveillance of pediatric health centers in 26 US states from March 15 to May 20, 2020. As with the New York cohort, a disproportionate number of children in this cohort were black (25%) and Hispanic or Latino (31%).

Similar to the New York cohort, 80% of the children in this group required intensive care, 48% received vasoactive support, 20% required invasive mechanical ventilation, and four children died. Skin rashes, gastrointestinal symptoms, cardiovascular and hematologic effects, mucous changes, and elevations of inflammatory biomarkers were also similarly observed.

The researchers note that, although many of the features of MIS-C overlap with Kawasaki disease, there are some important differences, particularly with respect to the nature of cardiovascular involvement. “Approximately 5% of children with Kawasaki’s disease in the United States present with cardiovascular shock leading to vasopressor or inotropic support, as compared with 50% of the patients in our series,” the authors write.

In addition, coronary-artery aneurysms affect approximately one quarter of Kawasaki disease patients within 21 days of disease onset. “In our series, a maximum z score of 2.5 or higher in the left anterior descending or right coronary artery was reported in 8% of the patients overall and in 9% of patients with echocardiograms,” they report.

Additional differentiating features include patient age and race/ethnicity. Kawasaki disease occurs most commonly in children younger than 5 years. The median age in the multistate study was 8.3 years, and nearly half of the children in the New York cohort were in the 6- to 12-year age group. Further, Kawasaki disease is disproportionately prevalent in children of Asian descent.

Despite the differences, “until more is known about long-term cardiac sequelae of MIS-C, providers could consider following Kawasaki’s disease guidelines for follow-up, which recommend repeat echocardiographic imaging at 1 to 2 weeks.”

As was the case in the New York series, treatment in the multistate cohort most commonly included intravenous immunoglobulin and systemic glucocorticoids. Optimal management, however, will require a better understanding of the pathogenesis of MIS-C, Feldstein and colleagues write.

Questions Remain

With the accumulating data on this syndrome, the MIS-C picture seems to be getting incrementally clearer, but there is still much uncertainty, according to Michael Levin, FMedSci, PhD, from the Department of Infectious Disease, Imperial College London, United Kingdom.

“The recognition and description of new diseases often resemble the parable of the blind men and the elephant, with each declaring that the part of the beast they have touched fully defines it,” he writes in an accompanying editorial.

“As the coronavirus disease 2019 (Covid-19) pandemic has evolved, case reports have appeared describing children with unusual febrile illnesses that have features of Kawasaki’s disease, toxic shock syndrome, acute abdominal conditions, and encephalopathy, along with other reports of children with fever, elevated inflammatory markers, and multisystem involvement. It is now apparent that these reports were describing different clinical presentations of a new childhood inflammatory disorder.”

Although a consistent clinical picture is emerging, “[t]he published reports have used a variety of hastily developed case definitions based on the most severe cases, possibly missing less serious cases,” Levin writes. In particular, both the CDC and World Health Organization definitions require evidence of SARS-CoV-2 infection or exposure, which might contribute to underrecognition and underreporting because asymptomatic infections are common and antibody testing is not universally available.

“There is concern that children meeting current diagnostic criteria for MIS-C are the ‘tip of the iceberg,’ and a bigger problem may be lurking below the waterline,” Levin states. With approximately 1000 cases of the syndrome reported worldwide, “do we now have a clear picture of the new disorder, or as in the story of the blind men and the elephant, has only part of the beast been described?”

Adrienne Randolph, MD, of Boston Children’s Hospital, who is a coauthor of the multistate report, agrees that there is still much to learn about MIS-C before the whole beast can be understood. In an interview with Medscape Medical News, she listed the following key questions that have yet to be answered:

• Why do some children get MIS-C and not others?
• What is the long-term outcome of children with MIS-C?
• How can we differentiate MIS-C from acute COVID-19 infection in children with respiratory failure?
• Does MIS-C occur in young adults?

Randolph said her team is taking the best path forward toward answering these questions, including conducting a second study to identify risk factors for MIS-C and longer-term follow-up studies with the National Institutes of Health. “We are also getting consent to collect blood samples and look at other tests to help distinguish MIS-C from acute COVID-19 infection,” she said. She encouraged heightened awareness among physicians who care for young adults to consider MIS-C in patients aged 21 years and older who present with similar signs and symptoms.

On the basis of the answers to these and additional questions, the case definitions for MIS-C may need refinement to capture the wider spectrum of illness, Levin writes in his editorial. “The challenges of this new condition will now be to understand its pathophysiological mechanisms, to develop diagnostics, and to define the best treatment.”

Kleinman has received grants from the Health Services Resources Administration outside the submitted work. Maddux has received grants from the NIH/NICHD and the Francis Family Foundation outside the submitted work. Randolph has received grants from Genentech and personal fees from La Jolla Pharma outside the submitted work and others from the CDC during the conduct of the study.

This article first appeared on Medscape.com.

New data from active surveillance of the severe inflammatory condition associated with COVID-19 in previously healthy children provide further insight into the prevalence and course of the rare syndrome, but experts are concerned that current diagnostic criteria may not capture the true scope of the problem.

In separate reports published online June 29 in the New England Journal of Medicine, researchers from the New York State Department of Health and the Centers for Disease Control and Prevention (CDC) describe the epidemiology and clinical features of multisystem inflammatory syndrome in children (MIS-C) on the basis of information derived from targeted surveillance programs in New York State and across the country.

For the New York study, Elizabeth M. Dufort, MD, from the New York Department of Health in Albany and colleagues analyzed MIS-C surveillance data from 106 hospitals across the state. Of 191 suspected MIS-C cases reported to the Department of Health from March 1 through May 10, 99 met the state’s interim case definition of the condition and were included in the analysis.

The incidence rate for MIS-C was two cases per 100,000 individuals younger than 21 years, whereas the incidence rate of confirmed COVID-19 cases in this age group was 322 per 100,000. Most cases occurred approximately 1 month after the state’s COVID-19 peak.

“Among our patients, predominantly from the New York Metropolitan Region, 40% were black and 36% were Hispanic. This may be a reflection of the well-documented elevated incidence of SARS-CoV-2 infection among black and Hispanic communities,” the authors report.

All children presented with fever or chills, and most had tachycardia (97%) and gastrointestinal symptoms (80%). Rash (60%), conjunctival infection (56%), hypotension (32%), and mucosal changes (27%) were reported. Among all of the children, levels of inflammatory markers were elevated, including levels of C-reactive protein (100%), D-dimer (91%), and troponin (71%). More than one third of the patients (36%) were diagnosed with myocarditis, and an additional 16% had clinical myocarditis.

Of the full cohort, 80% of the children required intensive care, 62% received vasopressor support, and two children died.

The high prevalence of cardiac dysfunction or depression, coagulopathy, gastrointestinal symptoms, mild respiratory symptoms, and indications for supplemental oxygen in patients with MIS-C stands in contrast to the clinical picture observed in most acute cases of COVID-19 in hospitalized children, the authors write.

“Although most children have mild or no illness from SARS-CoV-2 infection, MIS-C may follow Covid-19 or asymptomatic SARS-CoV-2 infection. Recognition of the syndrome and early identification of children with MIS-C, including early monitoring of blood pressure and electrocardiographic and echocardiographic evaluation, could inform appropriate supportive care and other potential therapeutic options,” they continue.

The incidence of MIS-C among children infected with SARS-CoV-2 is unclear because children with COVID-19 often have mild or no symptoms and because children are not tested as frequently, the authors state. For this reason, “[i]t is crucial to establish surveillance for MIS-C cases, particularly in communities with higher levels of SARS-CoV-2 transmission.”

Important Differences From Kawasaki Disease

In a separate study, Leora R. Feldstein, MD, of the CDC, and colleagues report 186 cases of MIS-C collected through targeted surveillance of pediatric health centers in 26 US states from March 15 to May 20, 2020. As with the New York cohort, a disproportionate number of children in this cohort were black (25%) and Hispanic or Latino (31%).

Similar to the New York cohort, 80% of the children in this group required intensive care, 48% received vasoactive support, 20% required invasive mechanical ventilation, and four children died. Skin rashes, gastrointestinal symptoms, cardiovascular and hematologic effects, mucous changes, and elevations of inflammatory biomarkers were also similarly observed.

The researchers note that, although many of the features of MIS-C overlap with Kawasaki disease, there are some important differences, particularly with respect to the nature of cardiovascular involvement. “Approximately 5% of children with Kawasaki’s disease in the United States present with cardiovascular shock leading to vasopressor or inotropic support, as compared with 50% of the patients in our series,” the authors write.

In addition, coronary-artery aneurysms affect approximately one quarter of Kawasaki disease patients within 21 days of disease onset. “In our series, a maximum z score of 2.5 or higher in the left anterior descending or right coronary artery was reported in 8% of the patients overall and in 9% of patients with echocardiograms,” they report.

Additional differentiating features include patient age and race/ethnicity. Kawasaki disease occurs most commonly in children younger than 5 years. The median age in the multistate study was 8.3 years, and nearly half of the children in the New York cohort were in the 6- to 12-year age group. Further, Kawasaki disease is disproportionately prevalent in children of Asian descent.

Despite the differences, “until more is known about long-term cardiac sequelae of MIS-C, providers could consider following Kawasaki’s disease guidelines for follow-up, which recommend repeat echocardiographic imaging at 1 to 2 weeks.”

As was the case in the New York series, treatment in the multistate cohort most commonly included intravenous immunoglobulin and systemic glucocorticoids. Optimal management, however, will require a better understanding of the pathogenesis of MIS-C, Feldstein and colleagues write.

Questions Remain

With the accumulating data on this syndrome, the MIS-C picture seems to be getting incrementally clearer, but there is still much uncertainty, according to Michael Levin, FMedSci, PhD, from the Department of Infectious Disease, Imperial College London, United Kingdom.

“The recognition and description of new diseases often resemble the parable of the blind men and the elephant, with each declaring that the part of the beast they have touched fully defines it,” he writes in an accompanying editorial.

“As the coronavirus disease 2019 (Covid-19) pandemic has evolved, case reports have appeared describing children with unusual febrile illnesses that have features of Kawasaki’s disease, toxic shock syndrome, acute abdominal conditions, and encephalopathy, along with other reports of children with fever, elevated inflammatory markers, and multisystem involvement. It is now apparent that these reports were describing different clinical presentations of a new childhood inflammatory disorder.”

Although a consistent clinical picture is emerging, “[t]he published reports have used a variety of hastily developed case definitions based on the most severe cases, possibly missing less serious cases,” Levin writes. In particular, both the CDC and World Health Organization definitions require evidence of SARS-CoV-2 infection or exposure, which might contribute to underrecognition and underreporting because asymptomatic infections are common and antibody testing is not universally available.

“There is concern that children meeting current diagnostic criteria for MIS-C are the ‘tip of the iceberg,’ and a bigger problem may be lurking below the waterline,” Levin states. With approximately 1000 cases of the syndrome reported worldwide, “do we now have a clear picture of the new disorder, or as in the story of the blind men and the elephant, has only part of the beast been described?”

Adrienne Randolph, MD, of Boston Children’s Hospital, who is a coauthor of the multistate report, agrees that there is still much to learn about MIS-C before the whole beast can be understood. In an interview with Medscape Medical News, she listed the following key questions that have yet to be answered:

• Why do some children get MIS-C and not others?
• What is the long-term outcome of children with MIS-C?
• How can we differentiate MIS-C from acute COVID-19 infection in children with respiratory failure?
• Does MIS-C occur in young adults?

Randolph said her team is taking the best path forward toward answering these questions, including conducting a second study to identify risk factors for MIS-C and longer-term follow-up studies with the National Institutes of Health. “We are also getting consent to collect blood samples and look at other tests to help distinguish MIS-C from acute COVID-19 infection,” she said. She encouraged heightened awareness among physicians who care for young adults to consider MIS-C in patients aged 21 years and older who present with similar signs and symptoms.

On the basis of the answers to these and additional questions, the case definitions for MIS-C may need refinement to capture the wider spectrum of illness, Levin writes in his editorial. “The challenges of this new condition will now be to understand its pathophysiological mechanisms, to develop diagnostics, and to define the best treatment.”

Kleinman has received grants from the Health Services Resources Administration outside the submitted work. Maddux has received grants from the NIH/NICHD and the Francis Family Foundation outside the submitted work. Randolph has received grants from Genentech and personal fees from La Jolla Pharma outside the submitted work and others from the CDC during the conduct of the study.

This article first appeared on Medscape.com.