MDedge Rheumatology

This transcript has been edited for clarity.

The ongoing longitudinal Nurses’ Health Study has served as an incredible database for evaluating disease states prospectively over decades, thanks to the robust input of its participants. Most recently, this allowed for an important analysis of the association between gastroesophageal reflux (GER) symptoms and sleep quality, the results of which were published in JAMA Network Open.

Approximately 49,000 women with a median age of 59 years (range, 48-69 years) provided data for this analysis. Starting in 2005, they were asked about their experience of GER symptoms. In 2017, they were also asked to respond to a questionnaire, a modified Pittsburgh Sleep Quality Index (PSQI). This is a tool we’ve used a lot in prospective studies looking at gastrointestinal diseases and sleep-related abnormalities. It’s unique in that it looks not only at sleep but also at next-day function and daytime sleepiness, which is important here for its implications related to reflux disease and sleep fragmentation.

In assessing these outcomes, the investigators found that the relative risk for association with sleep fragmentation was approximately 15% greater in those with GER symptoms occurring one to three times a month. For those with GER symptoms occurring once a week and more than once a week, the approximate relative risk increased by 30% and 53%, respectively. Clearly, the association of GER symptoms and relative sleep quality was really important.

It should be noted that the PSQI is a disease-independent, validated instrument. It’s not specific to GER disease or any diseases. It’s cross validated across 17 different languages. I think what’s most important about its use in the assessment here is the incorporation of next-day function and asking participants about daytime sleepiness, which we’ll discuss in more detail shortly.
 

The many causes of interrupted sleep

We’ve all experienced sleep fragmentation, whether in the form of having been on call during our medical training or common experiences like hearing a child cry in the night, a noisy truck pass by, or a dog barking. You may or may not remember that these happened the next day, but they’ve nonetheless interrupted your sleep efficiency.

When you transition laterally across the stages of sleep, that’s what establishes the circadian rhythm and ensures sleep hygiene. Typically, we require approximately 7 hours of restful sleep to do that. But if you fragment or interrupt this process, you more or less move your way erratically through the night, disrupting sleep hygiene and efficiency.

If you have a cognitive awakening during those disruptions, you may recall those events the next day. Or, you may not remember it at all, and such amnestic events are normal for some people with sleep disruptions.

You may also have a sensory arousal, whether it’s due to GER symptoms, auditory stimuli, bumping your toe, or whatever disruptive event. Any of these can cause you to lose that laterality of smooth transition through sleep.

Approximately 20% of the U.S. population have reported GER symptoms at least once a week. Incident data indicate that number may be increasing by as much as 5% a year. Much of that increase is tied to obesity. But nonetheless, it’s a problem on the rise.

It’s important to know this as we start to look at sleep. If GER is acting as a trigger to sleep disruption, you need to ask your patients with this condition about next-day function.

In particular, the next-day function questions to ask are, “How do you feel when you get up? Are you awake and refreshed? Do you have early fatigue? Do you drag yourself out of bed, have daytime somnolence, loss of concentration, or irritability?”

Those are key parameters we can use for looking back to the night before and gauging sleep efficiency. If you’re not asking those questions, you may miss out on identifying a patient having sleep fragmentation.
 

Sleep’s role in inflammatory disease processes

I now perform an interval assessment of this type not just in my patients with GER disease but across all my patients. I do so because sleep is physiologically important in so many ways.

In patients who have nonalcoholic fatty liver disease and a variety of other liver diseases, we’re finding an increased association with sleep fragmentation outside of sleep apnea.

The same is true with irritable bowel and other functional diseases.

When you have sleep fragmentation in inflammatory bowel disease, you turn on a variety of inflammatory proteins (e.g., C-reactive protein) and cytokines, such as interleukins and tumor necrosis factor alpha. These processes may actually tip somebody over to a pro-inflammatory state.

When it comes to what might be considered a relatively simpler condition like GER disease, Ronnie Fass and colleagues showed a number of years ago via Bernstein testing performed in patients with both fragmented and normal sleep that the sensory thresholds all get lowered in the former group. This is irrespective of whether you have a functional symptom or you’re awakened by bumping your toe, a headache, or having heartburn; your sensory thresholds are lower. As a result, the same stimulus provides a higher sense of awareness. By ramping up that awareness, you increase the interference with the next-day function.

We’ve shown that sleep fragmentation affects a variety of things, including immune function. This may be why many people get sick when they travel in between time zones.

There are also implications relating to things like obesity. When you have sleep dysfunction, you have effects on leptin and ghrelin, contrary to what you would normally want to have. This, in turn, causes adverse effects on stimulation or suppression of satiety or appetite. These are things that I counsel my patients about when I talk about reflux as well as those trying to lose weight.

Sleep disruption affects cortisol stimulation and has a significant correlation with type 2 diabetes, cardiovascular diseases, and even mortality statistics. 
 

Advice for counseling patients

This latest analysis from the Nurses’ Health Study reminds us that a lot of people have reflux and a lot of people have sleep fragmentation. We need to do better in asking our patients if they have symptoms specific not only to reflux but also to potentially sleep-related complications.

The more we do that, the more we individualize patient treatment rather than treating them as a disease state. This, in turn, will allow us to practice personalized medicine. The more we can engage our patients with reflux disease by asking the right questions about next-day function, the better we can do in improving their outcomes.

It’s time for us all to open our eyes to the value of closing them. Let’s talk to our patients with reflux disease in a little bit of a different light, providing a new perspective on strategies we can use to mitigate and deal with those symptoms, thereby preventing the consequences of sleep fragmentation.

Hopefully, this overview gives you some guidance the next time you have a conversation with your patients. It will apply across many, many disease states, and in almost everything we do in gastroenterology.

David A. Johnson, MD, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk, Va., and a past president of the American College of Gastroenterology. He reported advising with ISOTHRIVE and Johnson & Johnson.

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

This transcript has been edited for clarity.

The ongoing longitudinal Nurses’ Health Study has served as an incredible database for evaluating disease states prospectively over decades, thanks to the robust input of its participants. Most recently, this allowed for an important analysis of the association between gastroesophageal reflux (GER) symptoms and sleep quality, the results of which were published in JAMA Network Open.

Approximately 49,000 women with a median age of 59 years (range, 48-69 years) provided data for this analysis. Starting in 2005, they were asked about their experience of GER symptoms. In 2017, they were also asked to respond to a questionnaire, a modified Pittsburgh Sleep Quality Index (PSQI). This is a tool we’ve used a lot in prospective studies looking at gastrointestinal diseases and sleep-related abnormalities. It’s unique in that it looks not only at sleep but also at next-day function and daytime sleepiness, which is important here for its implications related to reflux disease and sleep fragmentation.

In assessing these outcomes, the investigators found that the relative risk for association with sleep fragmentation was approximately 15% greater in those with GER symptoms occurring one to three times a month. For those with GER symptoms occurring once a week and more than once a week, the approximate relative risk increased by 30% and 53%, respectively. Clearly, the association of GER symptoms and relative sleep quality was really important.

It should be noted that the PSQI is a disease-independent, validated instrument. It’s not specific to GER disease or any diseases. It’s cross validated across 17 different languages. I think what’s most important about its use in the assessment here is the incorporation of next-day function and asking participants about daytime sleepiness, which we’ll discuss in more detail shortly.
 

The many causes of interrupted sleep

We’ve all experienced sleep fragmentation, whether in the form of having been on call during our medical training or common experiences like hearing a child cry in the night, a noisy truck pass by, or a dog barking. You may or may not remember that these happened the next day, but they’ve nonetheless interrupted your sleep efficiency.

When you transition laterally across the stages of sleep, that’s what establishes the circadian rhythm and ensures sleep hygiene. Typically, we require approximately 7 hours of restful sleep to do that. But if you fragment or interrupt this process, you more or less move your way erratically through the night, disrupting sleep hygiene and efficiency.

If you have a cognitive awakening during those disruptions, you may recall those events the next day. Or, you may not remember it at all, and such amnestic events are normal for some people with sleep disruptions.

You may also have a sensory arousal, whether it’s due to GER symptoms, auditory stimuli, bumping your toe, or whatever disruptive event. Any of these can cause you to lose that laterality of smooth transition through sleep.

Approximately 20% of the U.S. population have reported GER symptoms at least once a week. Incident data indicate that number may be increasing by as much as 5% a year. Much of that increase is tied to obesity. But nonetheless, it’s a problem on the rise.

It’s important to know this as we start to look at sleep. If GER is acting as a trigger to sleep disruption, you need to ask your patients with this condition about next-day function.

In particular, the next-day function questions to ask are, “How do you feel when you get up? Are you awake and refreshed? Do you have early fatigue? Do you drag yourself out of bed, have daytime somnolence, loss of concentration, or irritability?”

Those are key parameters we can use for looking back to the night before and gauging sleep efficiency. If you’re not asking those questions, you may miss out on identifying a patient having sleep fragmentation.
 

Sleep’s role in inflammatory disease processes

I now perform an interval assessment of this type not just in my patients with GER disease but across all my patients. I do so because sleep is physiologically important in so many ways.

In patients who have nonalcoholic fatty liver disease and a variety of other liver diseases, we’re finding an increased association with sleep fragmentation outside of sleep apnea.

The same is true with irritable bowel and other functional diseases.

When you have sleep fragmentation in inflammatory bowel disease, you turn on a variety of inflammatory proteins (e.g., C-reactive protein) and cytokines, such as interleukins and tumor necrosis factor alpha. These processes may actually tip somebody over to a pro-inflammatory state.

When it comes to what might be considered a relatively simpler condition like GER disease, Ronnie Fass and colleagues showed a number of years ago via Bernstein testing performed in patients with both fragmented and normal sleep that the sensory thresholds all get lowered in the former group. This is irrespective of whether you have a functional symptom or you’re awakened by bumping your toe, a headache, or having heartburn; your sensory thresholds are lower. As a result, the same stimulus provides a higher sense of awareness. By ramping up that awareness, you increase the interference with the next-day function.

We’ve shown that sleep fragmentation affects a variety of things, including immune function. This may be why many people get sick when they travel in between time zones.

There are also implications relating to things like obesity. When you have sleep dysfunction, you have effects on leptin and ghrelin, contrary to what you would normally want to have. This, in turn, causes adverse effects on stimulation or suppression of satiety or appetite. These are things that I counsel my patients about when I talk about reflux as well as those trying to lose weight.

Sleep disruption affects cortisol stimulation and has a significant correlation with type 2 diabetes, cardiovascular diseases, and even mortality statistics. 
 

Advice for counseling patients

This latest analysis from the Nurses’ Health Study reminds us that a lot of people have reflux and a lot of people have sleep fragmentation. We need to do better in asking our patients if they have symptoms specific not only to reflux but also to potentially sleep-related complications.

The more we do that, the more we individualize patient treatment rather than treating them as a disease state. This, in turn, will allow us to practice personalized medicine. The more we can engage our patients with reflux disease by asking the right questions about next-day function, the better we can do in improving their outcomes.

It’s time for us all to open our eyes to the value of closing them. Let’s talk to our patients with reflux disease in a little bit of a different light, providing a new perspective on strategies we can use to mitigate and deal with those symptoms, thereby preventing the consequences of sleep fragmentation.

Hopefully, this overview gives you some guidance the next time you have a conversation with your patients. It will apply across many, many disease states, and in almost everything we do in gastroenterology.

David A. Johnson, MD, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk, Va., and a past president of the American College of Gastroenterology. He reported advising with ISOTHRIVE and Johnson & Johnson.

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

This transcript has been edited for clarity.

The ongoing longitudinal Nurses’ Health Study has served as an incredible database for evaluating disease states prospectively over decades, thanks to the robust input of its participants. Most recently, this allowed for an important analysis of the association between gastroesophageal reflux (GER) symptoms and sleep quality, the results of which were published in JAMA Network Open.

Approximately 49,000 women with a median age of 59 years (range, 48-69 years) provided data for this analysis. Starting in 2005, they were asked about their experience of GER symptoms. In 2017, they were also asked to respond to a questionnaire, a modified Pittsburgh Sleep Quality Index (PSQI). This is a tool we’ve used a lot in prospective studies looking at gastrointestinal diseases and sleep-related abnormalities. It’s unique in that it looks not only at sleep but also at next-day function and daytime sleepiness, which is important here for its implications related to reflux disease and sleep fragmentation.

In assessing these outcomes, the investigators found that the relative risk for association with sleep fragmentation was approximately 15% greater in those with GER symptoms occurring one to three times a month. For those with GER symptoms occurring once a week and more than once a week, the approximate relative risk increased by 30% and 53%, respectively. Clearly, the association of GER symptoms and relative sleep quality was really important.

It should be noted that the PSQI is a disease-independent, validated instrument. It’s not specific to GER disease or any diseases. It’s cross validated across 17 different languages. I think what’s most important about its use in the assessment here is the incorporation of next-day function and asking participants about daytime sleepiness, which we’ll discuss in more detail shortly.
 

The many causes of interrupted sleep

We’ve all experienced sleep fragmentation, whether in the form of having been on call during our medical training or common experiences like hearing a child cry in the night, a noisy truck pass by, or a dog barking. You may or may not remember that these happened the next day, but they’ve nonetheless interrupted your sleep efficiency.

When you transition laterally across the stages of sleep, that’s what establishes the circadian rhythm and ensures sleep hygiene. Typically, we require approximately 7 hours of restful sleep to do that. But if you fragment or interrupt this process, you more or less move your way erratically through the night, disrupting sleep hygiene and efficiency.

If you have a cognitive awakening during those disruptions, you may recall those events the next day. Or, you may not remember it at all, and such amnestic events are normal for some people with sleep disruptions.

You may also have a sensory arousal, whether it’s due to GER symptoms, auditory stimuli, bumping your toe, or whatever disruptive event. Any of these can cause you to lose that laterality of smooth transition through sleep.

Approximately 20% of the U.S. population have reported GER symptoms at least once a week. Incident data indicate that number may be increasing by as much as 5% a year. Much of that increase is tied to obesity. But nonetheless, it’s a problem on the rise.

It’s important to know this as we start to look at sleep. If GER is acting as a trigger to sleep disruption, you need to ask your patients with this condition about next-day function.

In particular, the next-day function questions to ask are, “How do you feel when you get up? Are you awake and refreshed? Do you have early fatigue? Do you drag yourself out of bed, have daytime somnolence, loss of concentration, or irritability?”

Those are key parameters we can use for looking back to the night before and gauging sleep efficiency. If you’re not asking those questions, you may miss out on identifying a patient having sleep fragmentation.
 

Sleep’s role in inflammatory disease processes

I now perform an interval assessment of this type not just in my patients with GER disease but across all my patients. I do so because sleep is physiologically important in so many ways.

In patients who have nonalcoholic fatty liver disease and a variety of other liver diseases, we’re finding an increased association with sleep fragmentation outside of sleep apnea.

The same is true with irritable bowel and other functional diseases.

When you have sleep fragmentation in inflammatory bowel disease, you turn on a variety of inflammatory proteins (e.g., C-reactive protein) and cytokines, such as interleukins and tumor necrosis factor alpha. These processes may actually tip somebody over to a pro-inflammatory state.

When it comes to what might be considered a relatively simpler condition like GER disease, Ronnie Fass and colleagues showed a number of years ago via Bernstein testing performed in patients with both fragmented and normal sleep that the sensory thresholds all get lowered in the former group. This is irrespective of whether you have a functional symptom or you’re awakened by bumping your toe, a headache, or having heartburn; your sensory thresholds are lower. As a result, the same stimulus provides a higher sense of awareness. By ramping up that awareness, you increase the interference with the next-day function.

We’ve shown that sleep fragmentation affects a variety of things, including immune function. This may be why many people get sick when they travel in between time zones.

There are also implications relating to things like obesity. When you have sleep dysfunction, you have effects on leptin and ghrelin, contrary to what you would normally want to have. This, in turn, causes adverse effects on stimulation or suppression of satiety or appetite. These are things that I counsel my patients about when I talk about reflux as well as those trying to lose weight.

Sleep disruption affects cortisol stimulation and has a significant correlation with type 2 diabetes, cardiovascular diseases, and even mortality statistics. 
 

Advice for counseling patients

This latest analysis from the Nurses’ Health Study reminds us that a lot of people have reflux and a lot of people have sleep fragmentation. We need to do better in asking our patients if they have symptoms specific not only to reflux but also to potentially sleep-related complications.

The more we do that, the more we individualize patient treatment rather than treating them as a disease state. This, in turn, will allow us to practice personalized medicine. The more we can engage our patients with reflux disease by asking the right questions about next-day function, the better we can do in improving their outcomes.

It’s time for us all to open our eyes to the value of closing them. Let’s talk to our patients with reflux disease in a little bit of a different light, providing a new perspective on strategies we can use to mitigate and deal with those symptoms, thereby preventing the consequences of sleep fragmentation.

Hopefully, this overview gives you some guidance the next time you have a conversation with your patients. It will apply across many, many disease states, and in almost everything we do in gastroenterology.

David A. Johnson, MD, is professor of medicine and chief of gastroenterology at Eastern Virginia Medical School, Norfolk, Va., and a past president of the American College of Gastroenterology. He reported advising with ISOTHRIVE and Johnson & Johnson.

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

The Food and Drug Administration has approved an intravenous (IV) formulation of secukinumab (Cosentyx) for the treatment of adults with psoriatic arthritis (PsA), ankylosing spondylitis (AS), and nonradiographic axial spondyloarthritis (nr-axSpA).

Secukinumab is the only treatment approved in an IV formulation that specifically targets and blocks interleukin-17A and the only non–tumor necrosis factor alpha IV option available to treat the three indications of PsA, AS, and nr-axSpA, according to a press release from the drug’s manufacturer, Novartis.

The approval marks the first new IV treatment in 6 years for these three conditions. The drug was first approved in 2015 and up to now has been available only as a subcutaneous injection.

The new formulation is also approved for secukinumab’s other indications of plaque psoriasis in people aged 6 years or older, children aged 2 years or older with PsA, and enthesitis-related arthritis in patients aged 4 years or older.

“A significant portion of the millions of PsA, AS, and nr-axSpA patients in the United States require treatment through IV infusions for a variety of reasons, including not being comfortable with self-injections or simply preferring to have treatments administered in their health care provider’s office,” Philip J. Mease, MD, clinical professor at the University of Washington, Seattle, and director of rheumatology research at the Swedish Medical Center, Seattle, said in the press release. “The approval of Cosentyx as an IV formulation is an important milestone for patients because it expands the treatment options available to them with a different mechanism of action than existing biologic IV therapies, along with the comfort and familiarity of an established treatment.”

This IV formulation is administered monthly in a 30-minute, weight-based dosing regimen. This new option will become available before the end of the year, Novartis said.

“With this approval of Cosentyx as an IV formulation, along with the subcutaneous formulation, we can broaden the use of Cosentyx to help more patients manage their condition with a medicine backed by more than a decade of clinical research and 8 years of real-world experience,” said Christy Siegel, vice president and head of immunology, Novartis U.S.

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

The Food and Drug Administration has approved an intravenous (IV) formulation of secukinumab (Cosentyx) for the treatment of adults with psoriatic arthritis (PsA), ankylosing spondylitis (AS), and nonradiographic axial spondyloarthritis (nr-axSpA).

Secukinumab is the only treatment approved in an IV formulation that specifically targets and blocks interleukin-17A and the only non–tumor necrosis factor alpha IV option available to treat the three indications of PsA, AS, and nr-axSpA, according to a press release from the drug’s manufacturer, Novartis.

The approval marks the first new IV treatment in 6 years for these three conditions. The drug was first approved in 2015 and up to now has been available only as a subcutaneous injection.

The new formulation is also approved for secukinumab’s other indications of plaque psoriasis in people aged 6 years or older, children aged 2 years or older with PsA, and enthesitis-related arthritis in patients aged 4 years or older.

“A significant portion of the millions of PsA, AS, and nr-axSpA patients in the United States require treatment through IV infusions for a variety of reasons, including not being comfortable with self-injections or simply preferring to have treatments administered in their health care provider’s office,” Philip J. Mease, MD, clinical professor at the University of Washington, Seattle, and director of rheumatology research at the Swedish Medical Center, Seattle, said in the press release. “The approval of Cosentyx as an IV formulation is an important milestone for patients because it expands the treatment options available to them with a different mechanism of action than existing biologic IV therapies, along with the comfort and familiarity of an established treatment.”

This IV formulation is administered monthly in a 30-minute, weight-based dosing regimen. This new option will become available before the end of the year, Novartis said.

“With this approval of Cosentyx as an IV formulation, along with the subcutaneous formulation, we can broaden the use of Cosentyx to help more patients manage their condition with a medicine backed by more than a decade of clinical research and 8 years of real-world experience,” said Christy Siegel, vice president and head of immunology, Novartis U.S.

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

The Food and Drug Administration has approved an intravenous (IV) formulation of secukinumab (Cosentyx) for the treatment of adults with psoriatic arthritis (PsA), ankylosing spondylitis (AS), and nonradiographic axial spondyloarthritis (nr-axSpA).

Secukinumab is the only treatment approved in an IV formulation that specifically targets and blocks interleukin-17A and the only non–tumor necrosis factor alpha IV option available to treat the three indications of PsA, AS, and nr-axSpA, according to a press release from the drug’s manufacturer, Novartis.

The approval marks the first new IV treatment in 6 years for these three conditions. The drug was first approved in 2015 and up to now has been available only as a subcutaneous injection.

The new formulation is also approved for secukinumab’s other indications of plaque psoriasis in people aged 6 years or older, children aged 2 years or older with PsA, and enthesitis-related arthritis in patients aged 4 years or older.

“A significant portion of the millions of PsA, AS, and nr-axSpA patients in the United States require treatment through IV infusions for a variety of reasons, including not being comfortable with self-injections or simply preferring to have treatments administered in their health care provider’s office,” Philip J. Mease, MD, clinical professor at the University of Washington, Seattle, and director of rheumatology research at the Swedish Medical Center, Seattle, said in the press release. “The approval of Cosentyx as an IV formulation is an important milestone for patients because it expands the treatment options available to them with a different mechanism of action than existing biologic IV therapies, along with the comfort and familiarity of an established treatment.”

This IV formulation is administered monthly in a 30-minute, weight-based dosing regimen. This new option will become available before the end of the year, Novartis said.

“With this approval of Cosentyx as an IV formulation, along with the subcutaneous formulation, we can broaden the use of Cosentyx to help more patients manage their condition with a medicine backed by more than a decade of clinical research and 8 years of real-world experience,” said Christy Siegel, vice president and head of immunology, Novartis U.S.

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

This transcript has been edited for clarity.

Michelle L. O’Donoghue, MD, MPH: I’m here in Amsterdam at the European Society of Cardiology (ESC) Congress 2023. Joining me for a great discussion is my friend Dr. Pam Taub, who is a cardiologist and a professor of medicine at UC San Diego. She has a particular interest in postural orthostatic tachycardia syndrome (POTS), so that’s what we’ll be talking about today.

Thanks for joining me, Pam. When we think about POTS, for those who are not familiar with the term, what does it actually mean and how do you diagnose it?
 

No tilt table required

Pam R. Taub, MD: As you said, it’s postural orthostatic tachycardia syndrome. What that means is when somebody stands up, they have an elevation in their heart rate that is usually 30 points from when they’re lying down. That’s typically associated with symptoms such as lightheadedness, dizziness, and cognitive difficulties such as brain fog. The diagnosis can be made by tilt-table testing, but it can also be made in the office with simple orthostats.

In my clinic, I have people lie down for 3-5 minutes. At the end of that period, you get a heart rate and blood pressure. Then you have them stand up for 3-5 minutes and then get heart rate and blood pressure, and you look at the differences. If the heart rate goes up by 30 points – so maybe they’re 80 beats/min when they’re lying down and when they stand up, it goes to 110 beats/min  – that’s POTS, so very objective criteria. Typically, these people don’t have what we call orthostatic hypotension, where there is a significant decrease in the blood pressure. It’s more a heart rate issue.

Dr. O’Donoghue: How symptomatically do they usually present?

Dr. Taub: It’s a spectrum. Some people have mild symptoms. After they’re in the upright position for maybe 10 minutes, they get symptoms. There are some people who, when they go from a lying to standing position, they’re extremely symptomatic and can’t really do any activities. There are some people that are even wheelchair-bound because the symptoms are so debilitating. There’s a wide spectrum.

Dr. O’Donoghue: There has been more discussion, I feel like, about the rising prevalence of POTS as a diagnosis, and in particular since the COVID pandemic. What’s our understanding of the relationship between COVID and POTS and what the mechanism might be?

Dr. Taub: We’ve known that POTS can be triggered by a viral infection. Before COVID, we knew that in certain individuals that we think have an underlying genetic predisposition, usually some autoimmune substrate, when they get certain types of infections, whether it’s influenza or mononucleosis, they get POTS.

Typically, when they get an infection, they start getting deconditioned. They don’t feel well, so they’re on bed rest. When they get long periods of bed rest, when they start to become active, they start to have overactivation of their sympathetic nervous system, and they have a large amount of cardiovascular deconditioning. It’s a cycle that is often triggered after an infection.

A huge increase of POTS has been seen after COVID-19 because we had so many people exposed to this virus. With COVID-19, there is a period where people don’t feel great and they are getting bed rest, so they’re getting deconditioned. We’ve seen so many patients referred for post-COVID POTS and also long COVID or the post-acute sequelae of COVID-19, where POTS is a part of that presentation.

Female sex and autoimmune conditions

Dr. O’Donoghue: We know that POTS seems to disproportionately affect women. Is that understood? Is it thought that that’s related to the perhaps the autoimmune component of that illness?

Dr. Taub: Yes. The theory is because women tend to have more autoimmune conditions, that’s why they’re more predisposed. There’s a large amount of genetic susceptibility. For instance, we know that there’s an association between POTS and conditions like Ehlers-Danlos syndrome and between POTS and mast cell activation. Some of those conditions are more prevalent in women as well.

Dr. O’Donoghue: I feel like many physicians don’t know how to manage POTS, and they’re actually a little fearful perhaps to take it on. Fortunately, there have been a growing number of POTS clinics with specialists that focus on that area. For the average practitioner who maybe can’t refer to a POTS clinic, how should they approach that?

Dr. Taub: The first thing is its diagnosis. When someone tells you that they have symptoms of orthostatic intolerance – so, activities that involve standing – you need to first have that on your differential diagnosis. You can make the diagnosis in the office with orthostats. You don’t need a tilt table. It’s sometimes helpful if you’re unsure about the diagnosis, but you can make the diagnosis.

Many times, you’re finding people that have very mild symptoms. You can treat that with some good lifestyle recommendations, such as increased hydration, increasing salt in their diet, and compression. And the exercise component is really important.

Many people with POTS are told to go exercise, go for a run, or go for a walk. That’s incorrect, because these people have symptoms when they’re in the upright position. The type of exercise they need to do initially is exercise in the lying or seated position – so exercises like rowing or a seated bike, and strength training. As they start to feel better, then they can do upright exercise.

You should never tell a person that has POTS to just initially start with upright exercise, because they’re going to feel so much worse and then they’re never going to want to exercise. It’s really important to give them the right exercise recommendations. I find that for many of these mild cases, if they do the right exercise and engage in the right lifestyle strategies, they get better.

Compression wear and drug therapy

Dr. O’Donoghue: When it comes to compression stockings, do you usually start with a particular length?

Dr. Taub: It’s interesting. There are many different compression stockings, medical grade. Through patients with POTS, I’ve gotten feedback on certain types of athletic wear that have built-in compression, and that’s a little bit easier for people to wear every day because they can do their errands and it doesn’t look like they’re wearing medical-grade compression stockings.

Basically, I’ve collected all the different recommendations that patients say help, and I give them a list. The medical-grade compression stockings sometimes are very challenging to put on, and sometimes people just need light compression or even just socks. Any kind of compression is going to help.

Dr. O’Donoghue: That’s a great tip, because I know there are many patients who refuse to wear the compression stockings. If there’s a fashionable alternative, that’s always good to reach for.

Dr. Taub: Another thing that patients have told me is that abdominal compression is also very helpful. There are many commercially available abdominal compression options, like shapewear. Many patients with POTS use that and that helps, too.

Dr. O’Donoghue: Good. For those patients with POTS that is refractory to the measures you’ve already discussed, what are the next steps after that?

Dr. Taub: Pharmacotherapy is very synergistic with lifestyle, and there are many different pharmacotherapy options. One of the first things that you want to think about is lowering that heart rate. The reason people feel horrible is because their heart rate is usually very high when they’re upright. If they’re upright for long periods of time and they’re having very high heart rates, they’re going to get really tired because it’s like they’re exercising for hours when they’re upright.

Heart rate lowering is the cornerstone of therapy. Traditionally, we’ve used beta-blockers for heart rate lowering. The problem is they also lower blood pressure. They can also cause fatigue, so not the ideal agent for patients with POTS.

One of the clinical trials that I led was with a drug called ivabradine, which selectively works on the SA node and decreases heart rate without affecting blood pressure. What’s really elegant about ivabradine is it has a more potent effect when the heart rate is higher. When the patient is standing, it’s going to have a more potent effect on heart rate lowering. It’s really well tolerated in patients with POTS. In our study, we showed an improvement in quality of life metrics. That’s one of the first-line drugs that I use for patients with POTS.

The other thing is some of them will also have a concomitant lowering of blood pressure. You can think about medications that increase blood pressure, like midodrine, fludrocortisone, and droxidopa. Sometimes that combination of a heart rate-lowering medication and a medication that increases blood pressure really works well.

Dr. O’Donoghue: That’s very helpful. I think that those kinds of practical tips are the ones that practitioners really want to reach for, because they need to have that algorithm in their mind to take on this condition. Thanks again for walking us through that.

I think it’s a very interesting space, and there’s more that we’re going to be learning over the next few years as we further flesh out these post-COVID cases and what we learn from that as well.

Dr. Taub: There are many clinical trials now starting in POTS, so it’s exciting.

Dr. O’Donoghue: Absolutely. Thank you again for joining me today. Signing off, this is Dr Michelle O’Donoghue.
 

Dr. O’Donoghue is a cardiologist at Brigham and Women’s Hospital and senior investigator with the TIMI Study Group. A strong believer in evidence-based medicine, she relishes discussions about the published literature. A native Canadian, Dr. O’Donoghue loves spending time outdoors with her family but admits with shame that she’s never strapped on hockey skates. She disclosed ties with Amgen, AstraZeneca Pharmaceuticals LP, CVS Minute Clinic, Eisai, GlaxoSmithKline, Janssen Pharmaceuticals, Merck, Novartis, and The Medicines Company. Dr. Taub is professor of Medicine, University of California San Diego Health, La Jolla. She disclosed ties with Amgen, Bayer, Boehringer Ingelheim, Medtronic, Merck, Novartis, Novo Nordisk, and Sanofi.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Michelle L. O’Donoghue, MD, MPH: I’m here in Amsterdam at the European Society of Cardiology (ESC) Congress 2023. Joining me for a great discussion is my friend Dr. Pam Taub, who is a cardiologist and a professor of medicine at UC San Diego. She has a particular interest in postural orthostatic tachycardia syndrome (POTS), so that’s what we’ll be talking about today.

Thanks for joining me, Pam. When we think about POTS, for those who are not familiar with the term, what does it actually mean and how do you diagnose it?
 

No tilt table required

Pam R. Taub, MD: As you said, it’s postural orthostatic tachycardia syndrome. What that means is when somebody stands up, they have an elevation in their heart rate that is usually 30 points from when they’re lying down. That’s typically associated with symptoms such as lightheadedness, dizziness, and cognitive difficulties such as brain fog. The diagnosis can be made by tilt-table testing, but it can also be made in the office with simple orthostats.

In my clinic, I have people lie down for 3-5 minutes. At the end of that period, you get a heart rate and blood pressure. Then you have them stand up for 3-5 minutes and then get heart rate and blood pressure, and you look at the differences. If the heart rate goes up by 30 points – so maybe they’re 80 beats/min when they’re lying down and when they stand up, it goes to 110 beats/min  – that’s POTS, so very objective criteria. Typically, these people don’t have what we call orthostatic hypotension, where there is a significant decrease in the blood pressure. It’s more a heart rate issue.

Dr. O’Donoghue: How symptomatically do they usually present?

Dr. Taub: It’s a spectrum. Some people have mild symptoms. After they’re in the upright position for maybe 10 minutes, they get symptoms. There are some people who, when they go from a lying to standing position, they’re extremely symptomatic and can’t really do any activities. There are some people that are even wheelchair-bound because the symptoms are so debilitating. There’s a wide spectrum.

Dr. O’Donoghue: There has been more discussion, I feel like, about the rising prevalence of POTS as a diagnosis, and in particular since the COVID pandemic. What’s our understanding of the relationship between COVID and POTS and what the mechanism might be?

Dr. Taub: We’ve known that POTS can be triggered by a viral infection. Before COVID, we knew that in certain individuals that we think have an underlying genetic predisposition, usually some autoimmune substrate, when they get certain types of infections, whether it’s influenza or mononucleosis, they get POTS.

Typically, when they get an infection, they start getting deconditioned. They don’t feel well, so they’re on bed rest. When they get long periods of bed rest, when they start to become active, they start to have overactivation of their sympathetic nervous system, and they have a large amount of cardiovascular deconditioning. It’s a cycle that is often triggered after an infection.

A huge increase of POTS has been seen after COVID-19 because we had so many people exposed to this virus. With COVID-19, there is a period where people don’t feel great and they are getting bed rest, so they’re getting deconditioned. We’ve seen so many patients referred for post-COVID POTS and also long COVID or the post-acute sequelae of COVID-19, where POTS is a part of that presentation.

Female sex and autoimmune conditions

Dr. O’Donoghue: We know that POTS seems to disproportionately affect women. Is that understood? Is it thought that that’s related to the perhaps the autoimmune component of that illness?

Dr. Taub: Yes. The theory is because women tend to have more autoimmune conditions, that’s why they’re more predisposed. There’s a large amount of genetic susceptibility. For instance, we know that there’s an association between POTS and conditions like Ehlers-Danlos syndrome and between POTS and mast cell activation. Some of those conditions are more prevalent in women as well.

Dr. O’Donoghue: I feel like many physicians don’t know how to manage POTS, and they’re actually a little fearful perhaps to take it on. Fortunately, there have been a growing number of POTS clinics with specialists that focus on that area. For the average practitioner who maybe can’t refer to a POTS clinic, how should they approach that?

Dr. Taub: The first thing is its diagnosis. When someone tells you that they have symptoms of orthostatic intolerance – so, activities that involve standing – you need to first have that on your differential diagnosis. You can make the diagnosis in the office with orthostats. You don’t need a tilt table. It’s sometimes helpful if you’re unsure about the diagnosis, but you can make the diagnosis.

Many times, you’re finding people that have very mild symptoms. You can treat that with some good lifestyle recommendations, such as increased hydration, increasing salt in their diet, and compression. And the exercise component is really important.

Many people with POTS are told to go exercise, go for a run, or go for a walk. That’s incorrect, because these people have symptoms when they’re in the upright position. The type of exercise they need to do initially is exercise in the lying or seated position – so exercises like rowing or a seated bike, and strength training. As they start to feel better, then they can do upright exercise.

You should never tell a person that has POTS to just initially start with upright exercise, because they’re going to feel so much worse and then they’re never going to want to exercise. It’s really important to give them the right exercise recommendations. I find that for many of these mild cases, if they do the right exercise and engage in the right lifestyle strategies, they get better.

Compression wear and drug therapy

Dr. O’Donoghue: When it comes to compression stockings, do you usually start with a particular length?

Dr. Taub: It’s interesting. There are many different compression stockings, medical grade. Through patients with POTS, I’ve gotten feedback on certain types of athletic wear that have built-in compression, and that’s a little bit easier for people to wear every day because they can do their errands and it doesn’t look like they’re wearing medical-grade compression stockings.

Basically, I’ve collected all the different recommendations that patients say help, and I give them a list. The medical-grade compression stockings sometimes are very challenging to put on, and sometimes people just need light compression or even just socks. Any kind of compression is going to help.

Dr. O’Donoghue: That’s a great tip, because I know there are many patients who refuse to wear the compression stockings. If there’s a fashionable alternative, that’s always good to reach for.

Dr. Taub: Another thing that patients have told me is that abdominal compression is also very helpful. There are many commercially available abdominal compression options, like shapewear. Many patients with POTS use that and that helps, too.

Dr. O’Donoghue: Good. For those patients with POTS that is refractory to the measures you’ve already discussed, what are the next steps after that?

Dr. Taub: Pharmacotherapy is very synergistic with lifestyle, and there are many different pharmacotherapy options. One of the first things that you want to think about is lowering that heart rate. The reason people feel horrible is because their heart rate is usually very high when they’re upright. If they’re upright for long periods of time and they’re having very high heart rates, they’re going to get really tired because it’s like they’re exercising for hours when they’re upright.

Heart rate lowering is the cornerstone of therapy. Traditionally, we’ve used beta-blockers for heart rate lowering. The problem is they also lower blood pressure. They can also cause fatigue, so not the ideal agent for patients with POTS.

One of the clinical trials that I led was with a drug called ivabradine, which selectively works on the SA node and decreases heart rate without affecting blood pressure. What’s really elegant about ivabradine is it has a more potent effect when the heart rate is higher. When the patient is standing, it’s going to have a more potent effect on heart rate lowering. It’s really well tolerated in patients with POTS. In our study, we showed an improvement in quality of life metrics. That’s one of the first-line drugs that I use for patients with POTS.

The other thing is some of them will also have a concomitant lowering of blood pressure. You can think about medications that increase blood pressure, like midodrine, fludrocortisone, and droxidopa. Sometimes that combination of a heart rate-lowering medication and a medication that increases blood pressure really works well.

Dr. O’Donoghue: That’s very helpful. I think that those kinds of practical tips are the ones that practitioners really want to reach for, because they need to have that algorithm in their mind to take on this condition. Thanks again for walking us through that.

I think it’s a very interesting space, and there’s more that we’re going to be learning over the next few years as we further flesh out these post-COVID cases and what we learn from that as well.

Dr. Taub: There are many clinical trials now starting in POTS, so it’s exciting.

Dr. O’Donoghue: Absolutely. Thank you again for joining me today. Signing off, this is Dr Michelle O’Donoghue.
 

Dr. O’Donoghue is a cardiologist at Brigham and Women’s Hospital and senior investigator with the TIMI Study Group. A strong believer in evidence-based medicine, she relishes discussions about the published literature. A native Canadian, Dr. O’Donoghue loves spending time outdoors with her family but admits with shame that she’s never strapped on hockey skates. She disclosed ties with Amgen, AstraZeneca Pharmaceuticals LP, CVS Minute Clinic, Eisai, GlaxoSmithKline, Janssen Pharmaceuticals, Merck, Novartis, and The Medicines Company. Dr. Taub is professor of Medicine, University of California San Diego Health, La Jolla. She disclosed ties with Amgen, Bayer, Boehringer Ingelheim, Medtronic, Merck, Novartis, Novo Nordisk, and Sanofi.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Michelle L. O’Donoghue, MD, MPH: I’m here in Amsterdam at the European Society of Cardiology (ESC) Congress 2023. Joining me for a great discussion is my friend Dr. Pam Taub, who is a cardiologist and a professor of medicine at UC San Diego. She has a particular interest in postural orthostatic tachycardia syndrome (POTS), so that’s what we’ll be talking about today.

Thanks for joining me, Pam. When we think about POTS, for those who are not familiar with the term, what does it actually mean and how do you diagnose it?
 

No tilt table required

Pam R. Taub, MD: As you said, it’s postural orthostatic tachycardia syndrome. What that means is when somebody stands up, they have an elevation in their heart rate that is usually 30 points from when they’re lying down. That’s typically associated with symptoms such as lightheadedness, dizziness, and cognitive difficulties such as brain fog. The diagnosis can be made by tilt-table testing, but it can also be made in the office with simple orthostats.

In my clinic, I have people lie down for 3-5 minutes. At the end of that period, you get a heart rate and blood pressure. Then you have them stand up for 3-5 minutes and then get heart rate and blood pressure, and you look at the differences. If the heart rate goes up by 30 points – so maybe they’re 80 beats/min when they’re lying down and when they stand up, it goes to 110 beats/min  – that’s POTS, so very objective criteria. Typically, these people don’t have what we call orthostatic hypotension, where there is a significant decrease in the blood pressure. It’s more a heart rate issue.

Dr. O’Donoghue: How symptomatically do they usually present?

Dr. Taub: It’s a spectrum. Some people have mild symptoms. After they’re in the upright position for maybe 10 minutes, they get symptoms. There are some people who, when they go from a lying to standing position, they’re extremely symptomatic and can’t really do any activities. There are some people that are even wheelchair-bound because the symptoms are so debilitating. There’s a wide spectrum.

Dr. O’Donoghue: There has been more discussion, I feel like, about the rising prevalence of POTS as a diagnosis, and in particular since the COVID pandemic. What’s our understanding of the relationship between COVID and POTS and what the mechanism might be?

Dr. Taub: We’ve known that POTS can be triggered by a viral infection. Before COVID, we knew that in certain individuals that we think have an underlying genetic predisposition, usually some autoimmune substrate, when they get certain types of infections, whether it’s influenza or mononucleosis, they get POTS.

Typically, when they get an infection, they start getting deconditioned. They don’t feel well, so they’re on bed rest. When they get long periods of bed rest, when they start to become active, they start to have overactivation of their sympathetic nervous system, and they have a large amount of cardiovascular deconditioning. It’s a cycle that is often triggered after an infection.

A huge increase of POTS has been seen after COVID-19 because we had so many people exposed to this virus. With COVID-19, there is a period where people don’t feel great and they are getting bed rest, so they’re getting deconditioned. We’ve seen so many patients referred for post-COVID POTS and also long COVID or the post-acute sequelae of COVID-19, where POTS is a part of that presentation.

Female sex and autoimmune conditions

Dr. O’Donoghue: We know that POTS seems to disproportionately affect women. Is that understood? Is it thought that that’s related to the perhaps the autoimmune component of that illness?

Dr. Taub: Yes. The theory is because women tend to have more autoimmune conditions, that’s why they’re more predisposed. There’s a large amount of genetic susceptibility. For instance, we know that there’s an association between POTS and conditions like Ehlers-Danlos syndrome and between POTS and mast cell activation. Some of those conditions are more prevalent in women as well.

Dr. O’Donoghue: I feel like many physicians don’t know how to manage POTS, and they’re actually a little fearful perhaps to take it on. Fortunately, there have been a growing number of POTS clinics with specialists that focus on that area. For the average practitioner who maybe can’t refer to a POTS clinic, how should they approach that?

Dr. Taub: The first thing is its diagnosis. When someone tells you that they have symptoms of orthostatic intolerance – so, activities that involve standing – you need to first have that on your differential diagnosis. You can make the diagnosis in the office with orthostats. You don’t need a tilt table. It’s sometimes helpful if you’re unsure about the diagnosis, but you can make the diagnosis.

Many times, you’re finding people that have very mild symptoms. You can treat that with some good lifestyle recommendations, such as increased hydration, increasing salt in their diet, and compression. And the exercise component is really important.

Many people with POTS are told to go exercise, go for a run, or go for a walk. That’s incorrect, because these people have symptoms when they’re in the upright position. The type of exercise they need to do initially is exercise in the lying or seated position – so exercises like rowing or a seated bike, and strength training. As they start to feel better, then they can do upright exercise.

You should never tell a person that has POTS to just initially start with upright exercise, because they’re going to feel so much worse and then they’re never going to want to exercise. It’s really important to give them the right exercise recommendations. I find that for many of these mild cases, if they do the right exercise and engage in the right lifestyle strategies, they get better.

Compression wear and drug therapy

Dr. O’Donoghue: When it comes to compression stockings, do you usually start with a particular length?

Dr. Taub: It’s interesting. There are many different compression stockings, medical grade. Through patients with POTS, I’ve gotten feedback on certain types of athletic wear that have built-in compression, and that’s a little bit easier for people to wear every day because they can do their errands and it doesn’t look like they’re wearing medical-grade compression stockings.

Basically, I’ve collected all the different recommendations that patients say help, and I give them a list. The medical-grade compression stockings sometimes are very challenging to put on, and sometimes people just need light compression or even just socks. Any kind of compression is going to help.

Dr. O’Donoghue: That’s a great tip, because I know there are many patients who refuse to wear the compression stockings. If there’s a fashionable alternative, that’s always good to reach for.

Dr. Taub: Another thing that patients have told me is that abdominal compression is also very helpful. There are many commercially available abdominal compression options, like shapewear. Many patients with POTS use that and that helps, too.

Dr. O’Donoghue: Good. For those patients with POTS that is refractory to the measures you’ve already discussed, what are the next steps after that?

Dr. Taub: Pharmacotherapy is very synergistic with lifestyle, and there are many different pharmacotherapy options. One of the first things that you want to think about is lowering that heart rate. The reason people feel horrible is because their heart rate is usually very high when they’re upright. If they’re upright for long periods of time and they’re having very high heart rates, they’re going to get really tired because it’s like they’re exercising for hours when they’re upright.

Heart rate lowering is the cornerstone of therapy. Traditionally, we’ve used beta-blockers for heart rate lowering. The problem is they also lower blood pressure. They can also cause fatigue, so not the ideal agent for patients with POTS.

One of the clinical trials that I led was with a drug called ivabradine, which selectively works on the SA node and decreases heart rate without affecting blood pressure. What’s really elegant about ivabradine is it has a more potent effect when the heart rate is higher. When the patient is standing, it’s going to have a more potent effect on heart rate lowering. It’s really well tolerated in patients with POTS. In our study, we showed an improvement in quality of life metrics. That’s one of the first-line drugs that I use for patients with POTS.

The other thing is some of them will also have a concomitant lowering of blood pressure. You can think about medications that increase blood pressure, like midodrine, fludrocortisone, and droxidopa. Sometimes that combination of a heart rate-lowering medication and a medication that increases blood pressure really works well.

Dr. O’Donoghue: That’s very helpful. I think that those kinds of practical tips are the ones that practitioners really want to reach for, because they need to have that algorithm in their mind to take on this condition. Thanks again for walking us through that.

I think it’s a very interesting space, and there’s more that we’re going to be learning over the next few years as we further flesh out these post-COVID cases and what we learn from that as well.

Dr. Taub: There are many clinical trials now starting in POTS, so it’s exciting.

Dr. O’Donoghue: Absolutely. Thank you again for joining me today. Signing off, this is Dr Michelle O’Donoghue.
 

Dr. O’Donoghue is a cardiologist at Brigham and Women’s Hospital and senior investigator with the TIMI Study Group. A strong believer in evidence-based medicine, she relishes discussions about the published literature. A native Canadian, Dr. O’Donoghue loves spending time outdoors with her family but admits with shame that she’s never strapped on hockey skates. She disclosed ties with Amgen, AstraZeneca Pharmaceuticals LP, CVS Minute Clinic, Eisai, GlaxoSmithKline, Janssen Pharmaceuticals, Merck, Novartis, and The Medicines Company. Dr. Taub is professor of Medicine, University of California San Diego Health, La Jolla. She disclosed ties with Amgen, Bayer, Boehringer Ingelheim, Medtronic, Merck, Novartis, Novo Nordisk, and Sanofi.

A version of this article appeared on Medscape.com.

The widening threat of the animal tranquilizer xylazine, otherwise known as tranq, which has been found in illegally manufactured fentanyl, necessitates wider testing, a better understanding of its effects, and more research on treatment options, according to a narrative review published in the Annals of Internal Medicine.

“A lot of doctors and providers are asking about this drug,” said Joseph D’Orazio, MD, an addiction medicine specialist and medical toxicologist at Cooper University Healthcare, Camden, N.J., who led the review.

Xylazine is believed to prolong or intensify the effects of opioids, making it a popular additive to illegally produced opioids, particularly fentanyl, according to the Drug Enforcement Administration. Users end up in a zombie-like state with slowed breathing, and they sometimes develop skin ulcers. Because xylazine is not an opioid, common antidotes such as naloxone are ineffective. The White House has called the fentanyl-xylazine combo an “emerging threat.”

“Xylazine is making the deadliest drug threat our country has ever faced, fentanyl, even deadlier,” said DEA administrator Anne Milgram, in a statement on the agency’s website. “DEA has seized xylazine and fentanyl mixtures in 48 of 50 States. The DEA Laboratory System is reporting that in 2022 approximately 23% of fentanyl powder and 7% of fentanyl pills seized by the DEA contained xylazine.”

Dr. D’Orazio paired clinical experience with available research to provide guidance on the care of patients exposed to xylazine.

He and his team issued a call for more research on the drug’s effects, including more details on dependency and withdrawal.

Testing a patient who may have been exposed to xylazine requires forensic lab capabilities, which makes testing complicated and costly. The review found no evidence of the origin of the drug or why it causes open sores.

The review calls for more education of providers, including primary care physicians, on the treatment and care of patients who have used xylazine and fentanyl. The authors also call for expanding standard urine analysis to test for xylazine and for intensifying surveillance of the drug supply and distribution of xylazine test strips.

The authors of an editorial that accompanied the journal article urged the health care community to get ahead of xylazine before the crisis worsens.

“Not testing for xylazine in current unaffected areas and populations may lead to delays in responding if and when the drug becomes prevalent in the drug supply,” the authors wrote.

Xylazine was detected in 90% of street opioid samples tested in Philadelphia in 2021, and a toxic surveillance study of drug paraphernalia in Maryland found xylazine in 80% of samples tested between 2021 and 2022.

Dr. D’Orazio stressed that although Narcan is ineffective in treating xylazine, because the sedative is almost always mixed with fentanyl or another opiate, the opioid antagonist should still be used in emergencies.

Angelique Campen, MD, an emergency medicine physician at Providence St. Joseph Medical Center, Burbank, Calif., said she has seen an increase in patients entering the emergency department under the influence of what seems like fentanyl or heroin, but standard treatments such as Narcan have a limited effect. These patients remain in a prolonged period of sedation.

Recently, she admitted to her hospital’s intensive care unit a patient suspected of a xylazine overdose who was not responding to treatment.

Dr. Campen said that patients are screened for fentanyl, but because no test is available for xylazine, she presumed xylazine was causing the complication.

“It makes perfect medical sense to me that that’s what was going on,” Dr. Campen, who has worked at St. Joseph’s for 25 years, said. “I’m hoping with physicians being more aware of it that we can have that part of our regular urine drug screen.”

Dr. Campen also said she hopes an antidote is soon developed.

“If we can just keep delivering that message, hopefully, [to] more and more people, it will get through to them,” she said. “Every time you’re taking this, even though you may have taken it a week before and been fine, you never know: The next dose you take may be the lethal dose.”

A review author reports being awarded $1,000 to cover travel cost for Best Overall Abstract at the American Society of Addiction Medicine 2023 Annual Meeting. Another author reports receiving payments for training conducted as part of a NJDMAHS training grant to educate on substance use disorders. Dr. D’Orazio reports a $500 honorarium for a one-time lecture on xylazine at Yale; and a $500 honorarium for speaking one to three times per year on various topics regarding opioid use disorder at the Health Federation of Philadelphia. No other disclosures were reported.

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

The widening threat of the animal tranquilizer xylazine, otherwise known as tranq, which has been found in illegally manufactured fentanyl, necessitates wider testing, a better understanding of its effects, and more research on treatment options, according to a narrative review published in the Annals of Internal Medicine.

“A lot of doctors and providers are asking about this drug,” said Joseph D’Orazio, MD, an addiction medicine specialist and medical toxicologist at Cooper University Healthcare, Camden, N.J., who led the review.

Xylazine is believed to prolong or intensify the effects of opioids, making it a popular additive to illegally produced opioids, particularly fentanyl, according to the Drug Enforcement Administration. Users end up in a zombie-like state with slowed breathing, and they sometimes develop skin ulcers. Because xylazine is not an opioid, common antidotes such as naloxone are ineffective. The White House has called the fentanyl-xylazine combo an “emerging threat.”

“Xylazine is making the deadliest drug threat our country has ever faced, fentanyl, even deadlier,” said DEA administrator Anne Milgram, in a statement on the agency’s website. “DEA has seized xylazine and fentanyl mixtures in 48 of 50 States. The DEA Laboratory System is reporting that in 2022 approximately 23% of fentanyl powder and 7% of fentanyl pills seized by the DEA contained xylazine.”

Dr. D’Orazio paired clinical experience with available research to provide guidance on the care of patients exposed to xylazine.

He and his team issued a call for more research on the drug’s effects, including more details on dependency and withdrawal.

Testing a patient who may have been exposed to xylazine requires forensic lab capabilities, which makes testing complicated and costly. The review found no evidence of the origin of the drug or why it causes open sores.

The review calls for more education of providers, including primary care physicians, on the treatment and care of patients who have used xylazine and fentanyl. The authors also call for expanding standard urine analysis to test for xylazine and for intensifying surveillance of the drug supply and distribution of xylazine test strips.

The authors of an editorial that accompanied the journal article urged the health care community to get ahead of xylazine before the crisis worsens.

“Not testing for xylazine in current unaffected areas and populations may lead to delays in responding if and when the drug becomes prevalent in the drug supply,” the authors wrote.

Xylazine was detected in 90% of street opioid samples tested in Philadelphia in 2021, and a toxic surveillance study of drug paraphernalia in Maryland found xylazine in 80% of samples tested between 2021 and 2022.

Dr. D’Orazio stressed that although Narcan is ineffective in treating xylazine, because the sedative is almost always mixed with fentanyl or another opiate, the opioid antagonist should still be used in emergencies.

Angelique Campen, MD, an emergency medicine physician at Providence St. Joseph Medical Center, Burbank, Calif., said she has seen an increase in patients entering the emergency department under the influence of what seems like fentanyl or heroin, but standard treatments such as Narcan have a limited effect. These patients remain in a prolonged period of sedation.

Recently, she admitted to her hospital’s intensive care unit a patient suspected of a xylazine overdose who was not responding to treatment.

Dr. Campen said that patients are screened for fentanyl, but because no test is available for xylazine, she presumed xylazine was causing the complication.

“It makes perfect medical sense to me that that’s what was going on,” Dr. Campen, who has worked at St. Joseph’s for 25 years, said. “I’m hoping with physicians being more aware of it that we can have that part of our regular urine drug screen.”

Dr. Campen also said she hopes an antidote is soon developed.

“If we can just keep delivering that message, hopefully, [to] more and more people, it will get through to them,” she said. “Every time you’re taking this, even though you may have taken it a week before and been fine, you never know: The next dose you take may be the lethal dose.”

A review author reports being awarded $1,000 to cover travel cost for Best Overall Abstract at the American Society of Addiction Medicine 2023 Annual Meeting. Another author reports receiving payments for training conducted as part of a NJDMAHS training grant to educate on substance use disorders. Dr. D’Orazio reports a $500 honorarium for a one-time lecture on xylazine at Yale; and a $500 honorarium for speaking one to three times per year on various topics regarding opioid use disorder at the Health Federation of Philadelphia. No other disclosures were reported.

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

The widening threat of the animal tranquilizer xylazine, otherwise known as tranq, which has been found in illegally manufactured fentanyl, necessitates wider testing, a better understanding of its effects, and more research on treatment options, according to a narrative review published in the Annals of Internal Medicine.

“A lot of doctors and providers are asking about this drug,” said Joseph D’Orazio, MD, an addiction medicine specialist and medical toxicologist at Cooper University Healthcare, Camden, N.J., who led the review.

Xylazine is believed to prolong or intensify the effects of opioids, making it a popular additive to illegally produced opioids, particularly fentanyl, according to the Drug Enforcement Administration. Users end up in a zombie-like state with slowed breathing, and they sometimes develop skin ulcers. Because xylazine is not an opioid, common antidotes such as naloxone are ineffective. The White House has called the fentanyl-xylazine combo an “emerging threat.”

“Xylazine is making the deadliest drug threat our country has ever faced, fentanyl, even deadlier,” said DEA administrator Anne Milgram, in a statement on the agency’s website. “DEA has seized xylazine and fentanyl mixtures in 48 of 50 States. The DEA Laboratory System is reporting that in 2022 approximately 23% of fentanyl powder and 7% of fentanyl pills seized by the DEA contained xylazine.”

Dr. D’Orazio paired clinical experience with available research to provide guidance on the care of patients exposed to xylazine.

He and his team issued a call for more research on the drug’s effects, including more details on dependency and withdrawal.

Testing a patient who may have been exposed to xylazine requires forensic lab capabilities, which makes testing complicated and costly. The review found no evidence of the origin of the drug or why it causes open sores.

The review calls for more education of providers, including primary care physicians, on the treatment and care of patients who have used xylazine and fentanyl. The authors also call for expanding standard urine analysis to test for xylazine and for intensifying surveillance of the drug supply and distribution of xylazine test strips.

The authors of an editorial that accompanied the journal article urged the health care community to get ahead of xylazine before the crisis worsens.

“Not testing for xylazine in current unaffected areas and populations may lead to delays in responding if and when the drug becomes prevalent in the drug supply,” the authors wrote.

Xylazine was detected in 90% of street opioid samples tested in Philadelphia in 2021, and a toxic surveillance study of drug paraphernalia in Maryland found xylazine in 80% of samples tested between 2021 and 2022.

Dr. D’Orazio stressed that although Narcan is ineffective in treating xylazine, because the sedative is almost always mixed with fentanyl or another opiate, the opioid antagonist should still be used in emergencies.

Angelique Campen, MD, an emergency medicine physician at Providence St. Joseph Medical Center, Burbank, Calif., said she has seen an increase in patients entering the emergency department under the influence of what seems like fentanyl or heroin, but standard treatments such as Narcan have a limited effect. These patients remain in a prolonged period of sedation.

Recently, she admitted to her hospital’s intensive care unit a patient suspected of a xylazine overdose who was not responding to treatment.

Dr. Campen said that patients are screened for fentanyl, but because no test is available for xylazine, she presumed xylazine was causing the complication.

“It makes perfect medical sense to me that that’s what was going on,” Dr. Campen, who has worked at St. Joseph’s for 25 years, said. “I’m hoping with physicians being more aware of it that we can have that part of our regular urine drug screen.”

Dr. Campen also said she hopes an antidote is soon developed.

“If we can just keep delivering that message, hopefully, [to] more and more people, it will get through to them,” she said. “Every time you’re taking this, even though you may have taken it a week before and been fine, you never know: The next dose you take may be the lethal dose.”

A review author reports being awarded $1,000 to cover travel cost for Best Overall Abstract at the American Society of Addiction Medicine 2023 Annual Meeting. Another author reports receiving payments for training conducted as part of a NJDMAHS training grant to educate on substance use disorders. Dr. D’Orazio reports a $500 honorarium for a one-time lecture on xylazine at Yale; and a $500 honorarium for speaking one to three times per year on various topics regarding opioid use disorder at the Health Federation of Philadelphia. No other disclosures were reported.

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

TOPLINE:

Matched cohort studies revealed infrequent adverse events (AEs) with either treatment, but the number needed to harm for any AE was more than three times higher with colchicine versus NSAIDs.

METHODOLOGY:

• The researchers conducted two matched retrospective cohort studies using the U.K. Clinical Practice Research Datalink and the Hospital Episode Statistics primary care datasets to compare AEs in adults initiating allopurinol for gout with and without colchicine or NSAID prophylaxis.
• For the study, 13,945 patients with gout who received colchicine were matched to 13,945 patients who received no prophylaxis. In addition, 25,980 patients with gout who received NSAIDs were matched to 25,980 who received no prophylaxis.
• The researchers used proportional hazard models to explore the associations between prophylaxis with either colchicine or NSAIDs and AEs.

TAKEAWAY:

• The incidence of most AEs was less than 200 per 10,000 patient-years, but the most common AE among patients given colchicine was diarrhea, with an incidence of 784.4 per 10,000 person-years, whereas the most common AE in those given NSAIDs was angina, with an incidence of 466.6 per 10,000 person-years.
• The number needed to harm in relation to any AE was 14.7 for colchicine, driven mainly by diarrhea, and 48.1 for NSAID.
• Compared with patients who started allopurinol without prophylaxis, those treated with colchicine were more likely to experience diarrhea, myocardial infarction, neuropathy, myalgia, and bone marrow suppression, whereas those treated with NSAIDs were more likely to experience angina, acute kidney injury, myocardial infarction, and peptic ulcer disease.
• Diarrhea, the most common AE, occurred in 17.9% of individuals who received colchicine.

IN PRACTICE:

“Our findings will provide much-needed information about the safety of flare prophylaxis that can inform treatment decisions and the choice between colchicine or NSAID for prophylaxis when initiating allopurinol, directly benefiting people with gout and their clinicians,” the authors write.

SOURCE:

First author Edward Roddy, MD, of Keele (England) University, and colleagues published their report online in BMJ’s Annals of the Rheumatic Diseases.

LIMITATIONS:

The study identified gout based on clinical diagnosis in primary care and only considered AEs serious enough to merit consultation or hospitalization; other limitations included the observational design and lack of data on the use of over-the-counter NSAIDs.

DISCLOSURES:

The study was supported by the National Institute for Health and Care Research’s Research for Patient Benefit program. The researchers had no financial conflicts to disclose.

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

TOPLINE:

Matched cohort studies revealed infrequent adverse events (AEs) with either treatment, but the number needed to harm for any AE was more than three times higher with colchicine versus NSAIDs.

METHODOLOGY:

• The researchers conducted two matched retrospective cohort studies using the U.K. Clinical Practice Research Datalink and the Hospital Episode Statistics primary care datasets to compare AEs in adults initiating allopurinol for gout with and without colchicine or NSAID prophylaxis.
• For the study, 13,945 patients with gout who received colchicine were matched to 13,945 patients who received no prophylaxis. In addition, 25,980 patients with gout who received NSAIDs were matched to 25,980 who received no prophylaxis.
• The researchers used proportional hazard models to explore the associations between prophylaxis with either colchicine or NSAIDs and AEs.

TAKEAWAY:

• The incidence of most AEs was less than 200 per 10,000 patient-years, but the most common AE among patients given colchicine was diarrhea, with an incidence of 784.4 per 10,000 person-years, whereas the most common AE in those given NSAIDs was angina, with an incidence of 466.6 per 10,000 person-years.
• The number needed to harm in relation to any AE was 14.7 for colchicine, driven mainly by diarrhea, and 48.1 for NSAID.
• Compared with patients who started allopurinol without prophylaxis, those treated with colchicine were more likely to experience diarrhea, myocardial infarction, neuropathy, myalgia, and bone marrow suppression, whereas those treated with NSAIDs were more likely to experience angina, acute kidney injury, myocardial infarction, and peptic ulcer disease.
• Diarrhea, the most common AE, occurred in 17.9% of individuals who received colchicine.

IN PRACTICE:

“Our findings will provide much-needed information about the safety of flare prophylaxis that can inform treatment decisions and the choice between colchicine or NSAID for prophylaxis when initiating allopurinol, directly benefiting people with gout and their clinicians,” the authors write.

SOURCE:

First author Edward Roddy, MD, of Keele (England) University, and colleagues published their report online in BMJ’s Annals of the Rheumatic Diseases.

LIMITATIONS:

The study identified gout based on clinical diagnosis in primary care and only considered AEs serious enough to merit consultation or hospitalization; other limitations included the observational design and lack of data on the use of over-the-counter NSAIDs.

DISCLOSURES:

The study was supported by the National Institute for Health and Care Research’s Research for Patient Benefit program. The researchers had no financial conflicts to disclose.

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

TOPLINE:

Matched cohort studies revealed infrequent adverse events (AEs) with either treatment, but the number needed to harm for any AE was more than three times higher with colchicine versus NSAIDs.

METHODOLOGY:

• The researchers conducted two matched retrospective cohort studies using the U.K. Clinical Practice Research Datalink and the Hospital Episode Statistics primary care datasets to compare AEs in adults initiating allopurinol for gout with and without colchicine or NSAID prophylaxis.
• For the study, 13,945 patients with gout who received colchicine were matched to 13,945 patients who received no prophylaxis. In addition, 25,980 patients with gout who received NSAIDs were matched to 25,980 who received no prophylaxis.
• The researchers used proportional hazard models to explore the associations between prophylaxis with either colchicine or NSAIDs and AEs.

TAKEAWAY:

• The incidence of most AEs was less than 200 per 10,000 patient-years, but the most common AE among patients given colchicine was diarrhea, with an incidence of 784.4 per 10,000 person-years, whereas the most common AE in those given NSAIDs was angina, with an incidence of 466.6 per 10,000 person-years.
• The number needed to harm in relation to any AE was 14.7 for colchicine, driven mainly by diarrhea, and 48.1 for NSAID.
• Compared with patients who started allopurinol without prophylaxis, those treated with colchicine were more likely to experience diarrhea, myocardial infarction, neuropathy, myalgia, and bone marrow suppression, whereas those treated with NSAIDs were more likely to experience angina, acute kidney injury, myocardial infarction, and peptic ulcer disease.
• Diarrhea, the most common AE, occurred in 17.9% of individuals who received colchicine.

IN PRACTICE:

“Our findings will provide much-needed information about the safety of flare prophylaxis that can inform treatment decisions and the choice between colchicine or NSAID for prophylaxis when initiating allopurinol, directly benefiting people with gout and their clinicians,” the authors write.

SOURCE:

First author Edward Roddy, MD, of Keele (England) University, and colleagues published their report online in BMJ’s Annals of the Rheumatic Diseases.

LIMITATIONS:

The study identified gout based on clinical diagnosis in primary care and only considered AEs serious enough to merit consultation or hospitalization; other limitations included the observational design and lack of data on the use of over-the-counter NSAIDs.

DISCLOSURES:

The study was supported by the National Institute for Health and Care Research’s Research for Patient Benefit program. The researchers had no financial conflicts to disclose.

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

TOPLINE:

Research from South Korea provides additional evidence for the connection between COVID-19 and an increased risk for autoimmune conditions post infection.

METHODOLOGY:

• In this retrospective study, researchers identified 354,527 individuals diagnosed with COVID-19 via polymerase chain reaction (PCR) testing from Oct. 8, 2020, to Dec. 31, 2021.
• Researchers compared the COVID-19 group with 6,134,940 healthy individuals who had no evidence of COVID-19 to quantify the risk for autoimmune and autoinflammatory connective tissue disorders.
• Patients were followed until diagnosis, death, or end of study period (Dec. 31, 2021).

TAKEAWAY:

• Risks for alopecia areata, alopecia totalis, antineutrophil cytoplasmic antibody–associated vasculitis, Crohn’s disease, and sarcoidosis were higher in the COVID-19 group.
• Patients with more severe COVID-19 (admitted to the ICU) were at greater risk for many autoimmune conditions, including alopecia totalis, psoriasis, vitiligo, and vasculitis.
•  

IN PRACTICE:

“Our results emphasize the need to focus on managing not only the acute stages of COVID-19 itself but also autoimmune diseases as complications of COVID-19,” the authors wrote.

SOURCE:

Sung Ha Lim, MD, of Yonsei University, Wonju, South Korea, was the first author of the study, published in JAMA Network Open.

LIMITATIONS:

The study was retrospective and was composed almost exclusively of individuals from a single ethnicity. The study could have included individuals with COVID-19 in the control group who did not undergo PCR testing. The analysis did not include detailed information on each patient, including genetic information, that could have contributed to autoimmune disease risk.

DISCLOSURES:

The study was supported by a fund from the research program of the Korea Medical Institute and by grants from the Korea Health Industry Development Institute, the Korean Ministry of Health & Welfare, and the National Research Foundation of Korea. The authors disclosed no relevant financial relationships.

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

TOPLINE:

Research from South Korea provides additional evidence for the connection between COVID-19 and an increased risk for autoimmune conditions post infection.

METHODOLOGY:

• In this retrospective study, researchers identified 354,527 individuals diagnosed with COVID-19 via polymerase chain reaction (PCR) testing from Oct. 8, 2020, to Dec. 31, 2021.
• Researchers compared the COVID-19 group with 6,134,940 healthy individuals who had no evidence of COVID-19 to quantify the risk for autoimmune and autoinflammatory connective tissue disorders.
• Patients were followed until diagnosis, death, or end of study period (Dec. 31, 2021).

TAKEAWAY:

• Risks for alopecia areata, alopecia totalis, antineutrophil cytoplasmic antibody–associated vasculitis, Crohn’s disease, and sarcoidosis were higher in the COVID-19 group.
• Patients with more severe COVID-19 (admitted to the ICU) were at greater risk for many autoimmune conditions, including alopecia totalis, psoriasis, vitiligo, and vasculitis.
•  

IN PRACTICE:

“Our results emphasize the need to focus on managing not only the acute stages of COVID-19 itself but also autoimmune diseases as complications of COVID-19,” the authors wrote.

SOURCE:

Sung Ha Lim, MD, of Yonsei University, Wonju, South Korea, was the first author of the study, published in JAMA Network Open.

LIMITATIONS:

The study was retrospective and was composed almost exclusively of individuals from a single ethnicity. The study could have included individuals with COVID-19 in the control group who did not undergo PCR testing. The analysis did not include detailed information on each patient, including genetic information, that could have contributed to autoimmune disease risk.

DISCLOSURES:

The study was supported by a fund from the research program of the Korea Medical Institute and by grants from the Korea Health Industry Development Institute, the Korean Ministry of Health & Welfare, and the National Research Foundation of Korea. The authors disclosed no relevant financial relationships.

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

TOPLINE:

Research from South Korea provides additional evidence for the connection between COVID-19 and an increased risk for autoimmune conditions post infection.

METHODOLOGY:

• In this retrospective study, researchers identified 354,527 individuals diagnosed with COVID-19 via polymerase chain reaction (PCR) testing from Oct. 8, 2020, to Dec. 31, 2021.
• Researchers compared the COVID-19 group with 6,134,940 healthy individuals who had no evidence of COVID-19 to quantify the risk for autoimmune and autoinflammatory connective tissue disorders.
• Patients were followed until diagnosis, death, or end of study period (Dec. 31, 2021).

TAKEAWAY:

• Risks for alopecia areata, alopecia totalis, antineutrophil cytoplasmic antibody–associated vasculitis, Crohn’s disease, and sarcoidosis were higher in the COVID-19 group.
• Patients with more severe COVID-19 (admitted to the ICU) were at greater risk for many autoimmune conditions, including alopecia totalis, psoriasis, vitiligo, and vasculitis.
•  

IN PRACTICE:

“Our results emphasize the need to focus on managing not only the acute stages of COVID-19 itself but also autoimmune diseases as complications of COVID-19,” the authors wrote.

SOURCE:

Sung Ha Lim, MD, of Yonsei University, Wonju, South Korea, was the first author of the study, published in JAMA Network Open.

LIMITATIONS:

The study was retrospective and was composed almost exclusively of individuals from a single ethnicity. The study could have included individuals with COVID-19 in the control group who did not undergo PCR testing. The analysis did not include detailed information on each patient, including genetic information, that could have contributed to autoimmune disease risk.

DISCLOSURES:

The study was supported by a fund from the research program of the Korea Medical Institute and by grants from the Korea Health Industry Development Institute, the Korean Ministry of Health & Welfare, and the National Research Foundation of Korea. The authors disclosed no relevant financial relationships.

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

CARLSBAD, CALIF. – With 11 different biologics approved for the treatment of plaque psoriasis on the market, settling on which one to prescribe can be tricky.

“When you look at the list of options it can be confusing to many clinicians in deciding which one to choose,” April W. Armstrong, MD, MPH, professor and chief of dermatology at the University of California, Los Angeles, said at the annual symposium of the California Society of Dermatology & Dermatologic Surgery.

Dr. Armstrong

One approach is to consider how the biologics compare in short- and long-term efficacy. “Several different meta-analyses of biologics have been conducted,” which include some head-to head studies, Dr. Armstrong said. “In terms of efficacy, [biologics] are similar at the population level,” she said.

In a meta-analysis of 71 randomized, controlled trials through July 2020, Dr. Armstrong and colleagues found that in the short-term, Psoriasis Area and Severity Index (PASI) 90 response rates at 10-16 weeks from baseline were highest for ixekizumab (72.9%), risankizumab (72.5%), and brodalumab (72%). These PASI 90 responses were significantly higher than among patients on guselkumab (65%), secukinumab (65%), infliximab (56.8%), certolizumab (400 mg: 49.6%; 200 mg: 42.2%), ustekinumab (90 mg: 47.9%; weight-based: 45.7%; 45 mg: 44.6%), adalimumab (43%), tildrakizumab (200 mg: 39.7%; 100 mg: 37.2%), etanercept (18.0%), apremilast (12.4%), and dimethyl fumarate (12.2%).

In a more recent meta-analysis, Dr. Armstrong and coauthors used area under the curve (AUC) analyses to compare the cumulative clinical benefits of biologics over 1 year. They found that the placebo-adjusted normalized maximum AUC for a PASI 100 response was greatest for ixekizumab (0.436), risankizumab (0.423), and brodalumab (0.378), followed by guselkumab (0.358), secukinumab (0.324), ustekinumab (0.201), adalimumab (0.183), and etanercept (0.087).

In Dr. Armstrong’s opinion, the tumor necrosis factor (TNF) inhibitors etanercept, infliximab, adalimumab, and certolizumab “have served their purpose for plaque psoriasis over time, but these days I would probably choose either an IL [interleukin]-17 inhibitor or an IL-23 inhibitor first,” she said. Still, TNF inhibitors “are certainly good for psoriatic arthritis, and certolizumab is appropriate for patients who are pregnant or breastfeeding,” she said. “Avoid them in patients with demyelinating disease and in those with hepatitis B. They are not preferred in patients with latent TB or advanced CHF.”

Dr. Armstrong said that there are robust efficacy data for the IL-17 inhibitors ixekizumab, secukinumab, and brodalumab in psoriasis and in the peripheral and axial forms of psoriatic arthritis (PsA). “Avoid using them in patients with a personal history of inflammatory bowel disease,” she advised.

Low rates of oral candidiasis have been reported in the literature, “but this has not been issue with our approved IL-17 inhibitors so far,” she said.

The IL-23 inhibitors guselkumab, risankizumab, tildrakizumab, and ustekinumab have robust data for psoriasis efficacy, she said, and three – guselkumab, risankizumab, and ustekinumab – are also approved for PsA. “These agents have the advantage of fewer injections, and the evidence [of efficacy] for IL-23 inhibitors continues to evolve, such as in patients with psoriatic arthritis involving the spine,” Dr. Armstrong said.

She also shared how she deals with patients who fail to respond to biologics. “Do you switch drugs, or do you dose escalate?” she asked. “In most cases, the strategy for dose escalation is to shorten the interval between the injections so the dosing is delivered more frequently.” In a case of primary failure, which Dr. Armstrong defined as a patient who has never responded optimally to a biologic, consider revisiting the diagnosis. “Maybe it’s cutaneous T-cell lymphoma or some other condition, because our current IL-17 and IL-23 medications work extremely well,” she said. “So, if you have a patient who is not responding at all, I would question the diagnosis and consider a biopsy.”

She generally waits about 6 months before switching a patient to another biologic, “to see if they’re one of the late bloomers who may catch up in efficacy,” she explained. “Switching the class of biologic is another consideration.”

If a patient had responded to the biologic for a long time and then lost response – known as secondary failure – Dr. Armstrong considers dose escalation or a switch to another agent within the same class “if it helps to address comorbidities such as PsA,” she said. “You can also try across-class switching.”

Dr. Armstrong disclosed ties with AbbVie, Arcutis, ASLAN, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Dermira, Dermavant, EPI, Galderma, InCyte, Janssen, Leo, Lilly, Meiji, Modmed, Nimbus, Novartis, Ortho Dermatologics, Parexel, Pfizer, Regeneron, Sanofi, Suna, UCB, and Ventyx.

CARLSBAD, CALIF. – With 11 different biologics approved for the treatment of plaque psoriasis on the market, settling on which one to prescribe can be tricky.

“When you look at the list of options it can be confusing to many clinicians in deciding which one to choose,” April W. Armstrong, MD, MPH, professor and chief of dermatology at the University of California, Los Angeles, said at the annual symposium of the California Society of Dermatology & Dermatologic Surgery.

Dr. Armstrong

One approach is to consider how the biologics compare in short- and long-term efficacy. “Several different meta-analyses of biologics have been conducted,” which include some head-to head studies, Dr. Armstrong said. “In terms of efficacy, [biologics] are similar at the population level,” she said.

In a meta-analysis of 71 randomized, controlled trials through July 2020, Dr. Armstrong and colleagues found that in the short-term, Psoriasis Area and Severity Index (PASI) 90 response rates at 10-16 weeks from baseline were highest for ixekizumab (72.9%), risankizumab (72.5%), and brodalumab (72%). These PASI 90 responses were significantly higher than among patients on guselkumab (65%), secukinumab (65%), infliximab (56.8%), certolizumab (400 mg: 49.6%; 200 mg: 42.2%), ustekinumab (90 mg: 47.9%; weight-based: 45.7%; 45 mg: 44.6%), adalimumab (43%), tildrakizumab (200 mg: 39.7%; 100 mg: 37.2%), etanercept (18.0%), apremilast (12.4%), and dimethyl fumarate (12.2%).

In a more recent meta-analysis, Dr. Armstrong and coauthors used area under the curve (AUC) analyses to compare the cumulative clinical benefits of biologics over 1 year. They found that the placebo-adjusted normalized maximum AUC for a PASI 100 response was greatest for ixekizumab (0.436), risankizumab (0.423), and brodalumab (0.378), followed by guselkumab (0.358), secukinumab (0.324), ustekinumab (0.201), adalimumab (0.183), and etanercept (0.087).

In Dr. Armstrong’s opinion, the tumor necrosis factor (TNF) inhibitors etanercept, infliximab, adalimumab, and certolizumab “have served their purpose for plaque psoriasis over time, but these days I would probably choose either an IL [interleukin]-17 inhibitor or an IL-23 inhibitor first,” she said. Still, TNF inhibitors “are certainly good for psoriatic arthritis, and certolizumab is appropriate for patients who are pregnant or breastfeeding,” she said. “Avoid them in patients with demyelinating disease and in those with hepatitis B. They are not preferred in patients with latent TB or advanced CHF.”

Dr. Armstrong said that there are robust efficacy data for the IL-17 inhibitors ixekizumab, secukinumab, and brodalumab in psoriasis and in the peripheral and axial forms of psoriatic arthritis (PsA). “Avoid using them in patients with a personal history of inflammatory bowel disease,” she advised.

Low rates of oral candidiasis have been reported in the literature, “but this has not been issue with our approved IL-17 inhibitors so far,” she said.

The IL-23 inhibitors guselkumab, risankizumab, tildrakizumab, and ustekinumab have robust data for psoriasis efficacy, she said, and three – guselkumab, risankizumab, and ustekinumab – are also approved for PsA. “These agents have the advantage of fewer injections, and the evidence [of efficacy] for IL-23 inhibitors continues to evolve, such as in patients with psoriatic arthritis involving the spine,” Dr. Armstrong said.

She also shared how she deals with patients who fail to respond to biologics. “Do you switch drugs, or do you dose escalate?” she asked. “In most cases, the strategy for dose escalation is to shorten the interval between the injections so the dosing is delivered more frequently.” In a case of primary failure, which Dr. Armstrong defined as a patient who has never responded optimally to a biologic, consider revisiting the diagnosis. “Maybe it’s cutaneous T-cell lymphoma or some other condition, because our current IL-17 and IL-23 medications work extremely well,” she said. “So, if you have a patient who is not responding at all, I would question the diagnosis and consider a biopsy.”

She generally waits about 6 months before switching a patient to another biologic, “to see if they’re one of the late bloomers who may catch up in efficacy,” she explained. “Switching the class of biologic is another consideration.”

If a patient had responded to the biologic for a long time and then lost response – known as secondary failure – Dr. Armstrong considers dose escalation or a switch to another agent within the same class “if it helps to address comorbidities such as PsA,” she said. “You can also try across-class switching.”

Dr. Armstrong disclosed ties with AbbVie, Arcutis, ASLAN, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Dermira, Dermavant, EPI, Galderma, InCyte, Janssen, Leo, Lilly, Meiji, Modmed, Nimbus, Novartis, Ortho Dermatologics, Parexel, Pfizer, Regeneron, Sanofi, Suna, UCB, and Ventyx.

CARLSBAD, CALIF. – With 11 different biologics approved for the treatment of plaque psoriasis on the market, settling on which one to prescribe can be tricky.

“When you look at the list of options it can be confusing to many clinicians in deciding which one to choose,” April W. Armstrong, MD, MPH, professor and chief of dermatology at the University of California, Los Angeles, said at the annual symposium of the California Society of Dermatology & Dermatologic Surgery.

Dr. Armstrong

One approach is to consider how the biologics compare in short- and long-term efficacy. “Several different meta-analyses of biologics have been conducted,” which include some head-to head studies, Dr. Armstrong said. “In terms of efficacy, [biologics] are similar at the population level,” she said.

In a meta-analysis of 71 randomized, controlled trials through July 2020, Dr. Armstrong and colleagues found that in the short-term, Psoriasis Area and Severity Index (PASI) 90 response rates at 10-16 weeks from baseline were highest for ixekizumab (72.9%), risankizumab (72.5%), and brodalumab (72%). These PASI 90 responses were significantly higher than among patients on guselkumab (65%), secukinumab (65%), infliximab (56.8%), certolizumab (400 mg: 49.6%; 200 mg: 42.2%), ustekinumab (90 mg: 47.9%; weight-based: 45.7%; 45 mg: 44.6%), adalimumab (43%), tildrakizumab (200 mg: 39.7%; 100 mg: 37.2%), etanercept (18.0%), apremilast (12.4%), and dimethyl fumarate (12.2%).

In a more recent meta-analysis, Dr. Armstrong and coauthors used area under the curve (AUC) analyses to compare the cumulative clinical benefits of biologics over 1 year. They found that the placebo-adjusted normalized maximum AUC for a PASI 100 response was greatest for ixekizumab (0.436), risankizumab (0.423), and brodalumab (0.378), followed by guselkumab (0.358), secukinumab (0.324), ustekinumab (0.201), adalimumab (0.183), and etanercept (0.087).

In Dr. Armstrong’s opinion, the tumor necrosis factor (TNF) inhibitors etanercept, infliximab, adalimumab, and certolizumab “have served their purpose for plaque psoriasis over time, but these days I would probably choose either an IL [interleukin]-17 inhibitor or an IL-23 inhibitor first,” she said. Still, TNF inhibitors “are certainly good for psoriatic arthritis, and certolizumab is appropriate for patients who are pregnant or breastfeeding,” she said. “Avoid them in patients with demyelinating disease and in those with hepatitis B. They are not preferred in patients with latent TB or advanced CHF.”

Dr. Armstrong said that there are robust efficacy data for the IL-17 inhibitors ixekizumab, secukinumab, and brodalumab in psoriasis and in the peripheral and axial forms of psoriatic arthritis (PsA). “Avoid using them in patients with a personal history of inflammatory bowel disease,” she advised.

Low rates of oral candidiasis have been reported in the literature, “but this has not been issue with our approved IL-17 inhibitors so far,” she said.

The IL-23 inhibitors guselkumab, risankizumab, tildrakizumab, and ustekinumab have robust data for psoriasis efficacy, she said, and three – guselkumab, risankizumab, and ustekinumab – are also approved for PsA. “These agents have the advantage of fewer injections, and the evidence [of efficacy] for IL-23 inhibitors continues to evolve, such as in patients with psoriatic arthritis involving the spine,” Dr. Armstrong said.

She also shared how she deals with patients who fail to respond to biologics. “Do you switch drugs, or do you dose escalate?” she asked. “In most cases, the strategy for dose escalation is to shorten the interval between the injections so the dosing is delivered more frequently.” In a case of primary failure, which Dr. Armstrong defined as a patient who has never responded optimally to a biologic, consider revisiting the diagnosis. “Maybe it’s cutaneous T-cell lymphoma or some other condition, because our current IL-17 and IL-23 medications work extremely well,” she said. “So, if you have a patient who is not responding at all, I would question the diagnosis and consider a biopsy.”

She generally waits about 6 months before switching a patient to another biologic, “to see if they’re one of the late bloomers who may catch up in efficacy,” she explained. “Switching the class of biologic is another consideration.”

If a patient had responded to the biologic for a long time and then lost response – known as secondary failure – Dr. Armstrong considers dose escalation or a switch to another agent within the same class “if it helps to address comorbidities such as PsA,” she said. “You can also try across-class switching.”

Dr. Armstrong disclosed ties with AbbVie, Arcutis, ASLAN, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Dermira, Dermavant, EPI, Galderma, InCyte, Janssen, Leo, Lilly, Meiji, Modmed, Nimbus, Novartis, Ortho Dermatologics, Parexel, Pfizer, Regeneron, Sanofi, Suna, UCB, and Ventyx.

On Oct. 6, the Food and Drug Administration approved the use of topical roflumilast cream 0.3% for the treatment of plaque psoriasis, including intertriginous areas, for children ages 6-11. This marks an expanded indication for the drug, which was first approved for the same indication in July, 2022, for individuals aged 12 and older.

Roflumilast cream 0.3% is a phosphodiesterase-4 inhibitor approved for once-daily topical treatment of mild, moderate, and severe plaque psoriasis. According to a press release from the manufacturer, Arcutis Biotherapeutics, approval of the expanded indication is based on data from a 4-week Maximal Usage Systemic Exposure (MUSE) study in children ages 6-11 years with plaque psoriasis. It stated that pharmacokinetic, safety, tolerability, and efficacy data from this study were “generally consistent” with data from the DERMIS-1 and DERMIS-2 pivotal phase 3 trials in adults.

According to the press release, a future FDA review is planned for the results from a second MUSE study in children ages 2-5 years, as well as data from an ongoing open-label extension study evaluating the long-term safety of roflumilast cream in individuals with plaque psoriasis aged 2 years and older. The company markets topical roflumilast as Zoryve.








 

On Oct. 6, the Food and Drug Administration approved the use of topical roflumilast cream 0.3% for the treatment of plaque psoriasis, including intertriginous areas, for children ages 6-11. This marks an expanded indication for the drug, which was first approved for the same indication in July, 2022, for individuals aged 12 and older.

Roflumilast cream 0.3% is a phosphodiesterase-4 inhibitor approved for once-daily topical treatment of mild, moderate, and severe plaque psoriasis. According to a press release from the manufacturer, Arcutis Biotherapeutics, approval of the expanded indication is based on data from a 4-week Maximal Usage Systemic Exposure (MUSE) study in children ages 6-11 years with plaque psoriasis. It stated that pharmacokinetic, safety, tolerability, and efficacy data from this study were “generally consistent” with data from the DERMIS-1 and DERMIS-2 pivotal phase 3 trials in adults.

According to the press release, a future FDA review is planned for the results from a second MUSE study in children ages 2-5 years, as well as data from an ongoing open-label extension study evaluating the long-term safety of roflumilast cream in individuals with plaque psoriasis aged 2 years and older. The company markets topical roflumilast as Zoryve.








 

On Oct. 6, the Food and Drug Administration approved the use of topical roflumilast cream 0.3% for the treatment of plaque psoriasis, including intertriginous areas, for children ages 6-11. This marks an expanded indication for the drug, which was first approved for the same indication in July, 2022, for individuals aged 12 and older.

Roflumilast cream 0.3% is a phosphodiesterase-4 inhibitor approved for once-daily topical treatment of mild, moderate, and severe plaque psoriasis. According to a press release from the manufacturer, Arcutis Biotherapeutics, approval of the expanded indication is based on data from a 4-week Maximal Usage Systemic Exposure (MUSE) study in children ages 6-11 years with plaque psoriasis. It stated that pharmacokinetic, safety, tolerability, and efficacy data from this study were “generally consistent” with data from the DERMIS-1 and DERMIS-2 pivotal phase 3 trials in adults.

According to the press release, a future FDA review is planned for the results from a second MUSE study in children ages 2-5 years, as well as data from an ongoing open-label extension study evaluating the long-term safety of roflumilast cream in individuals with plaque psoriasis aged 2 years and older. The company markets topical roflumilast as Zoryve.








 

The Food and Drug Administration has granted an interchangeability designation to adalimumab-afzb (Abrilada), according to an announcement from Pfizer.

This is the second adalimumab biosimilar granted interchangeability. The first, adalimumab-adbm (Cyltezo), became available in July.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Biosimilars introduce market competition that can help lower drug prices. Adalimumab-afzb is one of nine approved biosimilars for Humira, and the last to launch in 2023.

Adalimumab-afzb is indicated for:

• Adults with rheumatoid arthritis. 
• Polyarticular juvenile idiopathic arthritis in patients 2 years of age and older.
• Adults with psoriatic arthritis.
• Adults with ankylosing spondylitis.
• Crohn’s disease in adults and children 6 years of age and older.
• Adults with ulcerative colitis.
• Adults with plaque psoriasis.
• Adults with hidradenitis suppurativa.
• Adults with noninfectious intermediate and posterior uveitis and panuveitis.

“With this designation, Abrilada is now both biosimilar to and interchangeable with Humira, reinforcing confidence among physicians and pharmacists that there is no decrease in effectiveness or increase in safety risk associated with switching between Abrilada and the reference product,” Roy Fleischmann, MD, clinical professor of medicine, University of Texas Southwestern Medical Center, Dallas, said in Pfizer’s statement.

An interchangeability designation allows pharmacists to substitute the biosimilar for the reference product without involving the prescribing clinician (according to state law). To achieve this designation, Pfizer submitted data from a phase 3 study led by Dr. Fleischmann that evaluated adalimumab-afzb in patients with RA. Patients who were switched three times between the biosimilar and the reference product had outcomes similar to those of patients continuously treated with the reference product. 

Adalimumab-afzb will be available later in October at a 5% discount from Humira’s price. Later this year, the drug will launch at a second price, a 60% discount from Humira.

Full prescribing information for adalimumab-afzb is available here.

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

The Food and Drug Administration has granted an interchangeability designation to adalimumab-afzb (Abrilada), according to an announcement from Pfizer.

This is the second adalimumab biosimilar granted interchangeability. The first, adalimumab-adbm (Cyltezo), became available in July.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Biosimilars introduce market competition that can help lower drug prices. Adalimumab-afzb is one of nine approved biosimilars for Humira, and the last to launch in 2023.

Adalimumab-afzb is indicated for:

• Adults with rheumatoid arthritis. 
• Polyarticular juvenile idiopathic arthritis in patients 2 years of age and older.
• Adults with psoriatic arthritis.
• Adults with ankylosing spondylitis.
• Crohn’s disease in adults and children 6 years of age and older.
• Adults with ulcerative colitis.
• Adults with plaque psoriasis.
• Adults with hidradenitis suppurativa.
• Adults with noninfectious intermediate and posterior uveitis and panuveitis.

“With this designation, Abrilada is now both biosimilar to and interchangeable with Humira, reinforcing confidence among physicians and pharmacists that there is no decrease in effectiveness or increase in safety risk associated with switching between Abrilada and the reference product,” Roy Fleischmann, MD, clinical professor of medicine, University of Texas Southwestern Medical Center, Dallas, said in Pfizer’s statement.

An interchangeability designation allows pharmacists to substitute the biosimilar for the reference product without involving the prescribing clinician (according to state law). To achieve this designation, Pfizer submitted data from a phase 3 study led by Dr. Fleischmann that evaluated adalimumab-afzb in patients with RA. Patients who were switched three times between the biosimilar and the reference product had outcomes similar to those of patients continuously treated with the reference product. 

Adalimumab-afzb will be available later in October at a 5% discount from Humira’s price. Later this year, the drug will launch at a second price, a 60% discount from Humira.

Full prescribing information for adalimumab-afzb is available here.

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

The Food and Drug Administration has granted an interchangeability designation to adalimumab-afzb (Abrilada), according to an announcement from Pfizer.

This is the second adalimumab biosimilar granted interchangeability. The first, adalimumab-adbm (Cyltezo), became available in July.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Biosimilars introduce market competition that can help lower drug prices. Adalimumab-afzb is one of nine approved biosimilars for Humira, and the last to launch in 2023.

Adalimumab-afzb is indicated for:

• Adults with rheumatoid arthritis. 
• Polyarticular juvenile idiopathic arthritis in patients 2 years of age and older.
• Adults with psoriatic arthritis.
• Adults with ankylosing spondylitis.
• Crohn’s disease in adults and children 6 years of age and older.
• Adults with ulcerative colitis.
• Adults with plaque psoriasis.
• Adults with hidradenitis suppurativa.
• Adults with noninfectious intermediate and posterior uveitis and panuveitis.

“With this designation, Abrilada is now both biosimilar to and interchangeable with Humira, reinforcing confidence among physicians and pharmacists that there is no decrease in effectiveness or increase in safety risk associated with switching between Abrilada and the reference product,” Roy Fleischmann, MD, clinical professor of medicine, University of Texas Southwestern Medical Center, Dallas, said in Pfizer’s statement.

An interchangeability designation allows pharmacists to substitute the biosimilar for the reference product without involving the prescribing clinician (according to state law). To achieve this designation, Pfizer submitted data from a phase 3 study led by Dr. Fleischmann that evaluated adalimumab-afzb in patients with RA. Patients who were switched three times between the biosimilar and the reference product had outcomes similar to those of patients continuously treated with the reference product. 

Adalimumab-afzb will be available later in October at a 5% discount from Humira’s price. Later this year, the drug will launch at a second price, a 60% discount from Humira.

Full prescribing information for adalimumab-afzb is available here.

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

This transcript has been edited for clarity.

Recently, the Supreme Court of the United States struck down the use of affirmative action in admissions to colleges, universities, medical schools, and nursing schools. This has led to an enormous amount of worry and concern, particularly in medical school admissions in the world I’m in, where people start to say that diversity matters. Diversity is important.

I know many deans of medical schools immediately sent out messages of reassurance to their students, saying New York University or Stanford or Harvard or Minnesota or Case Western is still deeply concerned about diversity, and we’re going to do what we can to preserve attention to diversity.

I’ve served on admissions at a number of schools over the years for med school. I understand – and have been told – that diversity is important, and according to the Supreme Court, not explicitly by race. There are obviously many variables to take into account when trying to keep diversity at the forefront of admissions.

At the schools I’ve been at, including Columbia, NYU, University of Pittsburgh, University of Minnesota, and University of Pennsylvania, there are plenty of qualified students. Happily, we’ve always been engaged in some effort to try and whittle down the class to the size that we can manage and accept, and many qualified students don’t get admitted.

The first order of business for me is not to worry about how to maintain diversity. It’s to recognize that we need more doctors, nurses, and mental health care providers. I will, in a second, say a few words about diversity and where it fits into admissions, but I want to make the point clearly that what we should be doing is trying to expand the pool of students who are going to become doctors, nurses, mental health care providers, and social workers.

There are too many early retirements. We don’t have the person power we need to manage the health care challenges of an aging population. Let’s not get lost in arguing about what characteristics ought to get you into the finest medical schools. Let’s realize that we have to expand the number of schools we have.

We better be working pretty hard to expand our physician assistant programs, to make sure that we give full authority to qualified dentists and nurses who can help deliver some clinical care. We need more folks. That’s really where the battle ought to be: How do we get that done and how do we get it done quickly, not arguing about who’s in, who’s out, and why.

That said, diversity to me has never meant just race. I’m always interested in gender orientation, disability, and geographic input. Sometimes in decisions that you’re looking at, when I have students in front of me, they tell me they play a musical instrument or about the obstacles they had to overcome to get to medical school. Some of them will say they were involved in 4-H and did rodeo in high school or junior high school, which makes them a diverse potential student with characteristics that maybe some others don’t bring.

I’m not against diversity. I think having a rich set of experiences in any class – medicine, nursing, whatever it’s going to be – is beneficial to the students. They learn from each other. It is sometimes said that it’s also good for patients. I’m a little less excited about that, because I think our training goal should be to make every medical student and nursing student qualified to treat anybody.

I don’t think that, just because you’re Latinx or gay, that’s going to make a gay patient feel better. I think we should teach our students how to give care to everybody that they encounter. They shouldn’t have to match up characteristics to feel like they’re going to get quality care. That isn’t the right reason.

Diversity is important, I think, to teach our students, to broaden our research, and to make sure that bias doesn’t creep in to how we teach, learn, or behave. When you have a diverse set of providers, they can call that out and be on the alert for it, and that’s very important.

I also believe that we should think widely and broadly about diversity. Maybe race is out, but certainly other experiences related to income, background, struggle that got you to the point where you’re applying to medical school, motivation, the kinds of experiences you might have had caring for an elderly person, dealing with a disability or learning disability, and trying to overcome, let’s say, going to school in a poor area with not such a wonderful school, really help in terms of forming professionalism, empathy, and a caring point of view.

To me, the main goal is to expand our workforce. The secondary goal is to stay diverse, because we get better providers when we do so.

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

This transcript has been edited for clarity.

Recently, the Supreme Court of the United States struck down the use of affirmative action in admissions to colleges, universities, medical schools, and nursing schools. This has led to an enormous amount of worry and concern, particularly in medical school admissions in the world I’m in, where people start to say that diversity matters. Diversity is important.

I know many deans of medical schools immediately sent out messages of reassurance to their students, saying New York University or Stanford or Harvard or Minnesota or Case Western is still deeply concerned about diversity, and we’re going to do what we can to preserve attention to diversity.

I’ve served on admissions at a number of schools over the years for med school. I understand – and have been told – that diversity is important, and according to the Supreme Court, not explicitly by race. There are obviously many variables to take into account when trying to keep diversity at the forefront of admissions.

At the schools I’ve been at, including Columbia, NYU, University of Pittsburgh, University of Minnesota, and University of Pennsylvania, there are plenty of qualified students. Happily, we’ve always been engaged in some effort to try and whittle down the class to the size that we can manage and accept, and many qualified students don’t get admitted.

The first order of business for me is not to worry about how to maintain diversity. It’s to recognize that we need more doctors, nurses, and mental health care providers. I will, in a second, say a few words about diversity and where it fits into admissions, but I want to make the point clearly that what we should be doing is trying to expand the pool of students who are going to become doctors, nurses, mental health care providers, and social workers.

There are too many early retirements. We don’t have the person power we need to manage the health care challenges of an aging population. Let’s not get lost in arguing about what characteristics ought to get you into the finest medical schools. Let’s realize that we have to expand the number of schools we have.

We better be working pretty hard to expand our physician assistant programs, to make sure that we give full authority to qualified dentists and nurses who can help deliver some clinical care. We need more folks. That’s really where the battle ought to be: How do we get that done and how do we get it done quickly, not arguing about who’s in, who’s out, and why.

That said, diversity to me has never meant just race. I’m always interested in gender orientation, disability, and geographic input. Sometimes in decisions that you’re looking at, when I have students in front of me, they tell me they play a musical instrument or about the obstacles they had to overcome to get to medical school. Some of them will say they were involved in 4-H and did rodeo in high school or junior high school, which makes them a diverse potential student with characteristics that maybe some others don’t bring.

I’m not against diversity. I think having a rich set of experiences in any class – medicine, nursing, whatever it’s going to be – is beneficial to the students. They learn from each other. It is sometimes said that it’s also good for patients. I’m a little less excited about that, because I think our training goal should be to make every medical student and nursing student qualified to treat anybody.

I don’t think that, just because you’re Latinx or gay, that’s going to make a gay patient feel better. I think we should teach our students how to give care to everybody that they encounter. They shouldn’t have to match up characteristics to feel like they’re going to get quality care. That isn’t the right reason.

Diversity is important, I think, to teach our students, to broaden our research, and to make sure that bias doesn’t creep in to how we teach, learn, or behave. When you have a diverse set of providers, they can call that out and be on the alert for it, and that’s very important.

I also believe that we should think widely and broadly about diversity. Maybe race is out, but certainly other experiences related to income, background, struggle that got you to the point where you’re applying to medical school, motivation, the kinds of experiences you might have had caring for an elderly person, dealing with a disability or learning disability, and trying to overcome, let’s say, going to school in a poor area with not such a wonderful school, really help in terms of forming professionalism, empathy, and a caring point of view.

To me, the main goal is to expand our workforce. The secondary goal is to stay diverse, because we get better providers when we do so.

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

This transcript has been edited for clarity.

Recently, the Supreme Court of the United States struck down the use of affirmative action in admissions to colleges, universities, medical schools, and nursing schools. This has led to an enormous amount of worry and concern, particularly in medical school admissions in the world I’m in, where people start to say that diversity matters. Diversity is important.

I know many deans of medical schools immediately sent out messages of reassurance to their students, saying New York University or Stanford or Harvard or Minnesota or Case Western is still deeply concerned about diversity, and we’re going to do what we can to preserve attention to diversity.

I’ve served on admissions at a number of schools over the years for med school. I understand – and have been told – that diversity is important, and according to the Supreme Court, not explicitly by race. There are obviously many variables to take into account when trying to keep diversity at the forefront of admissions.

At the schools I’ve been at, including Columbia, NYU, University of Pittsburgh, University of Minnesota, and University of Pennsylvania, there are plenty of qualified students. Happily, we’ve always been engaged in some effort to try and whittle down the class to the size that we can manage and accept, and many qualified students don’t get admitted.

The first order of business for me is not to worry about how to maintain diversity. It’s to recognize that we need more doctors, nurses, and mental health care providers. I will, in a second, say a few words about diversity and where it fits into admissions, but I want to make the point clearly that what we should be doing is trying to expand the pool of students who are going to become doctors, nurses, mental health care providers, and social workers.

There are too many early retirements. We don’t have the person power we need to manage the health care challenges of an aging population. Let’s not get lost in arguing about what characteristics ought to get you into the finest medical schools. Let’s realize that we have to expand the number of schools we have.

We better be working pretty hard to expand our physician assistant programs, to make sure that we give full authority to qualified dentists and nurses who can help deliver some clinical care. We need more folks. That’s really where the battle ought to be: How do we get that done and how do we get it done quickly, not arguing about who’s in, who’s out, and why.

That said, diversity to me has never meant just race. I’m always interested in gender orientation, disability, and geographic input. Sometimes in decisions that you’re looking at, when I have students in front of me, they tell me they play a musical instrument or about the obstacles they had to overcome to get to medical school. Some of them will say they were involved in 4-H and did rodeo in high school or junior high school, which makes them a diverse potential student with characteristics that maybe some others don’t bring.

I’m not against diversity. I think having a rich set of experiences in any class – medicine, nursing, whatever it’s going to be – is beneficial to the students. They learn from each other. It is sometimes said that it’s also good for patients. I’m a little less excited about that, because I think our training goal should be to make every medical student and nursing student qualified to treat anybody.

I don’t think that, just because you’re Latinx or gay, that’s going to make a gay patient feel better. I think we should teach our students how to give care to everybody that they encounter. They shouldn’t have to match up characteristics to feel like they’re going to get quality care. That isn’t the right reason.

Diversity is important, I think, to teach our students, to broaden our research, and to make sure that bias doesn’t creep in to how we teach, learn, or behave. When you have a diverse set of providers, they can call that out and be on the alert for it, and that’s very important.

I also believe that we should think widely and broadly about diversity. Maybe race is out, but certainly other experiences related to income, background, struggle that got you to the point where you’re applying to medical school, motivation, the kinds of experiences you might have had caring for an elderly person, dealing with a disability or learning disability, and trying to overcome, let’s say, going to school in a poor area with not such a wonderful school, really help in terms of forming professionalism, empathy, and a caring point of view.

To me, the main goal is to expand our workforce. The secondary goal is to stay diverse, because we get better providers when we do so.

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