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Problematic alcohol use on the rise among physicians?
However, good data on exactly how common this is and on salient risk factors are lacking.
In a systematic literature review, investigators found the prevalence of self-reported problematic alcohol use varied widely, but could affect up to one third of physicians.
However, all studies were survey-based and self-reported, and definitions of problematic alcohol use were mixed, with inconsistent reporting on differences across sex, age, physician specialty, and career stage.
“Key epidemiologic information of the prevalence of problematic alcohol use in physicians and associated risk factors are unknown, hampering the ability to identify high-risk individuals for targeted interventions,” Manish Sood, MD, University of Ottawa, and colleagues wrote.
The findings were published online in JAMA Network Open.
Serious concern
The researchers noted that physicians are at a higher risk for burnout and mental health conditions, including depression and anxiety, than the general population, which could contribute to problematic drinking.
Problematic drinking among physicians poses a “serious concern” to their health and ability to provide care, the investigators wrote. Understanding the extent and characteristics of the issue is important to guide interventions.
To better characterize problematic drinking among physicians, the investigators reviewed 31 studies from 2006 to 2020 involving 51,680 residents, fellows, or staff physicians in 17 countries.
In the studies, problematic alcohol use was measured by a validated tool: the Alcohol Use Disorders Identification Test, AUDIT Version C (AUDIT-C), or the Cut down, Annoyed, Guilty, and Eye-opener (CAGE) questionnaire.
“Problematic alcohol use” included hazardous, potentially hazardous, risky, at-risk, harmful, problematic, or heavy drinking or alcohol use, as well as alcohol misuse, alcohol dependence, and alcohol use more than low-risk guidelines and alcohol use disorder.
Results showed problematic alcohol use “varied widely” regardless of measurement method used. The rate was 0%-34% with AUDIT, 9%-35% with AUDIT-C, and 4%-22% with CAGE.
The data also showed an increase in reported problematic alcohol use over time, rising from 16.3% between 2006 and 2010 to 26.8% between 2017 and 2020.
True prevalence unknown
“It remains unknown whether this increase is indeed accurate or whether it is due to increased transparency by physicians in self-reporting problematic alcohol use because of a changing culture of medicine,” the investigators wrote.
The data suggest that problematic alcohol use is more common in male than female physicians; but no firm conclusions can be drawn from the data on how problematic alcohol use varies based on physician age, sex, specialty, and career stage, the researchers noted.
True prevalence of problematic alcohol use among physicians remains unknown – and identifying this type of behavior is difficult, they pointed out.
They added that physicians with problematic use may be “high functioning,” making identifying potential impairment a challenge. Also, societal stigma and fear of reprisal from professional colleges for reporting or seeking care for problematic alcohol use may encourage physicians with alcohol problems to keep their problems hidden.
The researchers noted that future population-based studies with longitudinal designs or using health administrative data could help identify the prevalence of and salient risk factors for problematic alcohol use in physicians.
The study was supported by the Canadian Medical Association. The authors reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
However, good data on exactly how common this is and on salient risk factors are lacking.
In a systematic literature review, investigators found the prevalence of self-reported problematic alcohol use varied widely, but could affect up to one third of physicians.
However, all studies were survey-based and self-reported, and definitions of problematic alcohol use were mixed, with inconsistent reporting on differences across sex, age, physician specialty, and career stage.
“Key epidemiologic information of the prevalence of problematic alcohol use in physicians and associated risk factors are unknown, hampering the ability to identify high-risk individuals for targeted interventions,” Manish Sood, MD, University of Ottawa, and colleagues wrote.
The findings were published online in JAMA Network Open.
Serious concern
The researchers noted that physicians are at a higher risk for burnout and mental health conditions, including depression and anxiety, than the general population, which could contribute to problematic drinking.
Problematic drinking among physicians poses a “serious concern” to their health and ability to provide care, the investigators wrote. Understanding the extent and characteristics of the issue is important to guide interventions.
To better characterize problematic drinking among physicians, the investigators reviewed 31 studies from 2006 to 2020 involving 51,680 residents, fellows, or staff physicians in 17 countries.
In the studies, problematic alcohol use was measured by a validated tool: the Alcohol Use Disorders Identification Test, AUDIT Version C (AUDIT-C), or the Cut down, Annoyed, Guilty, and Eye-opener (CAGE) questionnaire.
“Problematic alcohol use” included hazardous, potentially hazardous, risky, at-risk, harmful, problematic, or heavy drinking or alcohol use, as well as alcohol misuse, alcohol dependence, and alcohol use more than low-risk guidelines and alcohol use disorder.
Results showed problematic alcohol use “varied widely” regardless of measurement method used. The rate was 0%-34% with AUDIT, 9%-35% with AUDIT-C, and 4%-22% with CAGE.
The data also showed an increase in reported problematic alcohol use over time, rising from 16.3% between 2006 and 2010 to 26.8% between 2017 and 2020.
True prevalence unknown
“It remains unknown whether this increase is indeed accurate or whether it is due to increased transparency by physicians in self-reporting problematic alcohol use because of a changing culture of medicine,” the investigators wrote.
The data suggest that problematic alcohol use is more common in male than female physicians; but no firm conclusions can be drawn from the data on how problematic alcohol use varies based on physician age, sex, specialty, and career stage, the researchers noted.
True prevalence of problematic alcohol use among physicians remains unknown – and identifying this type of behavior is difficult, they pointed out.
They added that physicians with problematic use may be “high functioning,” making identifying potential impairment a challenge. Also, societal stigma and fear of reprisal from professional colleges for reporting or seeking care for problematic alcohol use may encourage physicians with alcohol problems to keep their problems hidden.
The researchers noted that future population-based studies with longitudinal designs or using health administrative data could help identify the prevalence of and salient risk factors for problematic alcohol use in physicians.
The study was supported by the Canadian Medical Association. The authors reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
However, good data on exactly how common this is and on salient risk factors are lacking.
In a systematic literature review, investigators found the prevalence of self-reported problematic alcohol use varied widely, but could affect up to one third of physicians.
However, all studies were survey-based and self-reported, and definitions of problematic alcohol use were mixed, with inconsistent reporting on differences across sex, age, physician specialty, and career stage.
“Key epidemiologic information of the prevalence of problematic alcohol use in physicians and associated risk factors are unknown, hampering the ability to identify high-risk individuals for targeted interventions,” Manish Sood, MD, University of Ottawa, and colleagues wrote.
The findings were published online in JAMA Network Open.
Serious concern
The researchers noted that physicians are at a higher risk for burnout and mental health conditions, including depression and anxiety, than the general population, which could contribute to problematic drinking.
Problematic drinking among physicians poses a “serious concern” to their health and ability to provide care, the investigators wrote. Understanding the extent and characteristics of the issue is important to guide interventions.
To better characterize problematic drinking among physicians, the investigators reviewed 31 studies from 2006 to 2020 involving 51,680 residents, fellows, or staff physicians in 17 countries.
In the studies, problematic alcohol use was measured by a validated tool: the Alcohol Use Disorders Identification Test, AUDIT Version C (AUDIT-C), or the Cut down, Annoyed, Guilty, and Eye-opener (CAGE) questionnaire.
“Problematic alcohol use” included hazardous, potentially hazardous, risky, at-risk, harmful, problematic, or heavy drinking or alcohol use, as well as alcohol misuse, alcohol dependence, and alcohol use more than low-risk guidelines and alcohol use disorder.
Results showed problematic alcohol use “varied widely” regardless of measurement method used. The rate was 0%-34% with AUDIT, 9%-35% with AUDIT-C, and 4%-22% with CAGE.
The data also showed an increase in reported problematic alcohol use over time, rising from 16.3% between 2006 and 2010 to 26.8% between 2017 and 2020.
True prevalence unknown
“It remains unknown whether this increase is indeed accurate or whether it is due to increased transparency by physicians in self-reporting problematic alcohol use because of a changing culture of medicine,” the investigators wrote.
The data suggest that problematic alcohol use is more common in male than female physicians; but no firm conclusions can be drawn from the data on how problematic alcohol use varies based on physician age, sex, specialty, and career stage, the researchers noted.
True prevalence of problematic alcohol use among physicians remains unknown – and identifying this type of behavior is difficult, they pointed out.
They added that physicians with problematic use may be “high functioning,” making identifying potential impairment a challenge. Also, societal stigma and fear of reprisal from professional colleges for reporting or seeking care for problematic alcohol use may encourage physicians with alcohol problems to keep their problems hidden.
The researchers noted that future population-based studies with longitudinal designs or using health administrative data could help identify the prevalence of and salient risk factors for problematic alcohol use in physicians.
The study was supported by the Canadian Medical Association. The authors reported no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
A doctor saves a drowning family in a dangerous river
Is There a Doctor in the House? is a new series telling these stories.
I live on the Maumee River in Ohio, about 50 yards from the water. I had an early quit time and came home to meet my wife for lunch. Afterward, I went up to my barn across the main road to tinker around. It was a nice day out, so my wife had opened some windows. Suddenly, she heard screaming from the river. It did not sound like fun.
She ran down to the river’s edge and saw a dad and three boys struggling in the water. She phoned me screaming: “They’re drowning! They’re drowning!” I jumped in my truck and drove up our driveway through the yard right down to the river.
My wife was on the phone with 911 at that point, and I could see them about 75-100 yards out. The dad had two of the boys clinging around his neck. They were going under the water and coming up and going under again. The other boy was just floating nearby, face down, motionless.
I threw my shoes and scrubs off and started to walk towards the water. My wife screamed at me, “You’re not going in there!” I said, “I’m not going to stand here and watch this. It’s not going to happen.”
I’m not a kid anymore, but I was a high school swimmer, and to this day I work out all the time. I felt like I had to try something. So, I went in the water despite my wife yelling and I swam towards them.
What happens when you get in that deep water is that you panic. You can’t hear anyone because of the rapids, and your instinct is to swim back towards where you went in, which is against the current. Unless you’re a very strong swimmer, you’re just wasting your time, swimming in place.
But these guys weren’t trying to go anywhere. Dad was just trying to stay up and keep the boys alive. He was in about 10 feet of water. What they didn’t see or just didn’t know: About 20 yards upstream from that deep water is a little island.
When I got to them, I yelled at the dad to move towards the island, “Go backwards! Go back!” I flipped the boy over who wasn’t moving. He was the oldest of the three, around 10 or 11 years old. When I turned him over, he was blue and wasn’t breathing. I put my fingers on his neck and didn’t feel a pulse.
So, I’m treading water, holding him. I put an arm behind his back and started doing chest compressions on him. I probably did a dozen to 15 compressions – nothing. I thought, I’ve got to get some air in this kid. So, I gave him two deep breaths and then started doing compressions again. I know ACLS and CPR training would say we don’t do that anymore. But I couldn’t just sit there and give up. Shortly after that, he coughed out a large amount of water and started breathing.
The dad and the other two boys had made it to the island. So, I started moving towards it with the boy. It was a few minutes before he regained consciousness. Of course, he was unaware of what had happened. He started to scream, because here’s this strange man holding him. But he was breathing. That’s all I cared about.
When we got to the island, I saw that my neighbor downstream had launched his canoe. He’s a retired gentleman who lives next to me, a very physically fit man. He started rolling as hard as he could towards us, against the stream. I kind of gave him a thumbs up, like, “we’re safe now. We’re standing.” We loaded the kids and the dad in the canoe and made it back against the stream to the parking lot where they went in.
All this took probably 10 or 15 minutes, and by then the paramedics were there. Life Flight had been dispatched up by my barn where there’s room to land. So, they drove up there in the ambulance. The boy I revived was flown to the hospital. The others went in the ambulance.
I know all the ED docs, so I talked to somebody later who, with permission from the family, said they were all doing fine. They were getting x-rays on the boy’s lungs. And then I heard the dad and two boys were released that night. The other boy I worked on was observed overnight and discharged the following morning.
Four or 5 days later, I heard from their pediatrician, who also had permission to share. He sent me a very nice note through Epic that he had seen the boys. Besides some mental trauma, they were all healthy and doing fine.
The family lives in the area and the kids go to school 5 miles from my house. So, the following weekend they came over. It was Father’s Day, which was kind of cool. They brought me some flowers and candy and a card the boys had drawn to thank me.
I learned that the dad had brought the boys to the fishing site. They were horsing around in knee deep water. One of the boys walked off a little way and didn’t realize there was a drop off. He went in, and of course the dad went after him, and the other two followed.
I said to the parents: “Look, things like this happen for a reason. People like your son are saved and go on in this world because they’ve got special things to do. I can’t wait to see what kind of man he becomes.”
Two or 3 months later, it was football season, and I got at a message from the dad saying their son was playing football on Saturday at the school. He wondered if I could drop by. So, I kind of snuck over and watched, but I didn’t go say hi. There’s trauma there, and I didn’t want them to have to relive that.
I’m very fortunate that I exercise every day and I know how to do CPR and swim. And thank God the boy was floating when I got to him, or I never would’ve found him. The Maumee River is known as the “muddy Maumee.” You can’t see anything under the water.
Depending on the time of year, the river can be almost dry or overflowing into the parking lot with the current rushing hard. If it had been like that, I wouldn’t have considered going in. And they wouldn’t they have been there in the first place. They’d have been a mile downstream.
I took a risk. I could have gone out there and had the dad and two other kids jump on top of me. Then we all would have been in trouble. But like I told my wife, I couldn’t stand there and watch it. I’m just not that person.
I think it was also about being a dad myself and having grandkids now. Doctor or no doctor, I felt like I was in reasonably good shape and I had to go in there to help. This dad was trying his butt off, but three little kids is too many. You can’t do that by yourself. They were not going to make it.
I go to the hospital and I save lives as part of my job, and I don’t even come home and talk about it. But this is a whole different thing. Being able to save someone’s life when put in this situation is very gratifying. It’s a tremendous feeling. There’s a reason that young man is here today, and I’ll be watching for great things from him.
A version of this article first appeared on Medscape.com.
Daniel Cassavar, MD, is a cardiologist with ProMedica in Perrysburg, Ohio.
Is There a Doctor in the House? is a new series telling these stories.
I live on the Maumee River in Ohio, about 50 yards from the water. I had an early quit time and came home to meet my wife for lunch. Afterward, I went up to my barn across the main road to tinker around. It was a nice day out, so my wife had opened some windows. Suddenly, she heard screaming from the river. It did not sound like fun.
She ran down to the river’s edge and saw a dad and three boys struggling in the water. She phoned me screaming: “They’re drowning! They’re drowning!” I jumped in my truck and drove up our driveway through the yard right down to the river.
My wife was on the phone with 911 at that point, and I could see them about 75-100 yards out. The dad had two of the boys clinging around his neck. They were going under the water and coming up and going under again. The other boy was just floating nearby, face down, motionless.
I threw my shoes and scrubs off and started to walk towards the water. My wife screamed at me, “You’re not going in there!” I said, “I’m not going to stand here and watch this. It’s not going to happen.”
I’m not a kid anymore, but I was a high school swimmer, and to this day I work out all the time. I felt like I had to try something. So, I went in the water despite my wife yelling and I swam towards them.
What happens when you get in that deep water is that you panic. You can’t hear anyone because of the rapids, and your instinct is to swim back towards where you went in, which is against the current. Unless you’re a very strong swimmer, you’re just wasting your time, swimming in place.
But these guys weren’t trying to go anywhere. Dad was just trying to stay up and keep the boys alive. He was in about 10 feet of water. What they didn’t see or just didn’t know: About 20 yards upstream from that deep water is a little island.
When I got to them, I yelled at the dad to move towards the island, “Go backwards! Go back!” I flipped the boy over who wasn’t moving. He was the oldest of the three, around 10 or 11 years old. When I turned him over, he was blue and wasn’t breathing. I put my fingers on his neck and didn’t feel a pulse.
So, I’m treading water, holding him. I put an arm behind his back and started doing chest compressions on him. I probably did a dozen to 15 compressions – nothing. I thought, I’ve got to get some air in this kid. So, I gave him two deep breaths and then started doing compressions again. I know ACLS and CPR training would say we don’t do that anymore. But I couldn’t just sit there and give up. Shortly after that, he coughed out a large amount of water and started breathing.
The dad and the other two boys had made it to the island. So, I started moving towards it with the boy. It was a few minutes before he regained consciousness. Of course, he was unaware of what had happened. He started to scream, because here’s this strange man holding him. But he was breathing. That’s all I cared about.
When we got to the island, I saw that my neighbor downstream had launched his canoe. He’s a retired gentleman who lives next to me, a very physically fit man. He started rolling as hard as he could towards us, against the stream. I kind of gave him a thumbs up, like, “we’re safe now. We’re standing.” We loaded the kids and the dad in the canoe and made it back against the stream to the parking lot where they went in.
All this took probably 10 or 15 minutes, and by then the paramedics were there. Life Flight had been dispatched up by my barn where there’s room to land. So, they drove up there in the ambulance. The boy I revived was flown to the hospital. The others went in the ambulance.
I know all the ED docs, so I talked to somebody later who, with permission from the family, said they were all doing fine. They were getting x-rays on the boy’s lungs. And then I heard the dad and two boys were released that night. The other boy I worked on was observed overnight and discharged the following morning.
Four or 5 days later, I heard from their pediatrician, who also had permission to share. He sent me a very nice note through Epic that he had seen the boys. Besides some mental trauma, they were all healthy and doing fine.
The family lives in the area and the kids go to school 5 miles from my house. So, the following weekend they came over. It was Father’s Day, which was kind of cool. They brought me some flowers and candy and a card the boys had drawn to thank me.
I learned that the dad had brought the boys to the fishing site. They were horsing around in knee deep water. One of the boys walked off a little way and didn’t realize there was a drop off. He went in, and of course the dad went after him, and the other two followed.
I said to the parents: “Look, things like this happen for a reason. People like your son are saved and go on in this world because they’ve got special things to do. I can’t wait to see what kind of man he becomes.”
Two or 3 months later, it was football season, and I got at a message from the dad saying their son was playing football on Saturday at the school. He wondered if I could drop by. So, I kind of snuck over and watched, but I didn’t go say hi. There’s trauma there, and I didn’t want them to have to relive that.
I’m very fortunate that I exercise every day and I know how to do CPR and swim. And thank God the boy was floating when I got to him, or I never would’ve found him. The Maumee River is known as the “muddy Maumee.” You can’t see anything under the water.
Depending on the time of year, the river can be almost dry or overflowing into the parking lot with the current rushing hard. If it had been like that, I wouldn’t have considered going in. And they wouldn’t they have been there in the first place. They’d have been a mile downstream.
I took a risk. I could have gone out there and had the dad and two other kids jump on top of me. Then we all would have been in trouble. But like I told my wife, I couldn’t stand there and watch it. I’m just not that person.
I think it was also about being a dad myself and having grandkids now. Doctor or no doctor, I felt like I was in reasonably good shape and I had to go in there to help. This dad was trying his butt off, but three little kids is too many. You can’t do that by yourself. They were not going to make it.
I go to the hospital and I save lives as part of my job, and I don’t even come home and talk about it. But this is a whole different thing. Being able to save someone’s life when put in this situation is very gratifying. It’s a tremendous feeling. There’s a reason that young man is here today, and I’ll be watching for great things from him.
A version of this article first appeared on Medscape.com.
Daniel Cassavar, MD, is a cardiologist with ProMedica in Perrysburg, Ohio.
Is There a Doctor in the House? is a new series telling these stories.
I live on the Maumee River in Ohio, about 50 yards from the water. I had an early quit time and came home to meet my wife for lunch. Afterward, I went up to my barn across the main road to tinker around. It was a nice day out, so my wife had opened some windows. Suddenly, she heard screaming from the river. It did not sound like fun.
She ran down to the river’s edge and saw a dad and three boys struggling in the water. She phoned me screaming: “They’re drowning! They’re drowning!” I jumped in my truck and drove up our driveway through the yard right down to the river.
My wife was on the phone with 911 at that point, and I could see them about 75-100 yards out. The dad had two of the boys clinging around his neck. They were going under the water and coming up and going under again. The other boy was just floating nearby, face down, motionless.
I threw my shoes and scrubs off and started to walk towards the water. My wife screamed at me, “You’re not going in there!” I said, “I’m not going to stand here and watch this. It’s not going to happen.”
I’m not a kid anymore, but I was a high school swimmer, and to this day I work out all the time. I felt like I had to try something. So, I went in the water despite my wife yelling and I swam towards them.
What happens when you get in that deep water is that you panic. You can’t hear anyone because of the rapids, and your instinct is to swim back towards where you went in, which is against the current. Unless you’re a very strong swimmer, you’re just wasting your time, swimming in place.
But these guys weren’t trying to go anywhere. Dad was just trying to stay up and keep the boys alive. He was in about 10 feet of water. What they didn’t see or just didn’t know: About 20 yards upstream from that deep water is a little island.
When I got to them, I yelled at the dad to move towards the island, “Go backwards! Go back!” I flipped the boy over who wasn’t moving. He was the oldest of the three, around 10 or 11 years old. When I turned him over, he was blue and wasn’t breathing. I put my fingers on his neck and didn’t feel a pulse.
So, I’m treading water, holding him. I put an arm behind his back and started doing chest compressions on him. I probably did a dozen to 15 compressions – nothing. I thought, I’ve got to get some air in this kid. So, I gave him two deep breaths and then started doing compressions again. I know ACLS and CPR training would say we don’t do that anymore. But I couldn’t just sit there and give up. Shortly after that, he coughed out a large amount of water and started breathing.
The dad and the other two boys had made it to the island. So, I started moving towards it with the boy. It was a few minutes before he regained consciousness. Of course, he was unaware of what had happened. He started to scream, because here’s this strange man holding him. But he was breathing. That’s all I cared about.
When we got to the island, I saw that my neighbor downstream had launched his canoe. He’s a retired gentleman who lives next to me, a very physically fit man. He started rolling as hard as he could towards us, against the stream. I kind of gave him a thumbs up, like, “we’re safe now. We’re standing.” We loaded the kids and the dad in the canoe and made it back against the stream to the parking lot where they went in.
All this took probably 10 or 15 minutes, and by then the paramedics were there. Life Flight had been dispatched up by my barn where there’s room to land. So, they drove up there in the ambulance. The boy I revived was flown to the hospital. The others went in the ambulance.
I know all the ED docs, so I talked to somebody later who, with permission from the family, said they were all doing fine. They were getting x-rays on the boy’s lungs. And then I heard the dad and two boys were released that night. The other boy I worked on was observed overnight and discharged the following morning.
Four or 5 days later, I heard from their pediatrician, who also had permission to share. He sent me a very nice note through Epic that he had seen the boys. Besides some mental trauma, they were all healthy and doing fine.
The family lives in the area and the kids go to school 5 miles from my house. So, the following weekend they came over. It was Father’s Day, which was kind of cool. They brought me some flowers and candy and a card the boys had drawn to thank me.
I learned that the dad had brought the boys to the fishing site. They were horsing around in knee deep water. One of the boys walked off a little way and didn’t realize there was a drop off. He went in, and of course the dad went after him, and the other two followed.
I said to the parents: “Look, things like this happen for a reason. People like your son are saved and go on in this world because they’ve got special things to do. I can’t wait to see what kind of man he becomes.”
Two or 3 months later, it was football season, and I got at a message from the dad saying their son was playing football on Saturday at the school. He wondered if I could drop by. So, I kind of snuck over and watched, but I didn’t go say hi. There’s trauma there, and I didn’t want them to have to relive that.
I’m very fortunate that I exercise every day and I know how to do CPR and swim. And thank God the boy was floating when I got to him, or I never would’ve found him. The Maumee River is known as the “muddy Maumee.” You can’t see anything under the water.
Depending on the time of year, the river can be almost dry or overflowing into the parking lot with the current rushing hard. If it had been like that, I wouldn’t have considered going in. And they wouldn’t they have been there in the first place. They’d have been a mile downstream.
I took a risk. I could have gone out there and had the dad and two other kids jump on top of me. Then we all would have been in trouble. But like I told my wife, I couldn’t stand there and watch it. I’m just not that person.
I think it was also about being a dad myself and having grandkids now. Doctor or no doctor, I felt like I was in reasonably good shape and I had to go in there to help. This dad was trying his butt off, but three little kids is too many. You can’t do that by yourself. They were not going to make it.
I go to the hospital and I save lives as part of my job, and I don’t even come home and talk about it. But this is a whole different thing. Being able to save someone’s life when put in this situation is very gratifying. It’s a tremendous feeling. There’s a reason that young man is here today, and I’ll be watching for great things from him.
A version of this article first appeared on Medscape.com.
Daniel Cassavar, MD, is a cardiologist with ProMedica in Perrysburg, Ohio.
Endocarditis tied to drug use on the rise, spiked during COVID
A new study provides more evidence that endocarditis associated with drug use is a significant and growing health concern, and further demonstrates that this risk has been exacerbated by the COVID-19 pandemic.
The rate of infective endocarditis among individuals in the United States with opioid or cocaine use disorder increased in the 11-year period 2011 to 2022, with the steepest increase logged during the COVID-19 pandemic (2021-2022), according to the study.
A diagnosis of COVID-19 more than doubled the risk for a new diagnosis of endocarditis in patients with either cocaine (hazard ratio, 2.24) or opioid use disorder (HR, 2.23).
“Our data suggests that, in addition to the major social disruption from the pandemic, including disrupted access to health care, COVID-19 infection itself is a significant risk factor for new diagnosis of endocarditis in drug using populations,” authors Nora Volkow, MD, director of the National Institute on Drug Abuse, and colleagues wrote.
“Drug-using populations, particularly those who use cocaine or opioids, have some of the highest risk for endocarditis, and here we show that having a COVID-19 diagnoses further increases this risk,” they added.
The study was published online in Molecular Psychiatry.
The researchers analyzed electronic health record data collected from January 2011 to August 2022 for more than 109 million people across the United States, including more than 736,000 with an opioid use disorder and more than 379,000 with a cocaine use disorder.
In 2011, there were 4 cases of endocarditis per day for every 1 million people with opioid use disorder. By 2022, the rate had increased to 30 cases per day per 1 million people with opioid use disorder.
For people with cocaine use disorder, cases of endocarditis increased from 5 per 1 million in 2011 to 23 per 1 million in 2022.
Among individuals with cocaine or opioid use disorder, the risk of being hospitalized within 180 days following a diagnosis of endocarditis was higher in those with than without COVID-19 (67.5% vs. 58.7%; HR, 1.21).
The risk of dying within 180 days following new diagnosis of endocarditis was also higher in those with than without COVID-19 (9.2% vs. 8%; HR, 1.16).
The study also showed that Black and Hispanic individuals had a lower risk for COVID-19-associated endocarditis than non-Hispanic White individuals, which is consistent with a higher prevalence of injection drug use in non-Hispanic White populations, compared with Black or Hispanic populations, the researchers pointed out.
Dr. Volkow and colleagues said their findings highlight the need to screen drug users for endocarditis and link them to infectious disease and addiction treatment if they contract COVID-19.
“People with substance use disorder already face major impediments to proper health care due to lack of access and stigma,” Dr. Volkow said in a news release.
“Proven techniques like syringe service programs, which help people avoid infection from reused or shared injection equipment, can help prevent this often fatal and costly condition,” Dr. Volkow added.
The authors said it will also be important to determine exactly how SARS-CoV-2 viral infection exacerbates the risk for endocarditis in drug users.
Support for the study was provided by the National Institute on Aging, National Institute on Alcohol Abuse and Alcoholism, the Clinical and Translational Science Collaborative of Cleveland, and the National Cancer Institute Case Comprehensive Cancer Center. The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study provides more evidence that endocarditis associated with drug use is a significant and growing health concern, and further demonstrates that this risk has been exacerbated by the COVID-19 pandemic.
The rate of infective endocarditis among individuals in the United States with opioid or cocaine use disorder increased in the 11-year period 2011 to 2022, with the steepest increase logged during the COVID-19 pandemic (2021-2022), according to the study.
A diagnosis of COVID-19 more than doubled the risk for a new diagnosis of endocarditis in patients with either cocaine (hazard ratio, 2.24) or opioid use disorder (HR, 2.23).
“Our data suggests that, in addition to the major social disruption from the pandemic, including disrupted access to health care, COVID-19 infection itself is a significant risk factor for new diagnosis of endocarditis in drug using populations,” authors Nora Volkow, MD, director of the National Institute on Drug Abuse, and colleagues wrote.
“Drug-using populations, particularly those who use cocaine or opioids, have some of the highest risk for endocarditis, and here we show that having a COVID-19 diagnoses further increases this risk,” they added.
The study was published online in Molecular Psychiatry.
The researchers analyzed electronic health record data collected from January 2011 to August 2022 for more than 109 million people across the United States, including more than 736,000 with an opioid use disorder and more than 379,000 with a cocaine use disorder.
In 2011, there were 4 cases of endocarditis per day for every 1 million people with opioid use disorder. By 2022, the rate had increased to 30 cases per day per 1 million people with opioid use disorder.
For people with cocaine use disorder, cases of endocarditis increased from 5 per 1 million in 2011 to 23 per 1 million in 2022.
Among individuals with cocaine or opioid use disorder, the risk of being hospitalized within 180 days following a diagnosis of endocarditis was higher in those with than without COVID-19 (67.5% vs. 58.7%; HR, 1.21).
The risk of dying within 180 days following new diagnosis of endocarditis was also higher in those with than without COVID-19 (9.2% vs. 8%; HR, 1.16).
The study also showed that Black and Hispanic individuals had a lower risk for COVID-19-associated endocarditis than non-Hispanic White individuals, which is consistent with a higher prevalence of injection drug use in non-Hispanic White populations, compared with Black or Hispanic populations, the researchers pointed out.
Dr. Volkow and colleagues said their findings highlight the need to screen drug users for endocarditis and link them to infectious disease and addiction treatment if they contract COVID-19.
“People with substance use disorder already face major impediments to proper health care due to lack of access and stigma,” Dr. Volkow said in a news release.
“Proven techniques like syringe service programs, which help people avoid infection from reused or shared injection equipment, can help prevent this often fatal and costly condition,” Dr. Volkow added.
The authors said it will also be important to determine exactly how SARS-CoV-2 viral infection exacerbates the risk for endocarditis in drug users.
Support for the study was provided by the National Institute on Aging, National Institute on Alcohol Abuse and Alcoholism, the Clinical and Translational Science Collaborative of Cleveland, and the National Cancer Institute Case Comprehensive Cancer Center. The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study provides more evidence that endocarditis associated with drug use is a significant and growing health concern, and further demonstrates that this risk has been exacerbated by the COVID-19 pandemic.
The rate of infective endocarditis among individuals in the United States with opioid or cocaine use disorder increased in the 11-year period 2011 to 2022, with the steepest increase logged during the COVID-19 pandemic (2021-2022), according to the study.
A diagnosis of COVID-19 more than doubled the risk for a new diagnosis of endocarditis in patients with either cocaine (hazard ratio, 2.24) or opioid use disorder (HR, 2.23).
“Our data suggests that, in addition to the major social disruption from the pandemic, including disrupted access to health care, COVID-19 infection itself is a significant risk factor for new diagnosis of endocarditis in drug using populations,” authors Nora Volkow, MD, director of the National Institute on Drug Abuse, and colleagues wrote.
“Drug-using populations, particularly those who use cocaine or opioids, have some of the highest risk for endocarditis, and here we show that having a COVID-19 diagnoses further increases this risk,” they added.
The study was published online in Molecular Psychiatry.
The researchers analyzed electronic health record data collected from January 2011 to August 2022 for more than 109 million people across the United States, including more than 736,000 with an opioid use disorder and more than 379,000 with a cocaine use disorder.
In 2011, there were 4 cases of endocarditis per day for every 1 million people with opioid use disorder. By 2022, the rate had increased to 30 cases per day per 1 million people with opioid use disorder.
For people with cocaine use disorder, cases of endocarditis increased from 5 per 1 million in 2011 to 23 per 1 million in 2022.
Among individuals with cocaine or opioid use disorder, the risk of being hospitalized within 180 days following a diagnosis of endocarditis was higher in those with than without COVID-19 (67.5% vs. 58.7%; HR, 1.21).
The risk of dying within 180 days following new diagnosis of endocarditis was also higher in those with than without COVID-19 (9.2% vs. 8%; HR, 1.16).
The study also showed that Black and Hispanic individuals had a lower risk for COVID-19-associated endocarditis than non-Hispanic White individuals, which is consistent with a higher prevalence of injection drug use in non-Hispanic White populations, compared with Black or Hispanic populations, the researchers pointed out.
Dr. Volkow and colleagues said their findings highlight the need to screen drug users for endocarditis and link them to infectious disease and addiction treatment if they contract COVID-19.
“People with substance use disorder already face major impediments to proper health care due to lack of access and stigma,” Dr. Volkow said in a news release.
“Proven techniques like syringe service programs, which help people avoid infection from reused or shared injection equipment, can help prevent this often fatal and costly condition,” Dr. Volkow added.
The authors said it will also be important to determine exactly how SARS-CoV-2 viral infection exacerbates the risk for endocarditis in drug users.
Support for the study was provided by the National Institute on Aging, National Institute on Alcohol Abuse and Alcoholism, the Clinical and Translational Science Collaborative of Cleveland, and the National Cancer Institute Case Comprehensive Cancer Center. The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM MOLECULAR PSYCHIATRY
New PDT therapy for CTCL to be reviewed by FDA
based on phase 3 findings published in JAMA Dermatology.
The treatment employs an ointment formulation of synthetic hypericin (HyBryte), a photosensitizer, that is preferentially absorbed into malignant cells and activated with visible light – rather than ultraviolet light – approximately 24 hours later. Investigators saw significant clinical responses in both patch and plaque type lesions and across races during the 24-week placebo-controlled, double-blinded, phase 3, randomized clinical trial.
“Traditional phototherapy, ultraviolet B phototherapy, has a limited depth of penetration, so patients with thicker plaque lesions don’t respond as well ... and UVB phototherapy typically is less effective in penetrating pigmented skin,” Ellen J. Kim, MD, lead author of the FLASH phase 3 trial, said in an interview.
Visible light in the yellow-red spectrum (500-650 nm) “penetrates deeper into the skin” and is nonmutagenic in vitro, so “theoretically it should have a much more favorable long-term safety profile,” said Dr. Kim, a dermatologist at the University of Pennsylvania, Philadelphia.
Currently, she said, the risk of secondary malignancies inherent with UV PDT, including melanoma, is a deterrent for some patients, especially “patients with really fair skin and a history of skin cancer.”
Hypericin PDT also seems well suited for use with an at-home light unit. “In our field, it’s not about which therapy is [universally] better or best, but a matter of what works best for each patient at that moment in time, depending on the side-effect profile and other issues such as access,” Dr. Kim said. “It will be great to have another option for an incurable disease that requires chronic management.”
Mycosis fungoides (MF)/CTCL is considered an orphan disease, and the treatment has received orphan drug and fast track designations from the FDA, and orphan designation from the European Medicines Agency, according to a press release from its developer, Soligenix. The company is anticipating potential approval in the second half of 2023 and is targeting early 2024 for a U.S. launch, the statement said.
Phase 3 results
The pivotal trial involved 169 patients at 39 academic and community-based U.S. medical centers and consisted of several 6-week cycles of twice-weekly treatment punctuated by 2-week breaks. In cycle 1, patients were randomized 2:1 to receive hypericin or placebo treatment of three index lesions. Cycle 2 involved the crossover of placebo patients to active treatment of index lesions, and cycle 3 (optional) involved open-label treatment of all desired lesions (index and nonindex).
The trial defined the primary endpoint in phase 1 as 50% or greater improvement in the modified Composite Assessment of Index Lesion Severity score – a tool that’s endorsed by U.S. and international MF/CTCL specialty group consensus guidelines. For cycles 2 and 3, open-label response rates were secondary endpoints. Responses were assessed after 2-week rest periods to allow for treatment-induced skin reactions to subside.
After one cycle of treatment, topical hypericin PDT was more effective than placebo (an index lesion response rate of 16% vs. 4%; P =.04). The index lesion response rate with treatment increased to 40% after two cycles and 49% after three cycles. All were statistically significant changes.
Response rates were similar in patch and plaque-type lesions and regardless of age, sex, race, stage IA versus IB, time since diagnosis, and number of prior therapies. Adverse events were primarily mild application-site skin reactions. No serious drug-related adverse events occurred, Dr. Kim said, and “we had a low drop-out rate overall.”
Into the real world
The 24-week phase 3 trial duration is short, considering that “typically, phototherapy takes between 4 to 24 months [to achieve] full responses in CTCL,” Dr. Kim said in the interview.
So with real-world application, she said, “we’ll want to see where the overall response peaks with longer treatment, what the effects are of continuous treatment without any built-in breaks, and whether we will indeed see less skin cancer development in patients who are at higher risk of developing skin cancers from light treatment.”
Such questions will be explored as part of a new 4-year, 50-patient, open-label, multicenter study with the primary aim of investigating home-based hypericin PDT therapy in a supervised setting, said Dr. Kim, principal investigator of this study. Patients who are doing well after 6 weeks of twice-weekly therapy will be given at-home light units to continue therapy and achieve 1 year of treatment with no breaks. They will be monitored with video-based telemedicine.
“Long term, having a home unit should really improve patient access and compliance and hopefully effectiveness,” Dr. Kim said. Based on the phase 3 experience, “we think that continuous treatment will be well tolerated and that we may see greater responses.”
On Dec. 19, Soligenix announced that enrollment had begun in a phase 2a study of synthetic hypericin for treating patients with mild to moderate psoriasis.
Dr. Kim reported to JAMA Dermatology grants from Innate Pharma and Galderma; consulting/advisory fees from Almirall, Galderma, and Helsinn; and honoraria from Ology and UptoDate.
based on phase 3 findings published in JAMA Dermatology.
The treatment employs an ointment formulation of synthetic hypericin (HyBryte), a photosensitizer, that is preferentially absorbed into malignant cells and activated with visible light – rather than ultraviolet light – approximately 24 hours later. Investigators saw significant clinical responses in both patch and plaque type lesions and across races during the 24-week placebo-controlled, double-blinded, phase 3, randomized clinical trial.
“Traditional phototherapy, ultraviolet B phototherapy, has a limited depth of penetration, so patients with thicker plaque lesions don’t respond as well ... and UVB phototherapy typically is less effective in penetrating pigmented skin,” Ellen J. Kim, MD, lead author of the FLASH phase 3 trial, said in an interview.
Visible light in the yellow-red spectrum (500-650 nm) “penetrates deeper into the skin” and is nonmutagenic in vitro, so “theoretically it should have a much more favorable long-term safety profile,” said Dr. Kim, a dermatologist at the University of Pennsylvania, Philadelphia.
Currently, she said, the risk of secondary malignancies inherent with UV PDT, including melanoma, is a deterrent for some patients, especially “patients with really fair skin and a history of skin cancer.”
Hypericin PDT also seems well suited for use with an at-home light unit. “In our field, it’s not about which therapy is [universally] better or best, but a matter of what works best for each patient at that moment in time, depending on the side-effect profile and other issues such as access,” Dr. Kim said. “It will be great to have another option for an incurable disease that requires chronic management.”
Mycosis fungoides (MF)/CTCL is considered an orphan disease, and the treatment has received orphan drug and fast track designations from the FDA, and orphan designation from the European Medicines Agency, according to a press release from its developer, Soligenix. The company is anticipating potential approval in the second half of 2023 and is targeting early 2024 for a U.S. launch, the statement said.
Phase 3 results
The pivotal trial involved 169 patients at 39 academic and community-based U.S. medical centers and consisted of several 6-week cycles of twice-weekly treatment punctuated by 2-week breaks. In cycle 1, patients were randomized 2:1 to receive hypericin or placebo treatment of three index lesions. Cycle 2 involved the crossover of placebo patients to active treatment of index lesions, and cycle 3 (optional) involved open-label treatment of all desired lesions (index and nonindex).
The trial defined the primary endpoint in phase 1 as 50% or greater improvement in the modified Composite Assessment of Index Lesion Severity score – a tool that’s endorsed by U.S. and international MF/CTCL specialty group consensus guidelines. For cycles 2 and 3, open-label response rates were secondary endpoints. Responses were assessed after 2-week rest periods to allow for treatment-induced skin reactions to subside.
After one cycle of treatment, topical hypericin PDT was more effective than placebo (an index lesion response rate of 16% vs. 4%; P =.04). The index lesion response rate with treatment increased to 40% after two cycles and 49% after three cycles. All were statistically significant changes.
Response rates were similar in patch and plaque-type lesions and regardless of age, sex, race, stage IA versus IB, time since diagnosis, and number of prior therapies. Adverse events were primarily mild application-site skin reactions. No serious drug-related adverse events occurred, Dr. Kim said, and “we had a low drop-out rate overall.”
Into the real world
The 24-week phase 3 trial duration is short, considering that “typically, phototherapy takes between 4 to 24 months [to achieve] full responses in CTCL,” Dr. Kim said in the interview.
So with real-world application, she said, “we’ll want to see where the overall response peaks with longer treatment, what the effects are of continuous treatment without any built-in breaks, and whether we will indeed see less skin cancer development in patients who are at higher risk of developing skin cancers from light treatment.”
Such questions will be explored as part of a new 4-year, 50-patient, open-label, multicenter study with the primary aim of investigating home-based hypericin PDT therapy in a supervised setting, said Dr. Kim, principal investigator of this study. Patients who are doing well after 6 weeks of twice-weekly therapy will be given at-home light units to continue therapy and achieve 1 year of treatment with no breaks. They will be monitored with video-based telemedicine.
“Long term, having a home unit should really improve patient access and compliance and hopefully effectiveness,” Dr. Kim said. Based on the phase 3 experience, “we think that continuous treatment will be well tolerated and that we may see greater responses.”
On Dec. 19, Soligenix announced that enrollment had begun in a phase 2a study of synthetic hypericin for treating patients with mild to moderate psoriasis.
Dr. Kim reported to JAMA Dermatology grants from Innate Pharma and Galderma; consulting/advisory fees from Almirall, Galderma, and Helsinn; and honoraria from Ology and UptoDate.
based on phase 3 findings published in JAMA Dermatology.
The treatment employs an ointment formulation of synthetic hypericin (HyBryte), a photosensitizer, that is preferentially absorbed into malignant cells and activated with visible light – rather than ultraviolet light – approximately 24 hours later. Investigators saw significant clinical responses in both patch and plaque type lesions and across races during the 24-week placebo-controlled, double-blinded, phase 3, randomized clinical trial.
“Traditional phototherapy, ultraviolet B phototherapy, has a limited depth of penetration, so patients with thicker plaque lesions don’t respond as well ... and UVB phototherapy typically is less effective in penetrating pigmented skin,” Ellen J. Kim, MD, lead author of the FLASH phase 3 trial, said in an interview.
Visible light in the yellow-red spectrum (500-650 nm) “penetrates deeper into the skin” and is nonmutagenic in vitro, so “theoretically it should have a much more favorable long-term safety profile,” said Dr. Kim, a dermatologist at the University of Pennsylvania, Philadelphia.
Currently, she said, the risk of secondary malignancies inherent with UV PDT, including melanoma, is a deterrent for some patients, especially “patients with really fair skin and a history of skin cancer.”
Hypericin PDT also seems well suited for use with an at-home light unit. “In our field, it’s not about which therapy is [universally] better or best, but a matter of what works best for each patient at that moment in time, depending on the side-effect profile and other issues such as access,” Dr. Kim said. “It will be great to have another option for an incurable disease that requires chronic management.”
Mycosis fungoides (MF)/CTCL is considered an orphan disease, and the treatment has received orphan drug and fast track designations from the FDA, and orphan designation from the European Medicines Agency, according to a press release from its developer, Soligenix. The company is anticipating potential approval in the second half of 2023 and is targeting early 2024 for a U.S. launch, the statement said.
Phase 3 results
The pivotal trial involved 169 patients at 39 academic and community-based U.S. medical centers and consisted of several 6-week cycles of twice-weekly treatment punctuated by 2-week breaks. In cycle 1, patients were randomized 2:1 to receive hypericin or placebo treatment of three index lesions. Cycle 2 involved the crossover of placebo patients to active treatment of index lesions, and cycle 3 (optional) involved open-label treatment of all desired lesions (index and nonindex).
The trial defined the primary endpoint in phase 1 as 50% or greater improvement in the modified Composite Assessment of Index Lesion Severity score – a tool that’s endorsed by U.S. and international MF/CTCL specialty group consensus guidelines. For cycles 2 and 3, open-label response rates were secondary endpoints. Responses were assessed after 2-week rest periods to allow for treatment-induced skin reactions to subside.
After one cycle of treatment, topical hypericin PDT was more effective than placebo (an index lesion response rate of 16% vs. 4%; P =.04). The index lesion response rate with treatment increased to 40% after two cycles and 49% after three cycles. All were statistically significant changes.
Response rates were similar in patch and plaque-type lesions and regardless of age, sex, race, stage IA versus IB, time since diagnosis, and number of prior therapies. Adverse events were primarily mild application-site skin reactions. No serious drug-related adverse events occurred, Dr. Kim said, and “we had a low drop-out rate overall.”
Into the real world
The 24-week phase 3 trial duration is short, considering that “typically, phototherapy takes between 4 to 24 months [to achieve] full responses in CTCL,” Dr. Kim said in the interview.
So with real-world application, she said, “we’ll want to see where the overall response peaks with longer treatment, what the effects are of continuous treatment without any built-in breaks, and whether we will indeed see less skin cancer development in patients who are at higher risk of developing skin cancers from light treatment.”
Such questions will be explored as part of a new 4-year, 50-patient, open-label, multicenter study with the primary aim of investigating home-based hypericin PDT therapy in a supervised setting, said Dr. Kim, principal investigator of this study. Patients who are doing well after 6 weeks of twice-weekly therapy will be given at-home light units to continue therapy and achieve 1 year of treatment with no breaks. They will be monitored with video-based telemedicine.
“Long term, having a home unit should really improve patient access and compliance and hopefully effectiveness,” Dr. Kim said. Based on the phase 3 experience, “we think that continuous treatment will be well tolerated and that we may see greater responses.”
On Dec. 19, Soligenix announced that enrollment had begun in a phase 2a study of synthetic hypericin for treating patients with mild to moderate psoriasis.
Dr. Kim reported to JAMA Dermatology grants from Innate Pharma and Galderma; consulting/advisory fees from Almirall, Galderma, and Helsinn; and honoraria from Ology and UptoDate.
All the National Health Service wants for Christmas is tea and biscuits
Three cups of tea, two biscuit packs, and a Christmas study from the BMJ
Warning: The following content may contain excessive Britishness. Continue at your own risk.
It’s no secret that the world economy is in an … interesting spot right now. Belt tightening is occurring around the world despite the holiday season, and hospitals across the pond in Great Britain are no exception.
It was a simple sign that prompted the study, published in the Christmas edition of the BMJ: “Please do not take excessive quantities of these refreshments.” And if we all know one thing, you do not get between Brits and their tea and biscuits. So the researchers behind the study drafted a survey and sent it around to nearly 2,000 British health care workers and asked what they considered to be excessive consumption of work-provided hot drinks and biscuits.
In the hot drinks department (tea and coffee, though we appreciate the two people who voiced a preference for free hot whiskey, if it was available) the survey participants decreed that 3.32 drinks was the maximum before consumption became excessive. That’s pretty close to the actual number of hot drinks respondents drank daily (3.04), so it’s pretty fair to say that British health care workers do a good job of self-limiting.
It’s much the same story with biscuits: Health care workers reported that consuming 2.25 packets of free biscuits would be excessive. Notably, doctors would take more than nondoctors (2.35 vs. 2.14 – typical doctor behavior), and those who had been in their role for less than 2 years would consume nearly 3 packets a day before calling it quits.
The study did not include an official cost analysis, but calculations conducted on a biscuit wrapper (that’s not a joke, by the way) estimated that the combined cost for providing every National Health Service employee with three free drinks and two free biscuit packages a day would be about 160 million pounds a year. Now, that’s a lot of money for tea and biscuits, but, they added, it’s a meager 0.1% of the NHS annual budget. They also noted that most employees consider free hot drinks a more valuable workplace perk than free support for mental health.
In conclusion, the authors wrote, “As a target for cost-saving initiatives, limiting free refreshment consumption is really scraping the biscuit barrel (although some limits on hot whiskey availability may be necessary), and implementing, or continuing, perks that improve staff morale seems justifiable. … Healthcare employers should allow biscuits and hot drinks to be freely available to staff, and they should leave these grateful recipients to judge for themselves what constitutes reasonable consumption.”
Now there’s a Christmas sentiment we can all get behind.
We come not to bury sugar, but to improve it
When we think about sugar, healthy isn’t the first thing that comes to mind. Research also shows that artificial sweeteners, as well as processed foods in general, are bad for your body and brain. People, however, love the stuff. That’s why one of the leading brands in processed foods, Kraft Heinz, partnered with the Wyss Institute for Biologically Inspired Engineering at Harvard to find a way to reduce consumers’ sugar consumption.
The question that Kraft Heinz presented to Wyss was this: How could it reduce the fructose in its products without losing the functionality of regular sugar.
The Wyss team’s approach seems pretty simple: Use a naturally occurring enzyme to convert sugar to fiber. The trick was to add the enzymes into the food so they could convert the sugar to fiber after being consumed. The enzymes also needed to be able to be added to existing food products without changing their existing recipes, Kraft Heinz insisted.
How does it work? The crafted enzyme is encapsulated to remain dormant in the food until exposed to an increased pH level, as is found in the GI tract between the stomach and the intestine. It reduces the amount of sugar absorbed in the bloodstream and creates a healthy prebiotic fiber, the institute explained.
This opens a whole new window for consumers. People with diabetes can enjoy their favorite cookies from time to time, while parents can feel less guilty about their children bathing their chicken nuggets in unholy amounts of ketchup.
New genes, or not new genes? That is the question
… and the police report that no capybaras were harmed in the incident. What a relief. Now Action News 8 brings you Carol Espinosa’s exclusive interview with legendary scientist and zombie, Charles Darwin.
Carol: Thanks, Daryl. Tell us, Prof. Darwin, what have you been up to lately?
Prof. Darwin: Please, Carol, call me Chuck. As always, I’ve got my hands full with the whole evolution thing. The big news right now is a study published in Cell Reports that offers evidence of the continuing evolution of humans. Can I eat your brain now?
Carol: No, Chuck, you may not. So people are still evolving? It sure seems like we’ve reverted to survival of the dumbest.
Chuck Darwin: Good one, Carol, but evolution hasn’t stopped. The investigators used a previously published dataset of functionally relevant new genes to create an ancestral tree comparing humans with other vertebrate species. By tracking the genes across evolution, they found 155 from regions of unique DNA that arose from scratch and not from duplication events in the existing genome. That’s a big deal.
Carol: Anything made from scratch is always better. Everyone knows that. What else can you tell us, Chuck?
Chuck Darwin: So these 155 genes didn’t exist when humans separated from chimpanzees nearly 7 million years ago. Turns out that 44 of them are associated with growth defects in cell cultures and three “have disease-associated DNA markers that point to connections with ailments such as muscular dystrophy, retinitis pigmentosa, and Alazami syndrome.” At least that’s what the investigators said in a written statement. I must say, Carol, that your brain is looking particularly delicious tonight.
Carol: Ironic. For years I’ve been hoping a man would appreciate me for my brain, and now I get this. Back to you, Daryl.
Three cups of tea, two biscuit packs, and a Christmas study from the BMJ
Warning: The following content may contain excessive Britishness. Continue at your own risk.
It’s no secret that the world economy is in an … interesting spot right now. Belt tightening is occurring around the world despite the holiday season, and hospitals across the pond in Great Britain are no exception.
It was a simple sign that prompted the study, published in the Christmas edition of the BMJ: “Please do not take excessive quantities of these refreshments.” And if we all know one thing, you do not get between Brits and their tea and biscuits. So the researchers behind the study drafted a survey and sent it around to nearly 2,000 British health care workers and asked what they considered to be excessive consumption of work-provided hot drinks and biscuits.
In the hot drinks department (tea and coffee, though we appreciate the two people who voiced a preference for free hot whiskey, if it was available) the survey participants decreed that 3.32 drinks was the maximum before consumption became excessive. That’s pretty close to the actual number of hot drinks respondents drank daily (3.04), so it’s pretty fair to say that British health care workers do a good job of self-limiting.
It’s much the same story with biscuits: Health care workers reported that consuming 2.25 packets of free biscuits would be excessive. Notably, doctors would take more than nondoctors (2.35 vs. 2.14 – typical doctor behavior), and those who had been in their role for less than 2 years would consume nearly 3 packets a day before calling it quits.
The study did not include an official cost analysis, but calculations conducted on a biscuit wrapper (that’s not a joke, by the way) estimated that the combined cost for providing every National Health Service employee with three free drinks and two free biscuit packages a day would be about 160 million pounds a year. Now, that’s a lot of money for tea and biscuits, but, they added, it’s a meager 0.1% of the NHS annual budget. They also noted that most employees consider free hot drinks a more valuable workplace perk than free support for mental health.
In conclusion, the authors wrote, “As a target for cost-saving initiatives, limiting free refreshment consumption is really scraping the biscuit barrel (although some limits on hot whiskey availability may be necessary), and implementing, or continuing, perks that improve staff morale seems justifiable. … Healthcare employers should allow biscuits and hot drinks to be freely available to staff, and they should leave these grateful recipients to judge for themselves what constitutes reasonable consumption.”
Now there’s a Christmas sentiment we can all get behind.
We come not to bury sugar, but to improve it
When we think about sugar, healthy isn’t the first thing that comes to mind. Research also shows that artificial sweeteners, as well as processed foods in general, are bad for your body and brain. People, however, love the stuff. That’s why one of the leading brands in processed foods, Kraft Heinz, partnered with the Wyss Institute for Biologically Inspired Engineering at Harvard to find a way to reduce consumers’ sugar consumption.
The question that Kraft Heinz presented to Wyss was this: How could it reduce the fructose in its products without losing the functionality of regular sugar.
The Wyss team’s approach seems pretty simple: Use a naturally occurring enzyme to convert sugar to fiber. The trick was to add the enzymes into the food so they could convert the sugar to fiber after being consumed. The enzymes also needed to be able to be added to existing food products without changing their existing recipes, Kraft Heinz insisted.
How does it work? The crafted enzyme is encapsulated to remain dormant in the food until exposed to an increased pH level, as is found in the GI tract between the stomach and the intestine. It reduces the amount of sugar absorbed in the bloodstream and creates a healthy prebiotic fiber, the institute explained.
This opens a whole new window for consumers. People with diabetes can enjoy their favorite cookies from time to time, while parents can feel less guilty about their children bathing their chicken nuggets in unholy amounts of ketchup.
New genes, or not new genes? That is the question
… and the police report that no capybaras were harmed in the incident. What a relief. Now Action News 8 brings you Carol Espinosa’s exclusive interview with legendary scientist and zombie, Charles Darwin.
Carol: Thanks, Daryl. Tell us, Prof. Darwin, what have you been up to lately?
Prof. Darwin: Please, Carol, call me Chuck. As always, I’ve got my hands full with the whole evolution thing. The big news right now is a study published in Cell Reports that offers evidence of the continuing evolution of humans. Can I eat your brain now?
Carol: No, Chuck, you may not. So people are still evolving? It sure seems like we’ve reverted to survival of the dumbest.
Chuck Darwin: Good one, Carol, but evolution hasn’t stopped. The investigators used a previously published dataset of functionally relevant new genes to create an ancestral tree comparing humans with other vertebrate species. By tracking the genes across evolution, they found 155 from regions of unique DNA that arose from scratch and not from duplication events in the existing genome. That’s a big deal.
Carol: Anything made from scratch is always better. Everyone knows that. What else can you tell us, Chuck?
Chuck Darwin: So these 155 genes didn’t exist when humans separated from chimpanzees nearly 7 million years ago. Turns out that 44 of them are associated with growth defects in cell cultures and three “have disease-associated DNA markers that point to connections with ailments such as muscular dystrophy, retinitis pigmentosa, and Alazami syndrome.” At least that’s what the investigators said in a written statement. I must say, Carol, that your brain is looking particularly delicious tonight.
Carol: Ironic. For years I’ve been hoping a man would appreciate me for my brain, and now I get this. Back to you, Daryl.
Three cups of tea, two biscuit packs, and a Christmas study from the BMJ
Warning: The following content may contain excessive Britishness. Continue at your own risk.
It’s no secret that the world economy is in an … interesting spot right now. Belt tightening is occurring around the world despite the holiday season, and hospitals across the pond in Great Britain are no exception.
It was a simple sign that prompted the study, published in the Christmas edition of the BMJ: “Please do not take excessive quantities of these refreshments.” And if we all know one thing, you do not get between Brits and their tea and biscuits. So the researchers behind the study drafted a survey and sent it around to nearly 2,000 British health care workers and asked what they considered to be excessive consumption of work-provided hot drinks and biscuits.
In the hot drinks department (tea and coffee, though we appreciate the two people who voiced a preference for free hot whiskey, if it was available) the survey participants decreed that 3.32 drinks was the maximum before consumption became excessive. That’s pretty close to the actual number of hot drinks respondents drank daily (3.04), so it’s pretty fair to say that British health care workers do a good job of self-limiting.
It’s much the same story with biscuits: Health care workers reported that consuming 2.25 packets of free biscuits would be excessive. Notably, doctors would take more than nondoctors (2.35 vs. 2.14 – typical doctor behavior), and those who had been in their role for less than 2 years would consume nearly 3 packets a day before calling it quits.
The study did not include an official cost analysis, but calculations conducted on a biscuit wrapper (that’s not a joke, by the way) estimated that the combined cost for providing every National Health Service employee with three free drinks and two free biscuit packages a day would be about 160 million pounds a year. Now, that’s a lot of money for tea and biscuits, but, they added, it’s a meager 0.1% of the NHS annual budget. They also noted that most employees consider free hot drinks a more valuable workplace perk than free support for mental health.
In conclusion, the authors wrote, “As a target for cost-saving initiatives, limiting free refreshment consumption is really scraping the biscuit barrel (although some limits on hot whiskey availability may be necessary), and implementing, or continuing, perks that improve staff morale seems justifiable. … Healthcare employers should allow biscuits and hot drinks to be freely available to staff, and they should leave these grateful recipients to judge for themselves what constitutes reasonable consumption.”
Now there’s a Christmas sentiment we can all get behind.
We come not to bury sugar, but to improve it
When we think about sugar, healthy isn’t the first thing that comes to mind. Research also shows that artificial sweeteners, as well as processed foods in general, are bad for your body and brain. People, however, love the stuff. That’s why one of the leading brands in processed foods, Kraft Heinz, partnered with the Wyss Institute for Biologically Inspired Engineering at Harvard to find a way to reduce consumers’ sugar consumption.
The question that Kraft Heinz presented to Wyss was this: How could it reduce the fructose in its products without losing the functionality of regular sugar.
The Wyss team’s approach seems pretty simple: Use a naturally occurring enzyme to convert sugar to fiber. The trick was to add the enzymes into the food so they could convert the sugar to fiber after being consumed. The enzymes also needed to be able to be added to existing food products without changing their existing recipes, Kraft Heinz insisted.
How does it work? The crafted enzyme is encapsulated to remain dormant in the food until exposed to an increased pH level, as is found in the GI tract between the stomach and the intestine. It reduces the amount of sugar absorbed in the bloodstream and creates a healthy prebiotic fiber, the institute explained.
This opens a whole new window for consumers. People with diabetes can enjoy their favorite cookies from time to time, while parents can feel less guilty about their children bathing their chicken nuggets in unholy amounts of ketchup.
New genes, or not new genes? That is the question
… and the police report that no capybaras were harmed in the incident. What a relief. Now Action News 8 brings you Carol Espinosa’s exclusive interview with legendary scientist and zombie, Charles Darwin.
Carol: Thanks, Daryl. Tell us, Prof. Darwin, what have you been up to lately?
Prof. Darwin: Please, Carol, call me Chuck. As always, I’ve got my hands full with the whole evolution thing. The big news right now is a study published in Cell Reports that offers evidence of the continuing evolution of humans. Can I eat your brain now?
Carol: No, Chuck, you may not. So people are still evolving? It sure seems like we’ve reverted to survival of the dumbest.
Chuck Darwin: Good one, Carol, but evolution hasn’t stopped. The investigators used a previously published dataset of functionally relevant new genes to create an ancestral tree comparing humans with other vertebrate species. By tracking the genes across evolution, they found 155 from regions of unique DNA that arose from scratch and not from duplication events in the existing genome. That’s a big deal.
Carol: Anything made from scratch is always better. Everyone knows that. What else can you tell us, Chuck?
Chuck Darwin: So these 155 genes didn’t exist when humans separated from chimpanzees nearly 7 million years ago. Turns out that 44 of them are associated with growth defects in cell cultures and three “have disease-associated DNA markers that point to connections with ailments such as muscular dystrophy, retinitis pigmentosa, and Alazami syndrome.” At least that’s what the investigators said in a written statement. I must say, Carol, that your brain is looking particularly delicious tonight.
Carol: Ironic. For years I’ve been hoping a man would appreciate me for my brain, and now I get this. Back to you, Daryl.
Ten recommendations for building and growing a cosmetic dermatology practice
SAN DIEGO – When Omar A. Ibrahimi, MD, PhD, opened his own cosmetic dermatology practice in Stamford, Conn., in 2012, he sensed that he had his work cut out for him.
“I was a fellowship-trained Mohs surgeon who wanted to do aesthetics,” Dr. Ibrahimi, medical director of the Connecticut Skin Institute, recalled during the annual Masters of Aesthetics Symposium. “I was in a geographic area that was new to me. I didn’t know any referring doctors, but I started to network and tried to grow my practice.”
Someone once told him that the “three As” of being a medical specialist are “Available, Affable, and Ability,” so he applied that principle as he began to cultivate relationships with physicians in his geographic area. “I told my referring doctors, ‘If you’re kind enough to send me Mohs cases, I’ll help you out if there’s something you don’t like doing, whether it’s a nail biopsy or treating male genital warts,’” he said. “You want to make it easy for doctors to refer to you, but you also want to make their lives easier.”
Dr. Ibrahimi, who is also on the board of directors for the American Society for Dermatologic Surgery and the American Society for Laser Medicine and Surgery, offered . They include:
Know yourself. Do what you love to do, not what you feel like you should do. “Whatever you’re doing in your practice, it should be something that you’re passionate about and excited about,” he said. “I do a mix of Mohs surgery and procedural aesthetic dermatology. Most of my practice is shaped toward energy-based devices and laser procedures. Pick the things that you enjoy doing and try to deliver good results.”
Know your patients. When dermatologists who plan to open their own practice ask Dr. Ibrahimi what kind of laser they should buy, he typically responds by asking them to consider what procedures their patients are asking for. “Depending on where you are geographically and the economic profile of the community in which you practice, it can be a different answer,” Dr. Ibrahimi said. “If you practice in the Northeast and do a lot of medical dermatology, it might mean getting a vascular laser to treat rosacea. If you’re in Southern California, treating pigment might be a bigger concern than treating rosacea.” The annual ASDS Survey on Dermatologic Procedures provides a snapshot of trends and can be useful for decision-making, he said.
Know your practice. “Make sure you are capable of entering the aesthetics field,” he advised. “You cannot have a practice that runs like the DMV, with people waiting 30 to 40 minutes to be seen.” Proper training of staff is also key and representatives from device and injectable companies can provide advice and support. As for marketing, some dermatologists hire a public relations agency, but Dr. Ibrahimi finds that the best source of his referrals is word of mouth. “If I do a good job taking care of patients, they will send their friends and family over to me, but social media is also important,” he said. Taking quality before-and-after photos, and obtaining consent from patients to use them online in educational posts is a good approach, he noted.
Know your market. When Dr. Ibrahimi first opened his practice, offering laser hair removal was not a priority because so many other dermatologists and medical spas in his area were already providing it. With time, though, he added laser hair removal to his menu of treatment offerings because “I knew that if my patients weren’t getting that service from me, they would be getting it from somewhere else,” he said. “Initially it wasn’t important for me, but as my practice matured, I wanted to make sure that I was comprehensive.”
Start cautiously. Think safety first. “I tell people that starting a cosmetic practice is like baseball: don’t try to hit home runs,” Dr. Ibrahimi said. “Just aim for base hits and keep your patients happy. Make sure you deliver safe, good results.” This means knowing everything possible about the devices used in the office, because if the use of a laser is delegated to a staff member and a problem arises, “you have to know everything about how that device works so that you can troubleshoot,” he said. “A lot of problems that arise are from lack of intimacy with your device.”
Seek knowledge. Attend courses in cosmetic dermatology and read literature from journals like Dermatologic Surgery and Lasers in Surgery and Medicine, he advised. “People will see the success, but they won’t know how much hard work it takes to get there,” he said. “You have to develop your reputation to develop the kind of practice that you want.”
Understand the business of aesthetics. Most energy devices carry a steep price tag, and leasing or financing devices come with a monthly payment, he said. “Make sure that what you’re bringing in on that device is going to be sufficient to cover the monthly payment. With something like tissue microcoring, you don’t have to use that five times a day to cover that lease payment. But if you have a vascular laser, you probably need to be treating more than a couple patients per day to make that lease payment. If you can recover the amount the device costs in about a year, that’s going to be a good investment. Many devices come with consumables, so you have to remember that.”
Don’t be afraid to be unique/change directions. Becoming an early adopter of new technologies and procedures can make someone stand out. “Other providers feel more comfortable waiting to allow more data to come out about a new technology before they make a purchase,” he said. “But if you’re established and have a busy practice, that’s an opportunity that can draw people in.”
Have patience and realistic expectations. It’s smart to offer a variety of services, he said, such as medical or surgical dermatology in addition to cosmetic dermatology. “That’s going to help you through any kind of economic downturn,” he said. “Success depends on a lot of factors going right. Make sure you set short- and long-term goals.”
Dr. Ibrahimi disclosed that he is a member of the Advisory Board for Accure Acne, AbbVie, Cutera, Lutronic, Blueberry Therapeutics, Cytrellis, and Quthero. He also holds stock in many device and pharmaceutical companies.
SAN DIEGO – When Omar A. Ibrahimi, MD, PhD, opened his own cosmetic dermatology practice in Stamford, Conn., in 2012, he sensed that he had his work cut out for him.
“I was a fellowship-trained Mohs surgeon who wanted to do aesthetics,” Dr. Ibrahimi, medical director of the Connecticut Skin Institute, recalled during the annual Masters of Aesthetics Symposium. “I was in a geographic area that was new to me. I didn’t know any referring doctors, but I started to network and tried to grow my practice.”
Someone once told him that the “three As” of being a medical specialist are “Available, Affable, and Ability,” so he applied that principle as he began to cultivate relationships with physicians in his geographic area. “I told my referring doctors, ‘If you’re kind enough to send me Mohs cases, I’ll help you out if there’s something you don’t like doing, whether it’s a nail biopsy or treating male genital warts,’” he said. “You want to make it easy for doctors to refer to you, but you also want to make their lives easier.”
Dr. Ibrahimi, who is also on the board of directors for the American Society for Dermatologic Surgery and the American Society for Laser Medicine and Surgery, offered . They include:
Know yourself. Do what you love to do, not what you feel like you should do. “Whatever you’re doing in your practice, it should be something that you’re passionate about and excited about,” he said. “I do a mix of Mohs surgery and procedural aesthetic dermatology. Most of my practice is shaped toward energy-based devices and laser procedures. Pick the things that you enjoy doing and try to deliver good results.”
Know your patients. When dermatologists who plan to open their own practice ask Dr. Ibrahimi what kind of laser they should buy, he typically responds by asking them to consider what procedures their patients are asking for. “Depending on where you are geographically and the economic profile of the community in which you practice, it can be a different answer,” Dr. Ibrahimi said. “If you practice in the Northeast and do a lot of medical dermatology, it might mean getting a vascular laser to treat rosacea. If you’re in Southern California, treating pigment might be a bigger concern than treating rosacea.” The annual ASDS Survey on Dermatologic Procedures provides a snapshot of trends and can be useful for decision-making, he said.
Know your practice. “Make sure you are capable of entering the aesthetics field,” he advised. “You cannot have a practice that runs like the DMV, with people waiting 30 to 40 minutes to be seen.” Proper training of staff is also key and representatives from device and injectable companies can provide advice and support. As for marketing, some dermatologists hire a public relations agency, but Dr. Ibrahimi finds that the best source of his referrals is word of mouth. “If I do a good job taking care of patients, they will send their friends and family over to me, but social media is also important,” he said. Taking quality before-and-after photos, and obtaining consent from patients to use them online in educational posts is a good approach, he noted.
Know your market. When Dr. Ibrahimi first opened his practice, offering laser hair removal was not a priority because so many other dermatologists and medical spas in his area were already providing it. With time, though, he added laser hair removal to his menu of treatment offerings because “I knew that if my patients weren’t getting that service from me, they would be getting it from somewhere else,” he said. “Initially it wasn’t important for me, but as my practice matured, I wanted to make sure that I was comprehensive.”
Start cautiously. Think safety first. “I tell people that starting a cosmetic practice is like baseball: don’t try to hit home runs,” Dr. Ibrahimi said. “Just aim for base hits and keep your patients happy. Make sure you deliver safe, good results.” This means knowing everything possible about the devices used in the office, because if the use of a laser is delegated to a staff member and a problem arises, “you have to know everything about how that device works so that you can troubleshoot,” he said. “A lot of problems that arise are from lack of intimacy with your device.”
Seek knowledge. Attend courses in cosmetic dermatology and read literature from journals like Dermatologic Surgery and Lasers in Surgery and Medicine, he advised. “People will see the success, but they won’t know how much hard work it takes to get there,” he said. “You have to develop your reputation to develop the kind of practice that you want.”
Understand the business of aesthetics. Most energy devices carry a steep price tag, and leasing or financing devices come with a monthly payment, he said. “Make sure that what you’re bringing in on that device is going to be sufficient to cover the monthly payment. With something like tissue microcoring, you don’t have to use that five times a day to cover that lease payment. But if you have a vascular laser, you probably need to be treating more than a couple patients per day to make that lease payment. If you can recover the amount the device costs in about a year, that’s going to be a good investment. Many devices come with consumables, so you have to remember that.”
Don’t be afraid to be unique/change directions. Becoming an early adopter of new technologies and procedures can make someone stand out. “Other providers feel more comfortable waiting to allow more data to come out about a new technology before they make a purchase,” he said. “But if you’re established and have a busy practice, that’s an opportunity that can draw people in.”
Have patience and realistic expectations. It’s smart to offer a variety of services, he said, such as medical or surgical dermatology in addition to cosmetic dermatology. “That’s going to help you through any kind of economic downturn,” he said. “Success depends on a lot of factors going right. Make sure you set short- and long-term goals.”
Dr. Ibrahimi disclosed that he is a member of the Advisory Board for Accure Acne, AbbVie, Cutera, Lutronic, Blueberry Therapeutics, Cytrellis, and Quthero. He also holds stock in many device and pharmaceutical companies.
SAN DIEGO – When Omar A. Ibrahimi, MD, PhD, opened his own cosmetic dermatology practice in Stamford, Conn., in 2012, he sensed that he had his work cut out for him.
“I was a fellowship-trained Mohs surgeon who wanted to do aesthetics,” Dr. Ibrahimi, medical director of the Connecticut Skin Institute, recalled during the annual Masters of Aesthetics Symposium. “I was in a geographic area that was new to me. I didn’t know any referring doctors, but I started to network and tried to grow my practice.”
Someone once told him that the “three As” of being a medical specialist are “Available, Affable, and Ability,” so he applied that principle as he began to cultivate relationships with physicians in his geographic area. “I told my referring doctors, ‘If you’re kind enough to send me Mohs cases, I’ll help you out if there’s something you don’t like doing, whether it’s a nail biopsy or treating male genital warts,’” he said. “You want to make it easy for doctors to refer to you, but you also want to make their lives easier.”
Dr. Ibrahimi, who is also on the board of directors for the American Society for Dermatologic Surgery and the American Society for Laser Medicine and Surgery, offered . They include:
Know yourself. Do what you love to do, not what you feel like you should do. “Whatever you’re doing in your practice, it should be something that you’re passionate about and excited about,” he said. “I do a mix of Mohs surgery and procedural aesthetic dermatology. Most of my practice is shaped toward energy-based devices and laser procedures. Pick the things that you enjoy doing and try to deliver good results.”
Know your patients. When dermatologists who plan to open their own practice ask Dr. Ibrahimi what kind of laser they should buy, he typically responds by asking them to consider what procedures their patients are asking for. “Depending on where you are geographically and the economic profile of the community in which you practice, it can be a different answer,” Dr. Ibrahimi said. “If you practice in the Northeast and do a lot of medical dermatology, it might mean getting a vascular laser to treat rosacea. If you’re in Southern California, treating pigment might be a bigger concern than treating rosacea.” The annual ASDS Survey on Dermatologic Procedures provides a snapshot of trends and can be useful for decision-making, he said.
Know your practice. “Make sure you are capable of entering the aesthetics field,” he advised. “You cannot have a practice that runs like the DMV, with people waiting 30 to 40 minutes to be seen.” Proper training of staff is also key and representatives from device and injectable companies can provide advice and support. As for marketing, some dermatologists hire a public relations agency, but Dr. Ibrahimi finds that the best source of his referrals is word of mouth. “If I do a good job taking care of patients, they will send their friends and family over to me, but social media is also important,” he said. Taking quality before-and-after photos, and obtaining consent from patients to use them online in educational posts is a good approach, he noted.
Know your market. When Dr. Ibrahimi first opened his practice, offering laser hair removal was not a priority because so many other dermatologists and medical spas in his area were already providing it. With time, though, he added laser hair removal to his menu of treatment offerings because “I knew that if my patients weren’t getting that service from me, they would be getting it from somewhere else,” he said. “Initially it wasn’t important for me, but as my practice matured, I wanted to make sure that I was comprehensive.”
Start cautiously. Think safety first. “I tell people that starting a cosmetic practice is like baseball: don’t try to hit home runs,” Dr. Ibrahimi said. “Just aim for base hits and keep your patients happy. Make sure you deliver safe, good results.” This means knowing everything possible about the devices used in the office, because if the use of a laser is delegated to a staff member and a problem arises, “you have to know everything about how that device works so that you can troubleshoot,” he said. “A lot of problems that arise are from lack of intimacy with your device.”
Seek knowledge. Attend courses in cosmetic dermatology and read literature from journals like Dermatologic Surgery and Lasers in Surgery and Medicine, he advised. “People will see the success, but they won’t know how much hard work it takes to get there,” he said. “You have to develop your reputation to develop the kind of practice that you want.”
Understand the business of aesthetics. Most energy devices carry a steep price tag, and leasing or financing devices come with a monthly payment, he said. “Make sure that what you’re bringing in on that device is going to be sufficient to cover the monthly payment. With something like tissue microcoring, you don’t have to use that five times a day to cover that lease payment. But if you have a vascular laser, you probably need to be treating more than a couple patients per day to make that lease payment. If you can recover the amount the device costs in about a year, that’s going to be a good investment. Many devices come with consumables, so you have to remember that.”
Don’t be afraid to be unique/change directions. Becoming an early adopter of new technologies and procedures can make someone stand out. “Other providers feel more comfortable waiting to allow more data to come out about a new technology before they make a purchase,” he said. “But if you’re established and have a busy practice, that’s an opportunity that can draw people in.”
Have patience and realistic expectations. It’s smart to offer a variety of services, he said, such as medical or surgical dermatology in addition to cosmetic dermatology. “That’s going to help you through any kind of economic downturn,” he said. “Success depends on a lot of factors going right. Make sure you set short- and long-term goals.”
Dr. Ibrahimi disclosed that he is a member of the Advisory Board for Accure Acne, AbbVie, Cutera, Lutronic, Blueberry Therapeutics, Cytrellis, and Quthero. He also holds stock in many device and pharmaceutical companies.
AT MOAS 2022
For optimal results, fractional RF microneedling requires multiple treatments
SAN DIEGO – , according to Catherine M. DiGiorgio, MD.
Most core fractional RF microneedling indications – acne scars, rhytides, skin tightening – require multiple treatments, Dr. DiGiorgio, a laser and cosmetic dermatologist who practices in Boston, said at the annual Masters of Aesthetics Symposium. “That’s an important expectation to set for your patients,” she said. “You also want to select depth and density parameters based on pathophysiology of the condition being treated, and combination treatments always provide the best results. So, whether you’re treating someone for acne scars or rhytides, you want to treat them for their erythema or their dermatoheliosis. The same goes for skin tightening procedures.”
Many nonpolar and bipolar devices are available for use, most of which feature adjustable depths and energies. Tips can be insulated or noninsulated. Generally, the insulated tips are safer for darker skin types because the energy is not delivered to the epidermis. However, the Sylfirm X device from Benev has a noninsulated tip but is safe for all skin types because the energy is delivered from the tip of a conically shaped needle and moves proximally but never reaches the epidermis, said Dr. DiGiorgio. Continuous wave mode is used for tightening and wrinkles while pulsed mode is used for pigment and vascular lesions.
Treatment with most fractional RF microneedling devices is painful so topical anesthesia is required. Dr. DiGiorgio typically uses topical 23% lidocaine and 7% tetracaine. The downtime varies depending on which device is being used. For anesthesia prior to aggressive fractional microneedle RF treatments such as with the Profound RF for skin tightening, Dr. DiGiorgio typically uses a Mesoram needle with a cocktail of 30 ccs of 2% lidocaine with epinephrine, 15 ccs of bicarbonate, and 5 ccs of saline. “More aggressive RF procedures can result in bruising for 7 to 8 days,” she said. “It can be covered with makeup. Wearing masks during the COVID-19 pandemic have also helped patients cover the bruising.”
In her clinical experience, the ideal patient for skin tightening with fractional RF microneedling has mild to moderate skin laxity that does not require surgical intervention. “Nonsurgical treatments provide nonsurgical results,” she said. “If a patient comes in holding their skin back and there is a lot of laxity, this is not going to be the right treatment for that person.”
Dr. DiGiorgio offers fractional RF microneedling in the context of a full-face rejuvenation. She begins by addressing volume loss and dynamic rhytides with injectables prior to skin tightening devices such as fractional RF microneedling or ultrasound-based tightening devices such as Sofwave or Ulthera (also referred to as Ultherapy). “You can add an ablative fractional to target deeper rhytides or pigment-targeting laser to address their dermatoheliosis, which will enhance their results,” she said. “Finally, you can follow up with a thread lift two weeks after the microneedle RF to achieve greater skin tightening. If the thread lift is performed before the microneedle RF, you want to wait about 2 months because the microneedle RF can damage the thread.”
Despite the limited efficacy for tissue tightening with fractional RF microneedling, “it’s a good alternative to lasers, especially for darker skin types,” she said. “Combination treatments will always enhance your results.”
Dr. DiGiorgio disclosed that she is a member of the advisory board for Quthero. She is also a consultant for Revelle and has received equipment from Acclaro.
SAN DIEGO – , according to Catherine M. DiGiorgio, MD.
Most core fractional RF microneedling indications – acne scars, rhytides, skin tightening – require multiple treatments, Dr. DiGiorgio, a laser and cosmetic dermatologist who practices in Boston, said at the annual Masters of Aesthetics Symposium. “That’s an important expectation to set for your patients,” she said. “You also want to select depth and density parameters based on pathophysiology of the condition being treated, and combination treatments always provide the best results. So, whether you’re treating someone for acne scars or rhytides, you want to treat them for their erythema or their dermatoheliosis. The same goes for skin tightening procedures.”
Many nonpolar and bipolar devices are available for use, most of which feature adjustable depths and energies. Tips can be insulated or noninsulated. Generally, the insulated tips are safer for darker skin types because the energy is not delivered to the epidermis. However, the Sylfirm X device from Benev has a noninsulated tip but is safe for all skin types because the energy is delivered from the tip of a conically shaped needle and moves proximally but never reaches the epidermis, said Dr. DiGiorgio. Continuous wave mode is used for tightening and wrinkles while pulsed mode is used for pigment and vascular lesions.
Treatment with most fractional RF microneedling devices is painful so topical anesthesia is required. Dr. DiGiorgio typically uses topical 23% lidocaine and 7% tetracaine. The downtime varies depending on which device is being used. For anesthesia prior to aggressive fractional microneedle RF treatments such as with the Profound RF for skin tightening, Dr. DiGiorgio typically uses a Mesoram needle with a cocktail of 30 ccs of 2% lidocaine with epinephrine, 15 ccs of bicarbonate, and 5 ccs of saline. “More aggressive RF procedures can result in bruising for 7 to 8 days,” she said. “It can be covered with makeup. Wearing masks during the COVID-19 pandemic have also helped patients cover the bruising.”
In her clinical experience, the ideal patient for skin tightening with fractional RF microneedling has mild to moderate skin laxity that does not require surgical intervention. “Nonsurgical treatments provide nonsurgical results,” she said. “If a patient comes in holding their skin back and there is a lot of laxity, this is not going to be the right treatment for that person.”
Dr. DiGiorgio offers fractional RF microneedling in the context of a full-face rejuvenation. She begins by addressing volume loss and dynamic rhytides with injectables prior to skin tightening devices such as fractional RF microneedling or ultrasound-based tightening devices such as Sofwave or Ulthera (also referred to as Ultherapy). “You can add an ablative fractional to target deeper rhytides or pigment-targeting laser to address their dermatoheliosis, which will enhance their results,” she said. “Finally, you can follow up with a thread lift two weeks after the microneedle RF to achieve greater skin tightening. If the thread lift is performed before the microneedle RF, you want to wait about 2 months because the microneedle RF can damage the thread.”
Despite the limited efficacy for tissue tightening with fractional RF microneedling, “it’s a good alternative to lasers, especially for darker skin types,” she said. “Combination treatments will always enhance your results.”
Dr. DiGiorgio disclosed that she is a member of the advisory board for Quthero. She is also a consultant for Revelle and has received equipment from Acclaro.
SAN DIEGO – , according to Catherine M. DiGiorgio, MD.
Most core fractional RF microneedling indications – acne scars, rhytides, skin tightening – require multiple treatments, Dr. DiGiorgio, a laser and cosmetic dermatologist who practices in Boston, said at the annual Masters of Aesthetics Symposium. “That’s an important expectation to set for your patients,” she said. “You also want to select depth and density parameters based on pathophysiology of the condition being treated, and combination treatments always provide the best results. So, whether you’re treating someone for acne scars or rhytides, you want to treat them for their erythema or their dermatoheliosis. The same goes for skin tightening procedures.”
Many nonpolar and bipolar devices are available for use, most of which feature adjustable depths and energies. Tips can be insulated or noninsulated. Generally, the insulated tips are safer for darker skin types because the energy is not delivered to the epidermis. However, the Sylfirm X device from Benev has a noninsulated tip but is safe for all skin types because the energy is delivered from the tip of a conically shaped needle and moves proximally but never reaches the epidermis, said Dr. DiGiorgio. Continuous wave mode is used for tightening and wrinkles while pulsed mode is used for pigment and vascular lesions.
Treatment with most fractional RF microneedling devices is painful so topical anesthesia is required. Dr. DiGiorgio typically uses topical 23% lidocaine and 7% tetracaine. The downtime varies depending on which device is being used. For anesthesia prior to aggressive fractional microneedle RF treatments such as with the Profound RF for skin tightening, Dr. DiGiorgio typically uses a Mesoram needle with a cocktail of 30 ccs of 2% lidocaine with epinephrine, 15 ccs of bicarbonate, and 5 ccs of saline. “More aggressive RF procedures can result in bruising for 7 to 8 days,” she said. “It can be covered with makeup. Wearing masks during the COVID-19 pandemic have also helped patients cover the bruising.”
In her clinical experience, the ideal patient for skin tightening with fractional RF microneedling has mild to moderate skin laxity that does not require surgical intervention. “Nonsurgical treatments provide nonsurgical results,” she said. “If a patient comes in holding their skin back and there is a lot of laxity, this is not going to be the right treatment for that person.”
Dr. DiGiorgio offers fractional RF microneedling in the context of a full-face rejuvenation. She begins by addressing volume loss and dynamic rhytides with injectables prior to skin tightening devices such as fractional RF microneedling or ultrasound-based tightening devices such as Sofwave or Ulthera (also referred to as Ultherapy). “You can add an ablative fractional to target deeper rhytides or pigment-targeting laser to address their dermatoheliosis, which will enhance their results,” she said. “Finally, you can follow up with a thread lift two weeks after the microneedle RF to achieve greater skin tightening. If the thread lift is performed before the microneedle RF, you want to wait about 2 months because the microneedle RF can damage the thread.”
Despite the limited efficacy for tissue tightening with fractional RF microneedling, “it’s a good alternative to lasers, especially for darker skin types,” she said. “Combination treatments will always enhance your results.”
Dr. DiGiorgio disclosed that she is a member of the advisory board for Quthero. She is also a consultant for Revelle and has received equipment from Acclaro.
AT MOAS 2022
Violaceous-Purpuric Targetoid Macules and Patches With Bullae and Ulceration
The Diagnosis: Sweet Syndrome (Acute Febrile Neutrophilic Dermatosis)
A skin biopsy of the right lower extremity demonstrated diffuse interstitial, perivascular, and periadnexal neutrophilic dermal infiltrate in the reticular dermis (Figure 1), consistent with a diagnosis of Sweet syndrome without evidence of leukemia cutis or infection. The firm erythematous papulonodules with follicular accentuation on the face (Figure 2) also were confirmed as Sweet syndrome on histopathology. Concern for leukemic transformation was confirmed with bone biopsy revealing acute myeloid leukemia (AML). Our patient began a short course of prednisone, and the cutaneous lesions improved during hospitalization; however, he was lost to follow-up.
Sweet syndrome (also known as acute febrile neutrophilic dermatosis) is a rare inflammatory skin condition typically characterized by asymmetric, painful, erythematous to violaceous papules, plaques, or nodules involving the arms, face, and neck.1 It most commonly occurs in women and typically presents in patients aged 47 to 57 years. Although the pathogenesis of neutrophilic dermatoses is not completely understood, they are believed to be due to altered expression of inflammatory cytokines, irregular neutrophil function, and a genetic predisposition.2 There are 3 main categories of Sweet syndrome: classical (or idiopathic), drug induced, and malignancy associated.1 The lesions associated with Sweet syndrome vary from a few millimeters to several centimeters and may be annular or targetoid in the later stages. They also may form bullae and ulcerate. Fever, leukocytosis, and elevated acute-phase reactants also are common on presentation.1 Histopathologic analysis demonstrates an intense neutrophilic infiltrate within the reticular dermis with marked leukocytoclasia. Admixed within the neutrophil polymorphs are variable numbers of lymphocytes and histiocytes. Edema in the upper dermis also is characteristic.3 The exact pathogenesis of Sweet syndrome has yet to be elucidated but may involve a combination of cytokine dysregulation, hypersensitivity reactions, and genetics.4 Our case demonstrates 3 distinct morphologies of Sweet syndrome in a single patient, including classic edematous plaques, agminated targetoid plaques, and ulceration. Based on the clinical presentation, diagnostic workup for an undiagnosed malignancy was warranted, which confirmed AML. The malignancy-associated form of Sweet syndrome accounts for a substantial portion of cases, with approximately 21% of patients diagnosed with Sweet syndrome having an underlying malignancy, commonly a hematologic malignancy or myeloproliferative disorder with AML being the most common.1
The differential diagnosis for Sweet syndrome includes cutaneous small vessel vasculitis, which commonly presents with symmetric palpable purpura of the legs. Lesions may be round, port wine–colored plaques and even may form ulcers, vesicles, and targetoid lesions. However, skin biopsy shows polymorphonuclear infiltrate affecting postcapillary venules, fibrinoid deposits, and extravasation of red blood cells.5 Leukemia cutis describes any type of leukemia that manifests in the skin. It typically presents as violaceous or red-brown papules, nodules, and plaques most commonly on the legs. Histopathology varies by immunophenotype but generally demonstrates perivascular or periadnexal involvement or a diffuse, interstitial, or nodular infiltrate of the dermis or subcutis.6 Neutrophilic eccrine hidradenitis describes an aseptic neutrophilic infiltration around eccrine coils and glands. It may present as papules or plaques that usually are erythematous but also may be pigmented. Lesions can be asymptomatic or painful as in Sweet syndrome and are distributed proximally or on the distal extremities. Histopathologic examination demonstrates the degeneration of the eccrine gland and neutrophilic inflammatory infiltrates.7 Lastly, necrotizing fasciitis is a life-threatening infection of the deep soft tissue and fascia, classically caused by group A Streptococcus. The infected site may have erythema, tenderness, fluctuance, necrosis, and bullae.8 Although our patient had a fever, he did not display the tachycardia, hypotension, tachypnea, and rapid deterioration that is common in necrotizing fasciitis.
Sweet syndrome may present with various morphologies within the same patient. Painful, erythematous to violaceous papules, plaques, nodules, bullae, and ulcers may be seen. A workup for an underlying malignancy may be warranted based on clinical presentation. Most patients have a rapid and dramatic response to systemic corticosteroids.
- Cohen PR. Sweet’s syndrome—a comprehensive review of an acute febrile neutrophilic dermatosis. Orphanet J Rare Dis. 2007;2:34. doi:10.1186/1750-1172-2-34
- Nelson CA, Stephen S, Ashchyan HJ, et al. Neutrophilic dermatoses: pathogenesis, Sweet syndrome, neutrophilic eccrine hidradenitis, and Behçet disease. J Am Acad Dermatol. 2018;79:987-1006. doi:10.1016/J .JAAD.2017.11.064
- Pulido-Pérez A, Bergon-Sendin M, Sacks CA. Images in clinical medicine. N Engl J Med. 2020;16:382. doi:10.1056/NEJMicm1911025
- Marzano AV, Hilbrands L, Le ST, et al. Insights into the pathogenesis of Sweet’s syndrome. Front Immunol. 2019;10:414. doi:10.3389/fimmu.2019.00414
- Goeser MR, Laniosz V, Wetter DA. A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis. Am J Clin Dermatol. 2014;15:299-306. doi:10.1007/s40257-014-0076-6
- Hee Cho-Vega J, Jeffrey Medeiros L, Prieto VG, et al. Leukemia cutis. Am J Clin Pathol. 2008;129:130-142. doi:10.1309/WYAC YWF6NGM3WBRT
- Bachmeyer C, Aractingi S. Neutrophilic eccrine hidradenitis. Clin Dermatol. 2000;18:319-330. doi:10.1016/S0738-081X(99)00123-6
- Shimizu T, Tokuda Y. Necrotizing fasciitis. Intern Med. 2010; 49:1051-1057. doi:10.2169/internalmedicine.49.2964
The Diagnosis: Sweet Syndrome (Acute Febrile Neutrophilic Dermatosis)
A skin biopsy of the right lower extremity demonstrated diffuse interstitial, perivascular, and periadnexal neutrophilic dermal infiltrate in the reticular dermis (Figure 1), consistent with a diagnosis of Sweet syndrome without evidence of leukemia cutis or infection. The firm erythematous papulonodules with follicular accentuation on the face (Figure 2) also were confirmed as Sweet syndrome on histopathology. Concern for leukemic transformation was confirmed with bone biopsy revealing acute myeloid leukemia (AML). Our patient began a short course of prednisone, and the cutaneous lesions improved during hospitalization; however, he was lost to follow-up.
Sweet syndrome (also known as acute febrile neutrophilic dermatosis) is a rare inflammatory skin condition typically characterized by asymmetric, painful, erythematous to violaceous papules, plaques, or nodules involving the arms, face, and neck.1 It most commonly occurs in women and typically presents in patients aged 47 to 57 years. Although the pathogenesis of neutrophilic dermatoses is not completely understood, they are believed to be due to altered expression of inflammatory cytokines, irregular neutrophil function, and a genetic predisposition.2 There are 3 main categories of Sweet syndrome: classical (or idiopathic), drug induced, and malignancy associated.1 The lesions associated with Sweet syndrome vary from a few millimeters to several centimeters and may be annular or targetoid in the later stages. They also may form bullae and ulcerate. Fever, leukocytosis, and elevated acute-phase reactants also are common on presentation.1 Histopathologic analysis demonstrates an intense neutrophilic infiltrate within the reticular dermis with marked leukocytoclasia. Admixed within the neutrophil polymorphs are variable numbers of lymphocytes and histiocytes. Edema in the upper dermis also is characteristic.3 The exact pathogenesis of Sweet syndrome has yet to be elucidated but may involve a combination of cytokine dysregulation, hypersensitivity reactions, and genetics.4 Our case demonstrates 3 distinct morphologies of Sweet syndrome in a single patient, including classic edematous plaques, agminated targetoid plaques, and ulceration. Based on the clinical presentation, diagnostic workup for an undiagnosed malignancy was warranted, which confirmed AML. The malignancy-associated form of Sweet syndrome accounts for a substantial portion of cases, with approximately 21% of patients diagnosed with Sweet syndrome having an underlying malignancy, commonly a hematologic malignancy or myeloproliferative disorder with AML being the most common.1
The differential diagnosis for Sweet syndrome includes cutaneous small vessel vasculitis, which commonly presents with symmetric palpable purpura of the legs. Lesions may be round, port wine–colored plaques and even may form ulcers, vesicles, and targetoid lesions. However, skin biopsy shows polymorphonuclear infiltrate affecting postcapillary venules, fibrinoid deposits, and extravasation of red blood cells.5 Leukemia cutis describes any type of leukemia that manifests in the skin. It typically presents as violaceous or red-brown papules, nodules, and plaques most commonly on the legs. Histopathology varies by immunophenotype but generally demonstrates perivascular or periadnexal involvement or a diffuse, interstitial, or nodular infiltrate of the dermis or subcutis.6 Neutrophilic eccrine hidradenitis describes an aseptic neutrophilic infiltration around eccrine coils and glands. It may present as papules or plaques that usually are erythematous but also may be pigmented. Lesions can be asymptomatic or painful as in Sweet syndrome and are distributed proximally or on the distal extremities. Histopathologic examination demonstrates the degeneration of the eccrine gland and neutrophilic inflammatory infiltrates.7 Lastly, necrotizing fasciitis is a life-threatening infection of the deep soft tissue and fascia, classically caused by group A Streptococcus. The infected site may have erythema, tenderness, fluctuance, necrosis, and bullae.8 Although our patient had a fever, he did not display the tachycardia, hypotension, tachypnea, and rapid deterioration that is common in necrotizing fasciitis.
Sweet syndrome may present with various morphologies within the same patient. Painful, erythematous to violaceous papules, plaques, nodules, bullae, and ulcers may be seen. A workup for an underlying malignancy may be warranted based on clinical presentation. Most patients have a rapid and dramatic response to systemic corticosteroids.
The Diagnosis: Sweet Syndrome (Acute Febrile Neutrophilic Dermatosis)
A skin biopsy of the right lower extremity demonstrated diffuse interstitial, perivascular, and periadnexal neutrophilic dermal infiltrate in the reticular dermis (Figure 1), consistent with a diagnosis of Sweet syndrome without evidence of leukemia cutis or infection. The firm erythematous papulonodules with follicular accentuation on the face (Figure 2) also were confirmed as Sweet syndrome on histopathology. Concern for leukemic transformation was confirmed with bone biopsy revealing acute myeloid leukemia (AML). Our patient began a short course of prednisone, and the cutaneous lesions improved during hospitalization; however, he was lost to follow-up.
Sweet syndrome (also known as acute febrile neutrophilic dermatosis) is a rare inflammatory skin condition typically characterized by asymmetric, painful, erythematous to violaceous papules, plaques, or nodules involving the arms, face, and neck.1 It most commonly occurs in women and typically presents in patients aged 47 to 57 years. Although the pathogenesis of neutrophilic dermatoses is not completely understood, they are believed to be due to altered expression of inflammatory cytokines, irregular neutrophil function, and a genetic predisposition.2 There are 3 main categories of Sweet syndrome: classical (or idiopathic), drug induced, and malignancy associated.1 The lesions associated with Sweet syndrome vary from a few millimeters to several centimeters and may be annular or targetoid in the later stages. They also may form bullae and ulcerate. Fever, leukocytosis, and elevated acute-phase reactants also are common on presentation.1 Histopathologic analysis demonstrates an intense neutrophilic infiltrate within the reticular dermis with marked leukocytoclasia. Admixed within the neutrophil polymorphs are variable numbers of lymphocytes and histiocytes. Edema in the upper dermis also is characteristic.3 The exact pathogenesis of Sweet syndrome has yet to be elucidated but may involve a combination of cytokine dysregulation, hypersensitivity reactions, and genetics.4 Our case demonstrates 3 distinct morphologies of Sweet syndrome in a single patient, including classic edematous plaques, agminated targetoid plaques, and ulceration. Based on the clinical presentation, diagnostic workup for an undiagnosed malignancy was warranted, which confirmed AML. The malignancy-associated form of Sweet syndrome accounts for a substantial portion of cases, with approximately 21% of patients diagnosed with Sweet syndrome having an underlying malignancy, commonly a hematologic malignancy or myeloproliferative disorder with AML being the most common.1
The differential diagnosis for Sweet syndrome includes cutaneous small vessel vasculitis, which commonly presents with symmetric palpable purpura of the legs. Lesions may be round, port wine–colored plaques and even may form ulcers, vesicles, and targetoid lesions. However, skin biopsy shows polymorphonuclear infiltrate affecting postcapillary venules, fibrinoid deposits, and extravasation of red blood cells.5 Leukemia cutis describes any type of leukemia that manifests in the skin. It typically presents as violaceous or red-brown papules, nodules, and plaques most commonly on the legs. Histopathology varies by immunophenotype but generally demonstrates perivascular or periadnexal involvement or a diffuse, interstitial, or nodular infiltrate of the dermis or subcutis.6 Neutrophilic eccrine hidradenitis describes an aseptic neutrophilic infiltration around eccrine coils and glands. It may present as papules or plaques that usually are erythematous but also may be pigmented. Lesions can be asymptomatic or painful as in Sweet syndrome and are distributed proximally or on the distal extremities. Histopathologic examination demonstrates the degeneration of the eccrine gland and neutrophilic inflammatory infiltrates.7 Lastly, necrotizing fasciitis is a life-threatening infection of the deep soft tissue and fascia, classically caused by group A Streptococcus. The infected site may have erythema, tenderness, fluctuance, necrosis, and bullae.8 Although our patient had a fever, he did not display the tachycardia, hypotension, tachypnea, and rapid deterioration that is common in necrotizing fasciitis.
Sweet syndrome may present with various morphologies within the same patient. Painful, erythematous to violaceous papules, plaques, nodules, bullae, and ulcers may be seen. A workup for an underlying malignancy may be warranted based on clinical presentation. Most patients have a rapid and dramatic response to systemic corticosteroids.
- Cohen PR. Sweet’s syndrome—a comprehensive review of an acute febrile neutrophilic dermatosis. Orphanet J Rare Dis. 2007;2:34. doi:10.1186/1750-1172-2-34
- Nelson CA, Stephen S, Ashchyan HJ, et al. Neutrophilic dermatoses: pathogenesis, Sweet syndrome, neutrophilic eccrine hidradenitis, and Behçet disease. J Am Acad Dermatol. 2018;79:987-1006. doi:10.1016/J .JAAD.2017.11.064
- Pulido-Pérez A, Bergon-Sendin M, Sacks CA. Images in clinical medicine. N Engl J Med. 2020;16:382. doi:10.1056/NEJMicm1911025
- Marzano AV, Hilbrands L, Le ST, et al. Insights into the pathogenesis of Sweet’s syndrome. Front Immunol. 2019;10:414. doi:10.3389/fimmu.2019.00414
- Goeser MR, Laniosz V, Wetter DA. A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis. Am J Clin Dermatol. 2014;15:299-306. doi:10.1007/s40257-014-0076-6
- Hee Cho-Vega J, Jeffrey Medeiros L, Prieto VG, et al. Leukemia cutis. Am J Clin Pathol. 2008;129:130-142. doi:10.1309/WYAC YWF6NGM3WBRT
- Bachmeyer C, Aractingi S. Neutrophilic eccrine hidradenitis. Clin Dermatol. 2000;18:319-330. doi:10.1016/S0738-081X(99)00123-6
- Shimizu T, Tokuda Y. Necrotizing fasciitis. Intern Med. 2010; 49:1051-1057. doi:10.2169/internalmedicine.49.2964
- Cohen PR. Sweet’s syndrome—a comprehensive review of an acute febrile neutrophilic dermatosis. Orphanet J Rare Dis. 2007;2:34. doi:10.1186/1750-1172-2-34
- Nelson CA, Stephen S, Ashchyan HJ, et al. Neutrophilic dermatoses: pathogenesis, Sweet syndrome, neutrophilic eccrine hidradenitis, and Behçet disease. J Am Acad Dermatol. 2018;79:987-1006. doi:10.1016/J .JAAD.2017.11.064
- Pulido-Pérez A, Bergon-Sendin M, Sacks CA. Images in clinical medicine. N Engl J Med. 2020;16:382. doi:10.1056/NEJMicm1911025
- Marzano AV, Hilbrands L, Le ST, et al. Insights into the pathogenesis of Sweet’s syndrome. Front Immunol. 2019;10:414. doi:10.3389/fimmu.2019.00414
- Goeser MR, Laniosz V, Wetter DA. A practical approach to the diagnosis, evaluation, and management of cutaneous small-vessel vasculitis. Am J Clin Dermatol. 2014;15:299-306. doi:10.1007/s40257-014-0076-6
- Hee Cho-Vega J, Jeffrey Medeiros L, Prieto VG, et al. Leukemia cutis. Am J Clin Pathol. 2008;129:130-142. doi:10.1309/WYAC YWF6NGM3WBRT
- Bachmeyer C, Aractingi S. Neutrophilic eccrine hidradenitis. Clin Dermatol. 2000;18:319-330. doi:10.1016/S0738-081X(99)00123-6
- Shimizu T, Tokuda Y. Necrotizing fasciitis. Intern Med. 2010; 49:1051-1057. doi:10.2169/internalmedicine.49.2964
A 64-year-old man with long-standing myelofibrosis presented with neutropenic fevers as well as progressive painful lesions of 3 days’ duration on the legs. A bone marrow biopsy during this hospitalization demonstrated a recent progression of the patient’s myelofibrosis to acute myeloid leukemia. Physical examination revealed round to oval, violaceous, targetoid plaques. Within a week, new erythematous and nodular lesions appeared on the right arm and left vermilion border. The lesions on the legs enlarged, formed bullae, and ulcerated.
Juvenile Dermatomyositis–Associated Panniculitis
To the Editor:
Juvenile dermatomyositis (JDM) is an autoimmune disorder with childhood onset that predominantly affects the muscles and skin, among other organs. Since the recognition of dermatomyositis (DM) more than 100 years ago, a variety of clinical diagnostic criteria have been utilized. Classically, DM presents with muscle weakness and a pathognomonic cutaneous macular, violaceous, erythematous eruption. The juvenile variant is defined by onset prior to 16 years of age. Histologically, these entities are indistinguishable and demonstrate an interface dermatitis with epidermal atrophy. Clinically, JDM has a higher incidence of calcinosis cutis and is not associated with an increased risk for malignancy in contrast to the adult-onset variant.1 Panniculitis is a rare but serious complication in a subset of patients with DM and may represent a precursor to calcinosis cutis.2 We describe a case of JDM-associated panniculitis that was difficult to control with prednisone and rituximab.
A 21-year-old woman with fever, fatigue, muscle pain, and new-onset swelling of 2 weeks’ duration was admitted to the hospital. She had a 5-year history of intermittent muscle weakness and concomitant rash. Prior to presentation, she had been hospitalized twice for fever of unknown origin, and the source remained undetermined. Physical examination revealed prominent facial and periorbital edema. There was tender nonpitting edema present on all 4 extremities and hyperpigmented indurated nodules on the shins (Figure 1). A full laboratory and imaging workup was performed for autoantibodies and infectious etiologies. The complete blood cell count was notable for pancytopenia, and a thorough infectious workup was negative. Creatine kinase level was within reference range. A biopsy of the right shin was performed, and histopathology revealed a lobular panniculitis with fat necrosis and mixed inflammation with neutrophils with perieccrine involvement as well as an interface dermatitis (Figure 2). Periodic acid–Schiff, Grocott methenamine-silver, and Gram stains were negative. Myositis-specific antibody testing revealed anti-p155/140 autoantibodies, and magnetic resonance imaging did not reveal active myositis within the visualized muscles, consistent with stable nonprogressing DM. A diagnosis of JDM with panniculitis was made. The patient was started on oral prednisone. Subsequently, a trial of rituximab was initiated. Although the patient’s symptoms initially improved, the response was not sustained on rituximab, and the patient was continued on systemic steroids with initiation of cyclosporine.
Juvenile dermatomyositis is an autoimmune disorder with childhood onset that involves systemic inflammation of the muscles, skin, and internal organs. It often can present diagnostic and therapeutic challenges.2,3 Bohan and Peter4,5 clinical criteria may help identify potential patients with JDM, but magnetic resonance imaging, electromyography, and muscle biopsy often are required to confirm the diagnosis.6 Skin manifestations include heliotrope rash; V sign; shawl sign; Gottron papules; periorbital edema; and infrequently panniculitis, the subcutaneous inflammation of adipose tissue.3,7
Although panniculitis is found in approximately 10% of skin biopsies in patients with DM, our patient presented with anti-p155/140 antibodies.8-10 Fat involvement in these patients traditionally manifests as lipodystrophy. Panniculitis also may precede calcinosis cutis, a debilitating skin change that may occur in approximately 46% of patients with JDM and can cause severe morbidity.2,6,9
Subcutaneous edema rarely is described in DM-panniculitis, present in only 6% of 86 DM patients in one study.7 The pathophysiology of DM may be due to antibodies that target endothelial cells and activate complement, resulting in the membranolytic attack complex. This leads to microischemia, and microinfarction of the muscle fibers has been suggested to result in edema of the subcutaneous tissue in severe cases.7,11 Microinfarction has been found to be present 2.3 times more often in edematous DM compared with nonedematous DM.7 Subcutaneous edema may be an isolated presentation of DM that arises more quickly with severe disease activity. As such, recommendations have been made to consider edema in future classification schemes.7
Because of the severity of edematous and/or subcutaneous DM, aggressive therapy may be required. First-line therapy consists of corticosteroids with additional immunosuppressants and immunomodulatory agents if adequate response is not achieved.3,12 The effectiveness of rituximab in DM has been suggested.2,12,13 The Rituximab in Myositis (RIM) trial (N=200) was the first double-blind, placebo-controlled, phase 3 clinical trial to assess rituximab’s efficacy in refractory compared with early-onset inflammatory myopathies. Although outcomes were similar in both groups, 83% of patients overall, including the JDM subset, met the definition of improvement.12 In re-examining the RIM trial data and other cases using rituximab to treat inflammatory myopathies, an overall response rate of 78.3% was observed, with 52.1% of patients with DM reporting improvement in skin lesions (N=458, pooled from 48 studies).13 Further analysis of the RIM data revealed that panniculitis affected 10.4% of patients with JDM at baseline, which decreased to 6.8% at 36 weeks of rituximab therapy (N=48).12
As exhibited in our patient, subcutaneous tissue involvement, including calcinosis cutis and panniculitis, is seen more often in JDM than adult DM.2,6 However, panniculitis in anti-p155/140 patients is rare. Our patient also had antibody positivity, which likely predisposed her to a more severe course. Despite not having sustained improvement on rituximab, initiating aggressive therapy earlier in the disease course may be beneficial, and our patient continues with alternative therapies.
- Jorizzo JL, Vleugels RA. Dermatomyositis. In: Bolognia J, Schaffer J, Cerroni L. Dermatology. 4th ed. Elsevier; 2019:681-687.
- Aggarwal R, Loganathan P, Koontz D, et al. Cutaneous improvement in refractory adult and juvenile dermatomyositis after treatment with rituximab. Rheumatology. 2016;56:247-254.
- Santos-Briz A, Calle A, Linos K, et al. Dermatomyositis panniculitis: a clinicopathological and immunohistochemical study of 18 cases. J Eur Acad Dermatol Venereol. 2018;32:1352-1359.
- Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts). N Engl J Med. 1975;292:344-347.
- Bohan A, Peter JB. Polymyositis and dermatomyositis (second of two parts). N Engl J Med. 1975;292:403-407.
- Sakurai N, Hino-Shishikura A, Nozawa T, et al. Clinical significance of subcutaneous fat and fascial involvement in juvenile dermatomyositis. Mod Rheumatol. 2019;29:808-813.
- Milisenda JC, Doti PI, Prieto-Gonzalez S, et al. Dermatomyositis presenting with severe subcutaneous edema: five additional cases and review of the literature. Semin Arthritis Rheum. 2014;44:228-233.
- Janis JF, Winkelmann RK. Histopathology of the skin in dermatomyositis: a histopathologic study of 55 cases. Arch Dermatol. 1968;97:640-650.
- van Dongen HM, van Vugt RM, Stoof TJ. Extensive persistent panniculitis in the context of dermatomyositis. J Clin Rheumatol. 2020;26:e187-e188.
- Gunawardena H, Wedderburn LR, North J, et al. Clinical associations of autoantibodies to a p155/140 kDa doublet protein in juvenile dermatomyositis. Rheumatology. 2008;47:324-328.
- Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet. 2003;362:971-982.
- Oddis CV, Reed AM, Aggarwal R, et al. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial. Arthritis Rheum. 2013;65:314-324.
- Fasano S, Gordon P, Hajji R, et al. Rituximab in the treatment of inflammatory myopathies: a review. Rheumatology. 2016;56:26-36.
To the Editor:
Juvenile dermatomyositis (JDM) is an autoimmune disorder with childhood onset that predominantly affects the muscles and skin, among other organs. Since the recognition of dermatomyositis (DM) more than 100 years ago, a variety of clinical diagnostic criteria have been utilized. Classically, DM presents with muscle weakness and a pathognomonic cutaneous macular, violaceous, erythematous eruption. The juvenile variant is defined by onset prior to 16 years of age. Histologically, these entities are indistinguishable and demonstrate an interface dermatitis with epidermal atrophy. Clinically, JDM has a higher incidence of calcinosis cutis and is not associated with an increased risk for malignancy in contrast to the adult-onset variant.1 Panniculitis is a rare but serious complication in a subset of patients with DM and may represent a precursor to calcinosis cutis.2 We describe a case of JDM-associated panniculitis that was difficult to control with prednisone and rituximab.
A 21-year-old woman with fever, fatigue, muscle pain, and new-onset swelling of 2 weeks’ duration was admitted to the hospital. She had a 5-year history of intermittent muscle weakness and concomitant rash. Prior to presentation, she had been hospitalized twice for fever of unknown origin, and the source remained undetermined. Physical examination revealed prominent facial and periorbital edema. There was tender nonpitting edema present on all 4 extremities and hyperpigmented indurated nodules on the shins (Figure 1). A full laboratory and imaging workup was performed for autoantibodies and infectious etiologies. The complete blood cell count was notable for pancytopenia, and a thorough infectious workup was negative. Creatine kinase level was within reference range. A biopsy of the right shin was performed, and histopathology revealed a lobular panniculitis with fat necrosis and mixed inflammation with neutrophils with perieccrine involvement as well as an interface dermatitis (Figure 2). Periodic acid–Schiff, Grocott methenamine-silver, and Gram stains were negative. Myositis-specific antibody testing revealed anti-p155/140 autoantibodies, and magnetic resonance imaging did not reveal active myositis within the visualized muscles, consistent with stable nonprogressing DM. A diagnosis of JDM with panniculitis was made. The patient was started on oral prednisone. Subsequently, a trial of rituximab was initiated. Although the patient’s symptoms initially improved, the response was not sustained on rituximab, and the patient was continued on systemic steroids with initiation of cyclosporine.
Juvenile dermatomyositis is an autoimmune disorder with childhood onset that involves systemic inflammation of the muscles, skin, and internal organs. It often can present diagnostic and therapeutic challenges.2,3 Bohan and Peter4,5 clinical criteria may help identify potential patients with JDM, but magnetic resonance imaging, electromyography, and muscle biopsy often are required to confirm the diagnosis.6 Skin manifestations include heliotrope rash; V sign; shawl sign; Gottron papules; periorbital edema; and infrequently panniculitis, the subcutaneous inflammation of adipose tissue.3,7
Although panniculitis is found in approximately 10% of skin biopsies in patients with DM, our patient presented with anti-p155/140 antibodies.8-10 Fat involvement in these patients traditionally manifests as lipodystrophy. Panniculitis also may precede calcinosis cutis, a debilitating skin change that may occur in approximately 46% of patients with JDM and can cause severe morbidity.2,6,9
Subcutaneous edema rarely is described in DM-panniculitis, present in only 6% of 86 DM patients in one study.7 The pathophysiology of DM may be due to antibodies that target endothelial cells and activate complement, resulting in the membranolytic attack complex. This leads to microischemia, and microinfarction of the muscle fibers has been suggested to result in edema of the subcutaneous tissue in severe cases.7,11 Microinfarction has been found to be present 2.3 times more often in edematous DM compared with nonedematous DM.7 Subcutaneous edema may be an isolated presentation of DM that arises more quickly with severe disease activity. As such, recommendations have been made to consider edema in future classification schemes.7
Because of the severity of edematous and/or subcutaneous DM, aggressive therapy may be required. First-line therapy consists of corticosteroids with additional immunosuppressants and immunomodulatory agents if adequate response is not achieved.3,12 The effectiveness of rituximab in DM has been suggested.2,12,13 The Rituximab in Myositis (RIM) trial (N=200) was the first double-blind, placebo-controlled, phase 3 clinical trial to assess rituximab’s efficacy in refractory compared with early-onset inflammatory myopathies. Although outcomes were similar in both groups, 83% of patients overall, including the JDM subset, met the definition of improvement.12 In re-examining the RIM trial data and other cases using rituximab to treat inflammatory myopathies, an overall response rate of 78.3% was observed, with 52.1% of patients with DM reporting improvement in skin lesions (N=458, pooled from 48 studies).13 Further analysis of the RIM data revealed that panniculitis affected 10.4% of patients with JDM at baseline, which decreased to 6.8% at 36 weeks of rituximab therapy (N=48).12
As exhibited in our patient, subcutaneous tissue involvement, including calcinosis cutis and panniculitis, is seen more often in JDM than adult DM.2,6 However, panniculitis in anti-p155/140 patients is rare. Our patient also had antibody positivity, which likely predisposed her to a more severe course. Despite not having sustained improvement on rituximab, initiating aggressive therapy earlier in the disease course may be beneficial, and our patient continues with alternative therapies.
To the Editor:
Juvenile dermatomyositis (JDM) is an autoimmune disorder with childhood onset that predominantly affects the muscles and skin, among other organs. Since the recognition of dermatomyositis (DM) more than 100 years ago, a variety of clinical diagnostic criteria have been utilized. Classically, DM presents with muscle weakness and a pathognomonic cutaneous macular, violaceous, erythematous eruption. The juvenile variant is defined by onset prior to 16 years of age. Histologically, these entities are indistinguishable and demonstrate an interface dermatitis with epidermal atrophy. Clinically, JDM has a higher incidence of calcinosis cutis and is not associated with an increased risk for malignancy in contrast to the adult-onset variant.1 Panniculitis is a rare but serious complication in a subset of patients with DM and may represent a precursor to calcinosis cutis.2 We describe a case of JDM-associated panniculitis that was difficult to control with prednisone and rituximab.
A 21-year-old woman with fever, fatigue, muscle pain, and new-onset swelling of 2 weeks’ duration was admitted to the hospital. She had a 5-year history of intermittent muscle weakness and concomitant rash. Prior to presentation, she had been hospitalized twice for fever of unknown origin, and the source remained undetermined. Physical examination revealed prominent facial and periorbital edema. There was tender nonpitting edema present on all 4 extremities and hyperpigmented indurated nodules on the shins (Figure 1). A full laboratory and imaging workup was performed for autoantibodies and infectious etiologies. The complete blood cell count was notable for pancytopenia, and a thorough infectious workup was negative. Creatine kinase level was within reference range. A biopsy of the right shin was performed, and histopathology revealed a lobular panniculitis with fat necrosis and mixed inflammation with neutrophils with perieccrine involvement as well as an interface dermatitis (Figure 2). Periodic acid–Schiff, Grocott methenamine-silver, and Gram stains were negative. Myositis-specific antibody testing revealed anti-p155/140 autoantibodies, and magnetic resonance imaging did not reveal active myositis within the visualized muscles, consistent with stable nonprogressing DM. A diagnosis of JDM with panniculitis was made. The patient was started on oral prednisone. Subsequently, a trial of rituximab was initiated. Although the patient’s symptoms initially improved, the response was not sustained on rituximab, and the patient was continued on systemic steroids with initiation of cyclosporine.
Juvenile dermatomyositis is an autoimmune disorder with childhood onset that involves systemic inflammation of the muscles, skin, and internal organs. It often can present diagnostic and therapeutic challenges.2,3 Bohan and Peter4,5 clinical criteria may help identify potential patients with JDM, but magnetic resonance imaging, electromyography, and muscle biopsy often are required to confirm the diagnosis.6 Skin manifestations include heliotrope rash; V sign; shawl sign; Gottron papules; periorbital edema; and infrequently panniculitis, the subcutaneous inflammation of adipose tissue.3,7
Although panniculitis is found in approximately 10% of skin biopsies in patients with DM, our patient presented with anti-p155/140 antibodies.8-10 Fat involvement in these patients traditionally manifests as lipodystrophy. Panniculitis also may precede calcinosis cutis, a debilitating skin change that may occur in approximately 46% of patients with JDM and can cause severe morbidity.2,6,9
Subcutaneous edema rarely is described in DM-panniculitis, present in only 6% of 86 DM patients in one study.7 The pathophysiology of DM may be due to antibodies that target endothelial cells and activate complement, resulting in the membranolytic attack complex. This leads to microischemia, and microinfarction of the muscle fibers has been suggested to result in edema of the subcutaneous tissue in severe cases.7,11 Microinfarction has been found to be present 2.3 times more often in edematous DM compared with nonedematous DM.7 Subcutaneous edema may be an isolated presentation of DM that arises more quickly with severe disease activity. As such, recommendations have been made to consider edema in future classification schemes.7
Because of the severity of edematous and/or subcutaneous DM, aggressive therapy may be required. First-line therapy consists of corticosteroids with additional immunosuppressants and immunomodulatory agents if adequate response is not achieved.3,12 The effectiveness of rituximab in DM has been suggested.2,12,13 The Rituximab in Myositis (RIM) trial (N=200) was the first double-blind, placebo-controlled, phase 3 clinical trial to assess rituximab’s efficacy in refractory compared with early-onset inflammatory myopathies. Although outcomes were similar in both groups, 83% of patients overall, including the JDM subset, met the definition of improvement.12 In re-examining the RIM trial data and other cases using rituximab to treat inflammatory myopathies, an overall response rate of 78.3% was observed, with 52.1% of patients with DM reporting improvement in skin lesions (N=458, pooled from 48 studies).13 Further analysis of the RIM data revealed that panniculitis affected 10.4% of patients with JDM at baseline, which decreased to 6.8% at 36 weeks of rituximab therapy (N=48).12
As exhibited in our patient, subcutaneous tissue involvement, including calcinosis cutis and panniculitis, is seen more often in JDM than adult DM.2,6 However, panniculitis in anti-p155/140 patients is rare. Our patient also had antibody positivity, which likely predisposed her to a more severe course. Despite not having sustained improvement on rituximab, initiating aggressive therapy earlier in the disease course may be beneficial, and our patient continues with alternative therapies.
- Jorizzo JL, Vleugels RA. Dermatomyositis. In: Bolognia J, Schaffer J, Cerroni L. Dermatology. 4th ed. Elsevier; 2019:681-687.
- Aggarwal R, Loganathan P, Koontz D, et al. Cutaneous improvement in refractory adult and juvenile dermatomyositis after treatment with rituximab. Rheumatology. 2016;56:247-254.
- Santos-Briz A, Calle A, Linos K, et al. Dermatomyositis panniculitis: a clinicopathological and immunohistochemical study of 18 cases. J Eur Acad Dermatol Venereol. 2018;32:1352-1359.
- Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts). N Engl J Med. 1975;292:344-347.
- Bohan A, Peter JB. Polymyositis and dermatomyositis (second of two parts). N Engl J Med. 1975;292:403-407.
- Sakurai N, Hino-Shishikura A, Nozawa T, et al. Clinical significance of subcutaneous fat and fascial involvement in juvenile dermatomyositis. Mod Rheumatol. 2019;29:808-813.
- Milisenda JC, Doti PI, Prieto-Gonzalez S, et al. Dermatomyositis presenting with severe subcutaneous edema: five additional cases and review of the literature. Semin Arthritis Rheum. 2014;44:228-233.
- Janis JF, Winkelmann RK. Histopathology of the skin in dermatomyositis: a histopathologic study of 55 cases. Arch Dermatol. 1968;97:640-650.
- van Dongen HM, van Vugt RM, Stoof TJ. Extensive persistent panniculitis in the context of dermatomyositis. J Clin Rheumatol. 2020;26:e187-e188.
- Gunawardena H, Wedderburn LR, North J, et al. Clinical associations of autoantibodies to a p155/140 kDa doublet protein in juvenile dermatomyositis. Rheumatology. 2008;47:324-328.
- Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet. 2003;362:971-982.
- Oddis CV, Reed AM, Aggarwal R, et al. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial. Arthritis Rheum. 2013;65:314-324.
- Fasano S, Gordon P, Hajji R, et al. Rituximab in the treatment of inflammatory myopathies: a review. Rheumatology. 2016;56:26-36.
- Jorizzo JL, Vleugels RA. Dermatomyositis. In: Bolognia J, Schaffer J, Cerroni L. Dermatology. 4th ed. Elsevier; 2019:681-687.
- Aggarwal R, Loganathan P, Koontz D, et al. Cutaneous improvement in refractory adult and juvenile dermatomyositis after treatment with rituximab. Rheumatology. 2016;56:247-254.
- Santos-Briz A, Calle A, Linos K, et al. Dermatomyositis panniculitis: a clinicopathological and immunohistochemical study of 18 cases. J Eur Acad Dermatol Venereol. 2018;32:1352-1359.
- Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts). N Engl J Med. 1975;292:344-347.
- Bohan A, Peter JB. Polymyositis and dermatomyositis (second of two parts). N Engl J Med. 1975;292:403-407.
- Sakurai N, Hino-Shishikura A, Nozawa T, et al. Clinical significance of subcutaneous fat and fascial involvement in juvenile dermatomyositis. Mod Rheumatol. 2019;29:808-813.
- Milisenda JC, Doti PI, Prieto-Gonzalez S, et al. Dermatomyositis presenting with severe subcutaneous edema: five additional cases and review of the literature. Semin Arthritis Rheum. 2014;44:228-233.
- Janis JF, Winkelmann RK. Histopathology of the skin in dermatomyositis: a histopathologic study of 55 cases. Arch Dermatol. 1968;97:640-650.
- van Dongen HM, van Vugt RM, Stoof TJ. Extensive persistent panniculitis in the context of dermatomyositis. J Clin Rheumatol. 2020;26:e187-e188.
- Gunawardena H, Wedderburn LR, North J, et al. Clinical associations of autoantibodies to a p155/140 kDa doublet protein in juvenile dermatomyositis. Rheumatology. 2008;47:324-328.
- Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet. 2003;362:971-982.
- Oddis CV, Reed AM, Aggarwal R, et al. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial. Arthritis Rheum. 2013;65:314-324.
- Fasano S, Gordon P, Hajji R, et al. Rituximab in the treatment of inflammatory myopathies: a review. Rheumatology. 2016;56:26-36.
Practice Points
- Juvenile dermatomyositis is an autoimmune disorder with childhood onset that predominantly affects the muscles and skin.
- Juvenile dermatomyositis has a higher incidence of calcinosis cutis and is not associated with an increased risk for malignancy in contrast to the adult-onset variant, dermatomyositis (DM).
- Panniculitis is a rare but severe complication of DM, and this subset of DM may be challenging to treat, requiring aggressive therapy.
Skin Manifestations of Complex Regional Pain Syndrome
To the Editor:
Complex regional pain syndrome (CRPS) is a neurologic condition characterized by chronic pain and sensory changes, including allodynia and hyperalgesia, that usually affect the extremities.1,2 The syndrome is defined by the International Association for the Study of Pain (IASP) as a condition that appears regionally after an injury, with a variety of symptoms that often exceed the expected clinical course both in magnitude and duration, causing impairment of motor function and variable progression.3
Although CRPS most often is described following minor peripheral trauma, other precipitating causes include surgery and vascular events.4 Additional features of the condition include autonomic dysfunction, edema, and trophic changes.1 Symptoms of CRPS traditionally present in 3 stages, with notable skin changes most often documented in stages II and III.2
Skin changes are a known manifestation of the syndrome, but reports in the dermatologic literature are scarce. Qureshi and Friedman5 identified only 23 articles in the dermatology literature since 1990 in which skin changes in CRPS were described. We present a patient with a diagnosis of CRPS who developed hyperpigmentation and sclerotic changes, including skin thickening, induration, and skin tightening.
A middle-aged Black woman presented to dermatology for evaluation of progressive hyperpigmentation, hyperhidrosis, and sclerotic changes to the skin. Approximately 3 years prior, the patient was given a diagnosis of CRPS of the hands and feet. Pain symptoms started approximately 3 years prior to the onset of symptoms. Symptoms started in the left hand and eventually spread to the right arm, left leg, and subsequently to the right leg. The first dermatologic change the patient noticed was tightening of the skin in the affected area that led to decreased mobility, which improved over time—partly on its own and partly with physical therapy.
A biopsy performed by an outside dermatologist at the initial presentation demonstrated sclerodermalike changes, which were treated with creams but without improvement. Scleroderma was later ruled out by the same dermatologist. Skin tightening improved over time, with complete resolution approximately 1 year after the onset of symptoms.
Upon presentation to our clinic, the patient reported continuing intermittent flares of CRPS; however, she said she was most concerned about diffuse hyperpigmentation, which spread to include the face, arms, abdomen, legs (Figure), and buttocks and persisted after skin tightening resolved.
To treat the hyperpigmentation, a decision was made to first focus on a localized area. Facial hyperpigmentation was chosen because it was of greatest concern to the patient. She was instructed to use azelaic acid gel 15% in the morning, tretinoin cream 0.05% at night, and sunscreen daily. The patient had mild improvement in hyperpigmentation after a 4-month period but has been inconsistent in follow-up. She continues to have intermittent flares of CRPS, which may interfere with her response to treatment. In addition to the aforementioned regimen of azelaic acid gel and tretinoin, she has continued to work with a pain specialist to better control the neurologic symptoms and pain associated with her CRPS.
Complex regional pain syndrome, a neurological condition characterized by chronic pain, affects women 3 times more often than men. The syndrome is more common in the fourth and fifth decades of life.1,2
There are 2 subtypes of CRPS. Type I (also known as reflex sympathetic dystrophy) is more common and occurs following minor trauma without peripheral nerve injury. Type II (otherwise known as causalgia) occurs following more notable trauma with injury to a peripheral nerve.1,6 Onset of symptoms most often is secondary to minor peripheral trauma. More common triggers include soft-tissue injury (40%); fractures and subsequent orthopedic surgery (25%); and visceral lesions, such as myocardial infarction and cerebral vascular accident (12%).5 Regardless of the inciting event, prolonged immobilization of a limb has been identified as an important predisposing factor. One study found that 47% of patients who received a diagnosis of CRPS previously underwent immobilization of the same limb.7
The pathogenesis of CRPS has not been fully elucidated. Possible explanations include central nervous system sensitization to thermal, mechanical, and pain stimuli; sympathetic dysfunction leading to vasomotor, pseudomotor, and trophic changes; and inflammatory cytokine release and microcirculatory dysfunction, causing tissue injury.1,2,6
The diagnosis of CRPS is a based on clinical findings. Using the Budapest Criteria established to define CRPS, a clinical diagnosis can be made when all of the following criteria are met: chronic continuing pain disproportionate to any inciting event; 1 or more reported symptoms from 3 or more of the categories of involvement including sensory, vasomotor, pseudomotor, edema, and motor or trophic; 1 or more sign at the time of evaluation in 2 or more of the categories of involvement including sensory, vasomotor, pseudomotor, edema, and motor or trophic.8 Dermatologic findings are a common presenting feature of CRPS and are included in the Budapest Criteria used for diagnosis. In a retrospective chart review (N=26), researchers found that vascular findings were the most common dermatologic manifestation of CRPS—edema in 58% of patients and erythema in 54%.9 Other common manifestations included dermatitis (35%), erythematous papules (23%), and cutaneous atrophy (23%). Hyperpigmentation, which was present in our patient, was seen in 8% of patients in the chart review.9
Complex regional pain syndrome progresses through 3 stages; dermatologic changes are present in each stage and are more severe in later stages. Stage I lasts 2 or 3 months and is characterized by onset of pain, usually burning type, accompanied by allodynia and hyperalgesia. Early vasomotor and pseudomotor changes, such as erythema and edema, may become apparent.1,2 Stage II lasts 3 to 6 months and is characterized by more severe edema and more obvious trophic changes. Functional limitations, such as limited range of motion and muscle weakness, begin to manifest. Stage III—the final and most severe stage—is characterized by obvious hair, skin, and nail changes, as well as functional limitations.1,2 The waxy thickened skin changes and hyperpigmentation observed in our patient are characteristic of stage III. Furthermore, our patient experienced decreased mobility and limited range of motion secondary to tightening of the skin, a characteristic motor change of late-stage CRPS. Although chronic pain and allodynia are the most common characteristics of CRPS, skin changes also can cause notable distress and early dermatologic manifestations can be a chief concern.
Dermatologic management is focused to address the specific skin changes of CRPS. However, traditional treatment of the common dermatologic findings of CRPS is difficult and often unsuccessful; instead, the most successful treatment of skin findings involves controlling the underlying CRPS.9 Current treatment options include removal of any nidus of tissue trauma, sympathetic neural blockade with a local anesthetic, spinal cord stimulation to interrupt dysregulated sympathetic innervation, and physiotherapy or occupational therapy to desensitize skin.1,10
Given the complexity of CRPS and the variability of its presentation, management of the syndrome and its associated dermatologic conditions often requires interdisciplinary care and coordination of multiple specialties. Dermatologists can play an important role in both identification of CRPS and co-management of affected patients. Early diagnosis of CRPS has been universally identified as a key prognostic factor. For that reason, dermatologists should be aware of CRPS and include the syndrome in the differential diagnosis when presented with severe cutaneous findings following trauma either with or without peripheral nerve damage, suggestive of CRPS.
- Sebastin SJ. Complex regional pain syndrome. Indian J Plast Surg. 2011;44:298-307. doi:10.4103/0970-0358.85351
- Kabani R, Brassard A. Dermatological findings in early detection of complex regional pain syndrome. JAMA Dermatol. 2014;150:640-642. doi:10.1001/jamadermatol.2013.7459
- Moseley L. What is complex regional pain syndrome – in plain English. International Association for the Study of Pain website. Published 2009. Accessed December 15, 2022. https://www.iasp-pain.org/publications/relief-news/article/what-is-complex-pain-syndrome-in-plain-english/
- Pak TJ, Martin GM, Magness JL, et al. Reflex sympathetic dystrophy. Review of 140 cases. Minn Med. 1970;53:507-512.
- Qureshi AA, Friedman AJ. Complex regional pain syndrome: what the dermatologist should know. J Drugs Dermatol. 2018;17:532-536.
- Gorodkin R. Complex regional pain syndrome. Rheumatology. 2016;55(suppl 1):i12.
- Araki E, Tanioka M, Miyachi Y, et al. A case of complex regional pain syndrome: an underdiagnosed condition in dermatology. Acta Derm Venereol. 2007;87:440-441. doi:10.2340/00015555-0281
- Pergolizzi JV, LeQuang JA, Nalamachu S, et al. The Budapest criteria for complex regional pain syndrome: the diagnostic challenge. Anaesthesiol Clin Sci Res. 2018;2:1-10. doi:10.35841/anesthesiology.2.1.1-10
- Sundaram S, Webster GF. Vascular diseases are the most common cutaneous manifestations of reflex sympathetic dystrophy. J Am Acad Dermatol. 2001;44:1050-1051. doi:10.1067/mjd.2001.114299
- Taylor RS, Van Buyten J-P, Buchser E. Spinal stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature and assessment of prognostic factors. Eur J Pain. 2006;10:91-101. doi:10.1016/j.ejpain.2005.02.004
To the Editor:
Complex regional pain syndrome (CRPS) is a neurologic condition characterized by chronic pain and sensory changes, including allodynia and hyperalgesia, that usually affect the extremities.1,2 The syndrome is defined by the International Association for the Study of Pain (IASP) as a condition that appears regionally after an injury, with a variety of symptoms that often exceed the expected clinical course both in magnitude and duration, causing impairment of motor function and variable progression.3
Although CRPS most often is described following minor peripheral trauma, other precipitating causes include surgery and vascular events.4 Additional features of the condition include autonomic dysfunction, edema, and trophic changes.1 Symptoms of CRPS traditionally present in 3 stages, with notable skin changes most often documented in stages II and III.2
Skin changes are a known manifestation of the syndrome, but reports in the dermatologic literature are scarce. Qureshi and Friedman5 identified only 23 articles in the dermatology literature since 1990 in which skin changes in CRPS were described. We present a patient with a diagnosis of CRPS who developed hyperpigmentation and sclerotic changes, including skin thickening, induration, and skin tightening.
A middle-aged Black woman presented to dermatology for evaluation of progressive hyperpigmentation, hyperhidrosis, and sclerotic changes to the skin. Approximately 3 years prior, the patient was given a diagnosis of CRPS of the hands and feet. Pain symptoms started approximately 3 years prior to the onset of symptoms. Symptoms started in the left hand and eventually spread to the right arm, left leg, and subsequently to the right leg. The first dermatologic change the patient noticed was tightening of the skin in the affected area that led to decreased mobility, which improved over time—partly on its own and partly with physical therapy.
A biopsy performed by an outside dermatologist at the initial presentation demonstrated sclerodermalike changes, which were treated with creams but without improvement. Scleroderma was later ruled out by the same dermatologist. Skin tightening improved over time, with complete resolution approximately 1 year after the onset of symptoms.
Upon presentation to our clinic, the patient reported continuing intermittent flares of CRPS; however, she said she was most concerned about diffuse hyperpigmentation, which spread to include the face, arms, abdomen, legs (Figure), and buttocks and persisted after skin tightening resolved.
To treat the hyperpigmentation, a decision was made to first focus on a localized area. Facial hyperpigmentation was chosen because it was of greatest concern to the patient. She was instructed to use azelaic acid gel 15% in the morning, tretinoin cream 0.05% at night, and sunscreen daily. The patient had mild improvement in hyperpigmentation after a 4-month period but has been inconsistent in follow-up. She continues to have intermittent flares of CRPS, which may interfere with her response to treatment. In addition to the aforementioned regimen of azelaic acid gel and tretinoin, she has continued to work with a pain specialist to better control the neurologic symptoms and pain associated with her CRPS.
Complex regional pain syndrome, a neurological condition characterized by chronic pain, affects women 3 times more often than men. The syndrome is more common in the fourth and fifth decades of life.1,2
There are 2 subtypes of CRPS. Type I (also known as reflex sympathetic dystrophy) is more common and occurs following minor trauma without peripheral nerve injury. Type II (otherwise known as causalgia) occurs following more notable trauma with injury to a peripheral nerve.1,6 Onset of symptoms most often is secondary to minor peripheral trauma. More common triggers include soft-tissue injury (40%); fractures and subsequent orthopedic surgery (25%); and visceral lesions, such as myocardial infarction and cerebral vascular accident (12%).5 Regardless of the inciting event, prolonged immobilization of a limb has been identified as an important predisposing factor. One study found that 47% of patients who received a diagnosis of CRPS previously underwent immobilization of the same limb.7
The pathogenesis of CRPS has not been fully elucidated. Possible explanations include central nervous system sensitization to thermal, mechanical, and pain stimuli; sympathetic dysfunction leading to vasomotor, pseudomotor, and trophic changes; and inflammatory cytokine release and microcirculatory dysfunction, causing tissue injury.1,2,6
The diagnosis of CRPS is a based on clinical findings. Using the Budapest Criteria established to define CRPS, a clinical diagnosis can be made when all of the following criteria are met: chronic continuing pain disproportionate to any inciting event; 1 or more reported symptoms from 3 or more of the categories of involvement including sensory, vasomotor, pseudomotor, edema, and motor or trophic; 1 or more sign at the time of evaluation in 2 or more of the categories of involvement including sensory, vasomotor, pseudomotor, edema, and motor or trophic.8 Dermatologic findings are a common presenting feature of CRPS and are included in the Budapest Criteria used for diagnosis. In a retrospective chart review (N=26), researchers found that vascular findings were the most common dermatologic manifestation of CRPS—edema in 58% of patients and erythema in 54%.9 Other common manifestations included dermatitis (35%), erythematous papules (23%), and cutaneous atrophy (23%). Hyperpigmentation, which was present in our patient, was seen in 8% of patients in the chart review.9
Complex regional pain syndrome progresses through 3 stages; dermatologic changes are present in each stage and are more severe in later stages. Stage I lasts 2 or 3 months and is characterized by onset of pain, usually burning type, accompanied by allodynia and hyperalgesia. Early vasomotor and pseudomotor changes, such as erythema and edema, may become apparent.1,2 Stage II lasts 3 to 6 months and is characterized by more severe edema and more obvious trophic changes. Functional limitations, such as limited range of motion and muscle weakness, begin to manifest. Stage III—the final and most severe stage—is characterized by obvious hair, skin, and nail changes, as well as functional limitations.1,2 The waxy thickened skin changes and hyperpigmentation observed in our patient are characteristic of stage III. Furthermore, our patient experienced decreased mobility and limited range of motion secondary to tightening of the skin, a characteristic motor change of late-stage CRPS. Although chronic pain and allodynia are the most common characteristics of CRPS, skin changes also can cause notable distress and early dermatologic manifestations can be a chief concern.
Dermatologic management is focused to address the specific skin changes of CRPS. However, traditional treatment of the common dermatologic findings of CRPS is difficult and often unsuccessful; instead, the most successful treatment of skin findings involves controlling the underlying CRPS.9 Current treatment options include removal of any nidus of tissue trauma, sympathetic neural blockade with a local anesthetic, spinal cord stimulation to interrupt dysregulated sympathetic innervation, and physiotherapy or occupational therapy to desensitize skin.1,10
Given the complexity of CRPS and the variability of its presentation, management of the syndrome and its associated dermatologic conditions often requires interdisciplinary care and coordination of multiple specialties. Dermatologists can play an important role in both identification of CRPS and co-management of affected patients. Early diagnosis of CRPS has been universally identified as a key prognostic factor. For that reason, dermatologists should be aware of CRPS and include the syndrome in the differential diagnosis when presented with severe cutaneous findings following trauma either with or without peripheral nerve damage, suggestive of CRPS.
To the Editor:
Complex regional pain syndrome (CRPS) is a neurologic condition characterized by chronic pain and sensory changes, including allodynia and hyperalgesia, that usually affect the extremities.1,2 The syndrome is defined by the International Association for the Study of Pain (IASP) as a condition that appears regionally after an injury, with a variety of symptoms that often exceed the expected clinical course both in magnitude and duration, causing impairment of motor function and variable progression.3
Although CRPS most often is described following minor peripheral trauma, other precipitating causes include surgery and vascular events.4 Additional features of the condition include autonomic dysfunction, edema, and trophic changes.1 Symptoms of CRPS traditionally present in 3 stages, with notable skin changes most often documented in stages II and III.2
Skin changes are a known manifestation of the syndrome, but reports in the dermatologic literature are scarce. Qureshi and Friedman5 identified only 23 articles in the dermatology literature since 1990 in which skin changes in CRPS were described. We present a patient with a diagnosis of CRPS who developed hyperpigmentation and sclerotic changes, including skin thickening, induration, and skin tightening.
A middle-aged Black woman presented to dermatology for evaluation of progressive hyperpigmentation, hyperhidrosis, and sclerotic changes to the skin. Approximately 3 years prior, the patient was given a diagnosis of CRPS of the hands and feet. Pain symptoms started approximately 3 years prior to the onset of symptoms. Symptoms started in the left hand and eventually spread to the right arm, left leg, and subsequently to the right leg. The first dermatologic change the patient noticed was tightening of the skin in the affected area that led to decreased mobility, which improved over time—partly on its own and partly with physical therapy.
A biopsy performed by an outside dermatologist at the initial presentation demonstrated sclerodermalike changes, which were treated with creams but without improvement. Scleroderma was later ruled out by the same dermatologist. Skin tightening improved over time, with complete resolution approximately 1 year after the onset of symptoms.
Upon presentation to our clinic, the patient reported continuing intermittent flares of CRPS; however, she said she was most concerned about diffuse hyperpigmentation, which spread to include the face, arms, abdomen, legs (Figure), and buttocks and persisted after skin tightening resolved.
To treat the hyperpigmentation, a decision was made to first focus on a localized area. Facial hyperpigmentation was chosen because it was of greatest concern to the patient. She was instructed to use azelaic acid gel 15% in the morning, tretinoin cream 0.05% at night, and sunscreen daily. The patient had mild improvement in hyperpigmentation after a 4-month period but has been inconsistent in follow-up. She continues to have intermittent flares of CRPS, which may interfere with her response to treatment. In addition to the aforementioned regimen of azelaic acid gel and tretinoin, she has continued to work with a pain specialist to better control the neurologic symptoms and pain associated with her CRPS.
Complex regional pain syndrome, a neurological condition characterized by chronic pain, affects women 3 times more often than men. The syndrome is more common in the fourth and fifth decades of life.1,2
There are 2 subtypes of CRPS. Type I (also known as reflex sympathetic dystrophy) is more common and occurs following minor trauma without peripheral nerve injury. Type II (otherwise known as causalgia) occurs following more notable trauma with injury to a peripheral nerve.1,6 Onset of symptoms most often is secondary to minor peripheral trauma. More common triggers include soft-tissue injury (40%); fractures and subsequent orthopedic surgery (25%); and visceral lesions, such as myocardial infarction and cerebral vascular accident (12%).5 Regardless of the inciting event, prolonged immobilization of a limb has been identified as an important predisposing factor. One study found that 47% of patients who received a diagnosis of CRPS previously underwent immobilization of the same limb.7
The pathogenesis of CRPS has not been fully elucidated. Possible explanations include central nervous system sensitization to thermal, mechanical, and pain stimuli; sympathetic dysfunction leading to vasomotor, pseudomotor, and trophic changes; and inflammatory cytokine release and microcirculatory dysfunction, causing tissue injury.1,2,6
The diagnosis of CRPS is a based on clinical findings. Using the Budapest Criteria established to define CRPS, a clinical diagnosis can be made when all of the following criteria are met: chronic continuing pain disproportionate to any inciting event; 1 or more reported symptoms from 3 or more of the categories of involvement including sensory, vasomotor, pseudomotor, edema, and motor or trophic; 1 or more sign at the time of evaluation in 2 or more of the categories of involvement including sensory, vasomotor, pseudomotor, edema, and motor or trophic.8 Dermatologic findings are a common presenting feature of CRPS and are included in the Budapest Criteria used for diagnosis. In a retrospective chart review (N=26), researchers found that vascular findings were the most common dermatologic manifestation of CRPS—edema in 58% of patients and erythema in 54%.9 Other common manifestations included dermatitis (35%), erythematous papules (23%), and cutaneous atrophy (23%). Hyperpigmentation, which was present in our patient, was seen in 8% of patients in the chart review.9
Complex regional pain syndrome progresses through 3 stages; dermatologic changes are present in each stage and are more severe in later stages. Stage I lasts 2 or 3 months and is characterized by onset of pain, usually burning type, accompanied by allodynia and hyperalgesia. Early vasomotor and pseudomotor changes, such as erythema and edema, may become apparent.1,2 Stage II lasts 3 to 6 months and is characterized by more severe edema and more obvious trophic changes. Functional limitations, such as limited range of motion and muscle weakness, begin to manifest. Stage III—the final and most severe stage—is characterized by obvious hair, skin, and nail changes, as well as functional limitations.1,2 The waxy thickened skin changes and hyperpigmentation observed in our patient are characteristic of stage III. Furthermore, our patient experienced decreased mobility and limited range of motion secondary to tightening of the skin, a characteristic motor change of late-stage CRPS. Although chronic pain and allodynia are the most common characteristics of CRPS, skin changes also can cause notable distress and early dermatologic manifestations can be a chief concern.
Dermatologic management is focused to address the specific skin changes of CRPS. However, traditional treatment of the common dermatologic findings of CRPS is difficult and often unsuccessful; instead, the most successful treatment of skin findings involves controlling the underlying CRPS.9 Current treatment options include removal of any nidus of tissue trauma, sympathetic neural blockade with a local anesthetic, spinal cord stimulation to interrupt dysregulated sympathetic innervation, and physiotherapy or occupational therapy to desensitize skin.1,10
Given the complexity of CRPS and the variability of its presentation, management of the syndrome and its associated dermatologic conditions often requires interdisciplinary care and coordination of multiple specialties. Dermatologists can play an important role in both identification of CRPS and co-management of affected patients. Early diagnosis of CRPS has been universally identified as a key prognostic factor. For that reason, dermatologists should be aware of CRPS and include the syndrome in the differential diagnosis when presented with severe cutaneous findings following trauma either with or without peripheral nerve damage, suggestive of CRPS.
- Sebastin SJ. Complex regional pain syndrome. Indian J Plast Surg. 2011;44:298-307. doi:10.4103/0970-0358.85351
- Kabani R, Brassard A. Dermatological findings in early detection of complex regional pain syndrome. JAMA Dermatol. 2014;150:640-642. doi:10.1001/jamadermatol.2013.7459
- Moseley L. What is complex regional pain syndrome – in plain English. International Association for the Study of Pain website. Published 2009. Accessed December 15, 2022. https://www.iasp-pain.org/publications/relief-news/article/what-is-complex-pain-syndrome-in-plain-english/
- Pak TJ, Martin GM, Magness JL, et al. Reflex sympathetic dystrophy. Review of 140 cases. Minn Med. 1970;53:507-512.
- Qureshi AA, Friedman AJ. Complex regional pain syndrome: what the dermatologist should know. J Drugs Dermatol. 2018;17:532-536.
- Gorodkin R. Complex regional pain syndrome. Rheumatology. 2016;55(suppl 1):i12.
- Araki E, Tanioka M, Miyachi Y, et al. A case of complex regional pain syndrome: an underdiagnosed condition in dermatology. Acta Derm Venereol. 2007;87:440-441. doi:10.2340/00015555-0281
- Pergolizzi JV, LeQuang JA, Nalamachu S, et al. The Budapest criteria for complex regional pain syndrome: the diagnostic challenge. Anaesthesiol Clin Sci Res. 2018;2:1-10. doi:10.35841/anesthesiology.2.1.1-10
- Sundaram S, Webster GF. Vascular diseases are the most common cutaneous manifestations of reflex sympathetic dystrophy. J Am Acad Dermatol. 2001;44:1050-1051. doi:10.1067/mjd.2001.114299
- Taylor RS, Van Buyten J-P, Buchser E. Spinal stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature and assessment of prognostic factors. Eur J Pain. 2006;10:91-101. doi:10.1016/j.ejpain.2005.02.004
- Sebastin SJ. Complex regional pain syndrome. Indian J Plast Surg. 2011;44:298-307. doi:10.4103/0970-0358.85351
- Kabani R, Brassard A. Dermatological findings in early detection of complex regional pain syndrome. JAMA Dermatol. 2014;150:640-642. doi:10.1001/jamadermatol.2013.7459
- Moseley L. What is complex regional pain syndrome – in plain English. International Association for the Study of Pain website. Published 2009. Accessed December 15, 2022. https://www.iasp-pain.org/publications/relief-news/article/what-is-complex-pain-syndrome-in-plain-english/
- Pak TJ, Martin GM, Magness JL, et al. Reflex sympathetic dystrophy. Review of 140 cases. Minn Med. 1970;53:507-512.
- Qureshi AA, Friedman AJ. Complex regional pain syndrome: what the dermatologist should know. J Drugs Dermatol. 2018;17:532-536.
- Gorodkin R. Complex regional pain syndrome. Rheumatology. 2016;55(suppl 1):i12.
- Araki E, Tanioka M, Miyachi Y, et al. A case of complex regional pain syndrome: an underdiagnosed condition in dermatology. Acta Derm Venereol. 2007;87:440-441. doi:10.2340/00015555-0281
- Pergolizzi JV, LeQuang JA, Nalamachu S, et al. The Budapest criteria for complex regional pain syndrome: the diagnostic challenge. Anaesthesiol Clin Sci Res. 2018;2:1-10. doi:10.35841/anesthesiology.2.1.1-10
- Sundaram S, Webster GF. Vascular diseases are the most common cutaneous manifestations of reflex sympathetic dystrophy. J Am Acad Dermatol. 2001;44:1050-1051. doi:10.1067/mjd.2001.114299
- Taylor RS, Van Buyten J-P, Buchser E. Spinal stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature and assessment of prognostic factors. Eur J Pain. 2006;10:91-101. doi:10.1016/j.ejpain.2005.02.004
PRACTICE POINTS
- Common dermatologic manifestations of complex regional pain syndrome (CRPS), which often are nonspecific and often the presenting symptoms of the syndrome, include allodynia, edema, erythema, hypopigmentation or hyperpigmentation, and petechiae.
- Diagnosis and management of CRPS are the most important steps in treating dermatologic manifestations of the syndrome.
