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The danger when doctors don’t get mental health help
As medical professionals, you’re continually exposed to overwork, burnout, stressful situations, and challenging ethical decisions. Yet seeking help for mental health care may be last on your to-do list – or completely off your radar.
That’s sad and dangerous, since the American College of Emergency Physicians said 300-400 physicians die by suicide each year, and the stigma keeps 69% of female physicians from seeking mental health care, according to a prepandemic study.
In the 2022 Medscape Physician Suicide Report, 11% of female doctors and 9% of male doctors said they have had thoughts of suicide, and 64% experienced colloquial depression (feeling down, sad, or blue).
What’s more, physicians are typically seen as strong and capable and are often put on a pedestal by loved ones, patients, and the public and thought of as superhuman. No wonder it isn’t easy when you need to take time away to decompress and treat your mental well-being.
“There is a real fear for physicians when it comes to getting mental health care,” said Emil Tsai, MD, PhD, MAS, professor at the department of psychiatry and behavioral sciences at the University of California, Los Angeles, and an internationally reputed scientist in neurosciences and brain disorders.
The fear, said Dr. Tsai, comes from the stigma of mental health issues, potential repercussions to employment, and conceivable medical board suspension or revocation of your medical license.
Dr. Tsai said in an interview that to combat anxiety about “punishment” that many physicians fear when seeking care for their mental health, we must allow physicians to take time away from their day-to-day patient care for respite and treatment without reprisal.
Since the medical profession is high stress and has a high depression and suicide rate, finding solutions is imperative. And physicians must feel supported enough to seek treatment when needed. So how can we normalize seeking mental health care among physicians?
Get honest about stress and burnout
The only way to normalize any behavior is to be open and candid, Dr. Tsai said in an interview. The mental health conversation must occur across the board, not just within the medical profession.
“The greatest thing we can do to try and lift the burden that we place on physicians is to be willing to talk and be honest about the stress that physicians deal with and the importance of everyone feeling free to seek treatment and rest to strengthen their mental health,” said Dr. Tsai.
The more we talk about mental health and its treatment, the more we lessen the stigma, said Dr. Tsai. That could be more employer-employee check-ins, counseling as part of physician wellness, and programs structured so as not to construe a penal system.
“Mental health in the medical profession is a big issue and one that has to be met with the same compassion and care as it should be for any patient. We have annual physical checkups. Why don’t we offer annual mental health checkups for all, physicians included?” asked Dr. Tsai.
Evaluate the workload
Elizabeth Lombardo, PhD, psychologist, coach, and global keynote speaker, thinks that health care employers should reexamine their physicians’ workloads to see if they’re contributing to mental health issues.
The conversation on mental health in the workplace shouldn’t be about whether a certain person can handle stressors that are “normal” for health care settings. Instead, workplace managers in health care institutions should redefine workloads to ensure that physicians aren’t too heavily burdened with responsibilities that can cause overwork, burnout, and mental health problems,” she said.
Lessen the stigma
Even when physicians want to seek help for their psychological struggles, they may be weary of how their colleagues would react if they knew.
Raffaello Antonino, MD, clinical director at Therapy Central in London, said several underlying fears may exist at a physician’s core that prevent them from seeking care – being seen as weak, being judged as unfit to practice medicine, and the notion that “something is wrong with them.”
Dr. Antonino said we need to understand that physicians face challenges of bereavement and trauma derived from losing patients and the inability to save someone’s life. “These issues can easily develop into an accumulation of difficult, unprocessed emotions, later arising in symptoms and signs of PTSD, anxiety, and depression.”
Education is the best way to end this stigma, just like with any form of prejudice and stereotypes. For instance, we know that health care professionals are at risk of developing burnout. So, educating physicians on the symptoms and management of burnout and its consequences and prevention strategies is a must.
“Imagine what could happen if there were regular opportunities to work through the day’s events before signing out from a shift. The idea that individual weekly therapy is the only way to relieve mental distress is false,” said Lori McIsaac Bewsher, MSW, RSW, a trauma therapist and owner of a trauma-focused mental health clinic in New Brunswick.
“There are ways of integrating individual care into our doctor’s offices and hospitals that can be brief, effective, and confidential. The best way to introduce these interventions is early and collectively; no one is immune to the potential impact of exposure to trauma. The earlier these interventions can be accessed, the better the outcomes for everyone,” she said.
Dr. Antonino suggests, perhaps in the future, organizations can have “burnout checks” or mental health wellness checks for physicians akin to how we also have quick examinations for various physical ailments. What if physicians regularly answered a 10-question mental health survey as part of a burnout or trauma prevention strategy?
“Theirs is a profession and an identity which is often linked with a sense of strength, leadership and [benevolent] power: adjectives, which on the surface one might see as incompatible with what instead, unfortunately, and wrongly, may be associated with mental health issues,” said Dr. Antonino.
Keep it private
When it comes to removing the stigma from mental health care and treatment for physicians, privacy is top of mind. There needs to be some form of privacy protection for physicians who seek professional help for mental health reasons. Dr. Lombardo said physicians need to have the choice to keep their mental health journeys private. “Ideally, normalization should mean openly conversing about mental health, but for physicians, it can be a matter of life or death for their career, so the choice to remain private is something that should be afforded to them.”
Along those lines, the American Medical Association is pushing for system changes in legislative and regulatory arenas to support the mental health of practicing physicians, residents, and medical students. The organization is also urging health systems and state medical licensing bodies to remove questions on their applications that ask about prior treatment for mental health conditions.
Among many programs across the country, the Foundation of the Pennsylvania Medical Society has also created a Physicians’ Health Program, which provides confidential assessment, counseling, and referral services for physicians with mental health concerns.
“All of these initiatives are important in helping to destigmatize mental health issues among physicians,” said Harold Hong, MD, a board-certified psychiatrist in Raleigh, N.C.
Hail the benefits of treatment
Dr. Hong said to continue to destigmatize mental health among physicians and normalize its treatment, we not only have to emphasize how attending to mental health has individual benefits but also how it helps us help our patients.
“One key aspect that perhaps underpins this issue is the still present separation between mental and physical health, between mind and body, Dr. Hong said in an interview. “Feeling sad or angry or anxious should become a fact of life, a characteristic of being human, just like catching a cold or breaking a leg.”
It’s a normalization that, perhaps more than anything else, can lead the way for improving physicians’ mental health outcomes while also improving them for the rest of society. When society can finally see the health and well-being of someone in both their psychological and physical status, some of the stigmas may dissipate, and perhaps more physicians’ lives can be saved.
A version of this article first appeared on Medscape.com.
As medical professionals, you’re continually exposed to overwork, burnout, stressful situations, and challenging ethical decisions. Yet seeking help for mental health care may be last on your to-do list – or completely off your radar.
That’s sad and dangerous, since the American College of Emergency Physicians said 300-400 physicians die by suicide each year, and the stigma keeps 69% of female physicians from seeking mental health care, according to a prepandemic study.
In the 2022 Medscape Physician Suicide Report, 11% of female doctors and 9% of male doctors said they have had thoughts of suicide, and 64% experienced colloquial depression (feeling down, sad, or blue).
What’s more, physicians are typically seen as strong and capable and are often put on a pedestal by loved ones, patients, and the public and thought of as superhuman. No wonder it isn’t easy when you need to take time away to decompress and treat your mental well-being.
“There is a real fear for physicians when it comes to getting mental health care,” said Emil Tsai, MD, PhD, MAS, professor at the department of psychiatry and behavioral sciences at the University of California, Los Angeles, and an internationally reputed scientist in neurosciences and brain disorders.
The fear, said Dr. Tsai, comes from the stigma of mental health issues, potential repercussions to employment, and conceivable medical board suspension or revocation of your medical license.
Dr. Tsai said in an interview that to combat anxiety about “punishment” that many physicians fear when seeking care for their mental health, we must allow physicians to take time away from their day-to-day patient care for respite and treatment without reprisal.
Since the medical profession is high stress and has a high depression and suicide rate, finding solutions is imperative. And physicians must feel supported enough to seek treatment when needed. So how can we normalize seeking mental health care among physicians?
Get honest about stress and burnout
The only way to normalize any behavior is to be open and candid, Dr. Tsai said in an interview. The mental health conversation must occur across the board, not just within the medical profession.
“The greatest thing we can do to try and lift the burden that we place on physicians is to be willing to talk and be honest about the stress that physicians deal with and the importance of everyone feeling free to seek treatment and rest to strengthen their mental health,” said Dr. Tsai.
The more we talk about mental health and its treatment, the more we lessen the stigma, said Dr. Tsai. That could be more employer-employee check-ins, counseling as part of physician wellness, and programs structured so as not to construe a penal system.
“Mental health in the medical profession is a big issue and one that has to be met with the same compassion and care as it should be for any patient. We have annual physical checkups. Why don’t we offer annual mental health checkups for all, physicians included?” asked Dr. Tsai.
Evaluate the workload
Elizabeth Lombardo, PhD, psychologist, coach, and global keynote speaker, thinks that health care employers should reexamine their physicians’ workloads to see if they’re contributing to mental health issues.
The conversation on mental health in the workplace shouldn’t be about whether a certain person can handle stressors that are “normal” for health care settings. Instead, workplace managers in health care institutions should redefine workloads to ensure that physicians aren’t too heavily burdened with responsibilities that can cause overwork, burnout, and mental health problems,” she said.
Lessen the stigma
Even when physicians want to seek help for their psychological struggles, they may be weary of how their colleagues would react if they knew.
Raffaello Antonino, MD, clinical director at Therapy Central in London, said several underlying fears may exist at a physician’s core that prevent them from seeking care – being seen as weak, being judged as unfit to practice medicine, and the notion that “something is wrong with them.”
Dr. Antonino said we need to understand that physicians face challenges of bereavement and trauma derived from losing patients and the inability to save someone’s life. “These issues can easily develop into an accumulation of difficult, unprocessed emotions, later arising in symptoms and signs of PTSD, anxiety, and depression.”
Education is the best way to end this stigma, just like with any form of prejudice and stereotypes. For instance, we know that health care professionals are at risk of developing burnout. So, educating physicians on the symptoms and management of burnout and its consequences and prevention strategies is a must.
“Imagine what could happen if there were regular opportunities to work through the day’s events before signing out from a shift. The idea that individual weekly therapy is the only way to relieve mental distress is false,” said Lori McIsaac Bewsher, MSW, RSW, a trauma therapist and owner of a trauma-focused mental health clinic in New Brunswick.
“There are ways of integrating individual care into our doctor’s offices and hospitals that can be brief, effective, and confidential. The best way to introduce these interventions is early and collectively; no one is immune to the potential impact of exposure to trauma. The earlier these interventions can be accessed, the better the outcomes for everyone,” she said.
Dr. Antonino suggests, perhaps in the future, organizations can have “burnout checks” or mental health wellness checks for physicians akin to how we also have quick examinations for various physical ailments. What if physicians regularly answered a 10-question mental health survey as part of a burnout or trauma prevention strategy?
“Theirs is a profession and an identity which is often linked with a sense of strength, leadership and [benevolent] power: adjectives, which on the surface one might see as incompatible with what instead, unfortunately, and wrongly, may be associated with mental health issues,” said Dr. Antonino.
Keep it private
When it comes to removing the stigma from mental health care and treatment for physicians, privacy is top of mind. There needs to be some form of privacy protection for physicians who seek professional help for mental health reasons. Dr. Lombardo said physicians need to have the choice to keep their mental health journeys private. “Ideally, normalization should mean openly conversing about mental health, but for physicians, it can be a matter of life or death for their career, so the choice to remain private is something that should be afforded to them.”
Along those lines, the American Medical Association is pushing for system changes in legislative and regulatory arenas to support the mental health of practicing physicians, residents, and medical students. The organization is also urging health systems and state medical licensing bodies to remove questions on their applications that ask about prior treatment for mental health conditions.
Among many programs across the country, the Foundation of the Pennsylvania Medical Society has also created a Physicians’ Health Program, which provides confidential assessment, counseling, and referral services for physicians with mental health concerns.
“All of these initiatives are important in helping to destigmatize mental health issues among physicians,” said Harold Hong, MD, a board-certified psychiatrist in Raleigh, N.C.
Hail the benefits of treatment
Dr. Hong said to continue to destigmatize mental health among physicians and normalize its treatment, we not only have to emphasize how attending to mental health has individual benefits but also how it helps us help our patients.
“One key aspect that perhaps underpins this issue is the still present separation between mental and physical health, between mind and body, Dr. Hong said in an interview. “Feeling sad or angry or anxious should become a fact of life, a characteristic of being human, just like catching a cold or breaking a leg.”
It’s a normalization that, perhaps more than anything else, can lead the way for improving physicians’ mental health outcomes while also improving them for the rest of society. When society can finally see the health and well-being of someone in both their psychological and physical status, some of the stigmas may dissipate, and perhaps more physicians’ lives can be saved.
A version of this article first appeared on Medscape.com.
As medical professionals, you’re continually exposed to overwork, burnout, stressful situations, and challenging ethical decisions. Yet seeking help for mental health care may be last on your to-do list – or completely off your radar.
That’s sad and dangerous, since the American College of Emergency Physicians said 300-400 physicians die by suicide each year, and the stigma keeps 69% of female physicians from seeking mental health care, according to a prepandemic study.
In the 2022 Medscape Physician Suicide Report, 11% of female doctors and 9% of male doctors said they have had thoughts of suicide, and 64% experienced colloquial depression (feeling down, sad, or blue).
What’s more, physicians are typically seen as strong and capable and are often put on a pedestal by loved ones, patients, and the public and thought of as superhuman. No wonder it isn’t easy when you need to take time away to decompress and treat your mental well-being.
“There is a real fear for physicians when it comes to getting mental health care,” said Emil Tsai, MD, PhD, MAS, professor at the department of psychiatry and behavioral sciences at the University of California, Los Angeles, and an internationally reputed scientist in neurosciences and brain disorders.
The fear, said Dr. Tsai, comes from the stigma of mental health issues, potential repercussions to employment, and conceivable medical board suspension or revocation of your medical license.
Dr. Tsai said in an interview that to combat anxiety about “punishment” that many physicians fear when seeking care for their mental health, we must allow physicians to take time away from their day-to-day patient care for respite and treatment without reprisal.
Since the medical profession is high stress and has a high depression and suicide rate, finding solutions is imperative. And physicians must feel supported enough to seek treatment when needed. So how can we normalize seeking mental health care among physicians?
Get honest about stress and burnout
The only way to normalize any behavior is to be open and candid, Dr. Tsai said in an interview. The mental health conversation must occur across the board, not just within the medical profession.
“The greatest thing we can do to try and lift the burden that we place on physicians is to be willing to talk and be honest about the stress that physicians deal with and the importance of everyone feeling free to seek treatment and rest to strengthen their mental health,” said Dr. Tsai.
The more we talk about mental health and its treatment, the more we lessen the stigma, said Dr. Tsai. That could be more employer-employee check-ins, counseling as part of physician wellness, and programs structured so as not to construe a penal system.
“Mental health in the medical profession is a big issue and one that has to be met with the same compassion and care as it should be for any patient. We have annual physical checkups. Why don’t we offer annual mental health checkups for all, physicians included?” asked Dr. Tsai.
Evaluate the workload
Elizabeth Lombardo, PhD, psychologist, coach, and global keynote speaker, thinks that health care employers should reexamine their physicians’ workloads to see if they’re contributing to mental health issues.
The conversation on mental health in the workplace shouldn’t be about whether a certain person can handle stressors that are “normal” for health care settings. Instead, workplace managers in health care institutions should redefine workloads to ensure that physicians aren’t too heavily burdened with responsibilities that can cause overwork, burnout, and mental health problems,” she said.
Lessen the stigma
Even when physicians want to seek help for their psychological struggles, they may be weary of how their colleagues would react if they knew.
Raffaello Antonino, MD, clinical director at Therapy Central in London, said several underlying fears may exist at a physician’s core that prevent them from seeking care – being seen as weak, being judged as unfit to practice medicine, and the notion that “something is wrong with them.”
Dr. Antonino said we need to understand that physicians face challenges of bereavement and trauma derived from losing patients and the inability to save someone’s life. “These issues can easily develop into an accumulation of difficult, unprocessed emotions, later arising in symptoms and signs of PTSD, anxiety, and depression.”
Education is the best way to end this stigma, just like with any form of prejudice and stereotypes. For instance, we know that health care professionals are at risk of developing burnout. So, educating physicians on the symptoms and management of burnout and its consequences and prevention strategies is a must.
“Imagine what could happen if there were regular opportunities to work through the day’s events before signing out from a shift. The idea that individual weekly therapy is the only way to relieve mental distress is false,” said Lori McIsaac Bewsher, MSW, RSW, a trauma therapist and owner of a trauma-focused mental health clinic in New Brunswick.
“There are ways of integrating individual care into our doctor’s offices and hospitals that can be brief, effective, and confidential. The best way to introduce these interventions is early and collectively; no one is immune to the potential impact of exposure to trauma. The earlier these interventions can be accessed, the better the outcomes for everyone,” she said.
Dr. Antonino suggests, perhaps in the future, organizations can have “burnout checks” or mental health wellness checks for physicians akin to how we also have quick examinations for various physical ailments. What if physicians regularly answered a 10-question mental health survey as part of a burnout or trauma prevention strategy?
“Theirs is a profession and an identity which is often linked with a sense of strength, leadership and [benevolent] power: adjectives, which on the surface one might see as incompatible with what instead, unfortunately, and wrongly, may be associated with mental health issues,” said Dr. Antonino.
Keep it private
When it comes to removing the stigma from mental health care and treatment for physicians, privacy is top of mind. There needs to be some form of privacy protection for physicians who seek professional help for mental health reasons. Dr. Lombardo said physicians need to have the choice to keep their mental health journeys private. “Ideally, normalization should mean openly conversing about mental health, but for physicians, it can be a matter of life or death for their career, so the choice to remain private is something that should be afforded to them.”
Along those lines, the American Medical Association is pushing for system changes in legislative and regulatory arenas to support the mental health of practicing physicians, residents, and medical students. The organization is also urging health systems and state medical licensing bodies to remove questions on their applications that ask about prior treatment for mental health conditions.
Among many programs across the country, the Foundation of the Pennsylvania Medical Society has also created a Physicians’ Health Program, which provides confidential assessment, counseling, and referral services for physicians with mental health concerns.
“All of these initiatives are important in helping to destigmatize mental health issues among physicians,” said Harold Hong, MD, a board-certified psychiatrist in Raleigh, N.C.
Hail the benefits of treatment
Dr. Hong said to continue to destigmatize mental health among physicians and normalize its treatment, we not only have to emphasize how attending to mental health has individual benefits but also how it helps us help our patients.
“One key aspect that perhaps underpins this issue is the still present separation between mental and physical health, between mind and body, Dr. Hong said in an interview. “Feeling sad or angry or anxious should become a fact of life, a characteristic of being human, just like catching a cold or breaking a leg.”
It’s a normalization that, perhaps more than anything else, can lead the way for improving physicians’ mental health outcomes while also improving them for the rest of society. When society can finally see the health and well-being of someone in both their psychological and physical status, some of the stigmas may dissipate, and perhaps more physicians’ lives can be saved.
A version of this article first appeared on Medscape.com.
Med students dismayed that residency match process won’t change
– mostly medical students, residents, and fellows – who supported the change.
The program’s decision comes after nearly 3 months of feedback from the public, medical students, and education community. Although about 60% of public respondents believed the change could reduce stress and allow students more time for momentous career decisions, the program’s board of directors decided the disadvantages were “of greater consequence,” according to a Oct. 28 statement.
Those disadvantages included introducing application or interview behaviors that could increase students’ stress; potentially identifying partially matched or unmatched applicants, which could lead to bias; and extending the match process time for those applicants.
In addition, members of 12 medical education and student organizations raised other concerns, such as the proposed change not addressing high application numbers, according to the statement. NRMP has reported record numbers of applicants over the past few years, typically with more applicants than available program slots.
“While the testimony gave nod to the positive aspects of the proposal ... there was substantially more concern voiced about the potential negative consequences identified in the public comments,” NRMP President and CEO Donna L. Lamb, DHSc, MBA, BSN, told this news organization. Some of those issues could not be addressed without further study, so the board decided not to proceed with the proposal, she explained.
The proposal would have separated the Main Residency Match into two phases and replaced the Supplemental Offer and Acceptance Program (SOAP), in which unmatched or partially matched applicants apply for unfilled residency positions. Under the proposed change, each phase would have operated the same way, from rank order lists and using a matching algorithm to a pair of Match Days instead of a single day.
The two-phase process would have given students who didn’t match more time to carefully weigh residency programs – they can apply to up to 45 placements as part of SOAP – that will guide their career path for the next few years, PGY-1 intern Asim A., who asked not to be identified further, told this news organization. The alternative is a hasty decision once students learn which residency spots are available, he added. “Applicants would have breathing room to make a more informed decision.”
Asim, who is Canadian, said he is participating in a transitional year in internal medicine in the hopes of being matched into internal medicine or psychiatry. He said Canada’s two-phase match is a “lot less stressful” than the U.S. system.
Meanwhile, students on Reddit’s medical school community also questioned NRMP’s decision.
“A significant majority of those surveyed thought it would be beneficial. But NRMP decides to not go through with it,” one Reddit user wrote. Another posted, “The one thing that could have improved the match and they chose not to do it.”
Others supported the decision to retain a 1-day match.
“I think this was the right call,” Bryan Carmody, MD, an outspoken medical education blogger, tweeted after learning of NRMP’s decision. Dr. Carmody, a pediatric nephrologist, previously expressed to this news organization misgivings about whether the two-phase match would make it difficult for programs to thoroughly review candidates and vice versa. He was concerned that it would compress the interview season and pressure programs to rapidly review applicants and conduct interviews.
More than 8,000 people responded to the public survey that began in August and ran for a month. Nearly two-thirds of the respondents (60%) were students, residents, or fellows. About 25% included faculty, program directors, and staff. Among the survey findings, respondents were equally divided between whether the two-phase match would be modestly advantageous (30%) or significantly advantageous (30%) compared to 20% who viewed it as modestly or significantly disadvantageous.
The NRMP said it would continue engaging with the community through focus groups and other means to improve the match experience and transition to residency.
“It is important to remember that a proposal is just that,” Dr. Lamb told this news orgnization, “an opportunity to discuss the pros and cons of an idea or framework ... and to mitigate unwanted consequences determined to be detrimental to learners and programs.”
The NRMP will involve the community in future discussions “to continue to give learners a voice,” she said.
A version of this article first appeared on Medscape.com.
– mostly medical students, residents, and fellows – who supported the change.
The program’s decision comes after nearly 3 months of feedback from the public, medical students, and education community. Although about 60% of public respondents believed the change could reduce stress and allow students more time for momentous career decisions, the program’s board of directors decided the disadvantages were “of greater consequence,” according to a Oct. 28 statement.
Those disadvantages included introducing application or interview behaviors that could increase students’ stress; potentially identifying partially matched or unmatched applicants, which could lead to bias; and extending the match process time for those applicants.
In addition, members of 12 medical education and student organizations raised other concerns, such as the proposed change not addressing high application numbers, according to the statement. NRMP has reported record numbers of applicants over the past few years, typically with more applicants than available program slots.
“While the testimony gave nod to the positive aspects of the proposal ... there was substantially more concern voiced about the potential negative consequences identified in the public comments,” NRMP President and CEO Donna L. Lamb, DHSc, MBA, BSN, told this news organization. Some of those issues could not be addressed without further study, so the board decided not to proceed with the proposal, she explained.
The proposal would have separated the Main Residency Match into two phases and replaced the Supplemental Offer and Acceptance Program (SOAP), in which unmatched or partially matched applicants apply for unfilled residency positions. Under the proposed change, each phase would have operated the same way, from rank order lists and using a matching algorithm to a pair of Match Days instead of a single day.
The two-phase process would have given students who didn’t match more time to carefully weigh residency programs – they can apply to up to 45 placements as part of SOAP – that will guide their career path for the next few years, PGY-1 intern Asim A., who asked not to be identified further, told this news organization. The alternative is a hasty decision once students learn which residency spots are available, he added. “Applicants would have breathing room to make a more informed decision.”
Asim, who is Canadian, said he is participating in a transitional year in internal medicine in the hopes of being matched into internal medicine or psychiatry. He said Canada’s two-phase match is a “lot less stressful” than the U.S. system.
Meanwhile, students on Reddit’s medical school community also questioned NRMP’s decision.
“A significant majority of those surveyed thought it would be beneficial. But NRMP decides to not go through with it,” one Reddit user wrote. Another posted, “The one thing that could have improved the match and they chose not to do it.”
Others supported the decision to retain a 1-day match.
“I think this was the right call,” Bryan Carmody, MD, an outspoken medical education blogger, tweeted after learning of NRMP’s decision. Dr. Carmody, a pediatric nephrologist, previously expressed to this news organization misgivings about whether the two-phase match would make it difficult for programs to thoroughly review candidates and vice versa. He was concerned that it would compress the interview season and pressure programs to rapidly review applicants and conduct interviews.
More than 8,000 people responded to the public survey that began in August and ran for a month. Nearly two-thirds of the respondents (60%) were students, residents, or fellows. About 25% included faculty, program directors, and staff. Among the survey findings, respondents were equally divided between whether the two-phase match would be modestly advantageous (30%) or significantly advantageous (30%) compared to 20% who viewed it as modestly or significantly disadvantageous.
The NRMP said it would continue engaging with the community through focus groups and other means to improve the match experience and transition to residency.
“It is important to remember that a proposal is just that,” Dr. Lamb told this news orgnization, “an opportunity to discuss the pros and cons of an idea or framework ... and to mitigate unwanted consequences determined to be detrimental to learners and programs.”
The NRMP will involve the community in future discussions “to continue to give learners a voice,” she said.
A version of this article first appeared on Medscape.com.
– mostly medical students, residents, and fellows – who supported the change.
The program’s decision comes after nearly 3 months of feedback from the public, medical students, and education community. Although about 60% of public respondents believed the change could reduce stress and allow students more time for momentous career decisions, the program’s board of directors decided the disadvantages were “of greater consequence,” according to a Oct. 28 statement.
Those disadvantages included introducing application or interview behaviors that could increase students’ stress; potentially identifying partially matched or unmatched applicants, which could lead to bias; and extending the match process time for those applicants.
In addition, members of 12 medical education and student organizations raised other concerns, such as the proposed change not addressing high application numbers, according to the statement. NRMP has reported record numbers of applicants over the past few years, typically with more applicants than available program slots.
“While the testimony gave nod to the positive aspects of the proposal ... there was substantially more concern voiced about the potential negative consequences identified in the public comments,” NRMP President and CEO Donna L. Lamb, DHSc, MBA, BSN, told this news organization. Some of those issues could not be addressed without further study, so the board decided not to proceed with the proposal, she explained.
The proposal would have separated the Main Residency Match into two phases and replaced the Supplemental Offer and Acceptance Program (SOAP), in which unmatched or partially matched applicants apply for unfilled residency positions. Under the proposed change, each phase would have operated the same way, from rank order lists and using a matching algorithm to a pair of Match Days instead of a single day.
The two-phase process would have given students who didn’t match more time to carefully weigh residency programs – they can apply to up to 45 placements as part of SOAP – that will guide their career path for the next few years, PGY-1 intern Asim A., who asked not to be identified further, told this news organization. The alternative is a hasty decision once students learn which residency spots are available, he added. “Applicants would have breathing room to make a more informed decision.”
Asim, who is Canadian, said he is participating in a transitional year in internal medicine in the hopes of being matched into internal medicine or psychiatry. He said Canada’s two-phase match is a “lot less stressful” than the U.S. system.
Meanwhile, students on Reddit’s medical school community also questioned NRMP’s decision.
“A significant majority of those surveyed thought it would be beneficial. But NRMP decides to not go through with it,” one Reddit user wrote. Another posted, “The one thing that could have improved the match and they chose not to do it.”
Others supported the decision to retain a 1-day match.
“I think this was the right call,” Bryan Carmody, MD, an outspoken medical education blogger, tweeted after learning of NRMP’s decision. Dr. Carmody, a pediatric nephrologist, previously expressed to this news organization misgivings about whether the two-phase match would make it difficult for programs to thoroughly review candidates and vice versa. He was concerned that it would compress the interview season and pressure programs to rapidly review applicants and conduct interviews.
More than 8,000 people responded to the public survey that began in August and ran for a month. Nearly two-thirds of the respondents (60%) were students, residents, or fellows. About 25% included faculty, program directors, and staff. Among the survey findings, respondents were equally divided between whether the two-phase match would be modestly advantageous (30%) or significantly advantageous (30%) compared to 20% who viewed it as modestly or significantly disadvantageous.
The NRMP said it would continue engaging with the community through focus groups and other means to improve the match experience and transition to residency.
“It is important to remember that a proposal is just that,” Dr. Lamb told this news orgnization, “an opportunity to discuss the pros and cons of an idea or framework ... and to mitigate unwanted consequences determined to be detrimental to learners and programs.”
The NRMP will involve the community in future discussions “to continue to give learners a voice,” she said.
A version of this article first appeared on Medscape.com.
Lego introduces first character with vitiligo
The
The character appears with the customizable array of players to assemble for a table football team.
It’s the latest representation of the disease as toymakers diversify their lines.
In May 2022, Mattel released a Ken doll with vitiligo after a Barbie with vitiligo was released in 2020. Rainbow High and other toy makers also have character versions.
The Lego addition follows a big summer medically for vitiligo as the first treatment was approved for repigmentation. In July, a cream formulation of ruxolitinib (Opzelura), a Janus kinase inhibitor, became the first repigmentation treatment approved by the Food and Drug Administration for nonsegmental vitiligo, the most common form of the disease.
Vitiligo is estimated to affect 1.9 million–2.8 million adults in the United States and more than 100 million people worldwide. It cuts across races and genders and can be psychologically painful for many who live with it.
John E. Harris, MD, director of the Vitiligo Clinic and Research Center at the University of Massachusetts, Worcester, wrote about the Lego character in his blog “Speaking of Vitiligo ...” saying: “I could not be more excited. This new minifigure also serves as a way to educate both children and adults who are not familiar with vitiligo about the disease.”
He noted that until recently vitiligo representation in kids’ toys has been limited. “By adding diversity such as representations of vitiligo in toys, it can help remove stigmas associated with vitiligo and give children more options that they can relate to.”
Erika Page of Richmond, Va., who founded and edits the vitiligo blog “Living Dappled,” told this news organization she was thrilled to see the new Lego character.
“Growing up I didn’t know anyone who looked like me, let alone a toy or a character,” she said. The message the representations send is important not just for the kids but for the parents of kids with vitiligo who want to help their kids in any way they can.
Ms. Page was diagnosed with vitiligo at age 7 and struggled emotionally in her high school and college years when she often looked in the mirror, saw “giraffe-like” spots, and cried. Over time she lost 100% of her pigment to the condition and today at age 33, lives with universal vitiligo or overall very pale skin.
She founded the Living Dappled blog 6 years ago to help people with the disease feel less alone. The Lego character will also help with that, she said.
“Growing up with vitiligo was so isolating and you felt so different,” Ms. Page said. “Today we see billboards and models and dolls and now Legos that look like us. I hope this is a first of many to come for Lego.”
Dr. Harris and Ms. Page declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The
The character appears with the customizable array of players to assemble for a table football team.
It’s the latest representation of the disease as toymakers diversify their lines.
In May 2022, Mattel released a Ken doll with vitiligo after a Barbie with vitiligo was released in 2020. Rainbow High and other toy makers also have character versions.
The Lego addition follows a big summer medically for vitiligo as the first treatment was approved for repigmentation. In July, a cream formulation of ruxolitinib (Opzelura), a Janus kinase inhibitor, became the first repigmentation treatment approved by the Food and Drug Administration for nonsegmental vitiligo, the most common form of the disease.
Vitiligo is estimated to affect 1.9 million–2.8 million adults in the United States and more than 100 million people worldwide. It cuts across races and genders and can be psychologically painful for many who live with it.
John E. Harris, MD, director of the Vitiligo Clinic and Research Center at the University of Massachusetts, Worcester, wrote about the Lego character in his blog “Speaking of Vitiligo ...” saying: “I could not be more excited. This new minifigure also serves as a way to educate both children and adults who are not familiar with vitiligo about the disease.”
He noted that until recently vitiligo representation in kids’ toys has been limited. “By adding diversity such as representations of vitiligo in toys, it can help remove stigmas associated with vitiligo and give children more options that they can relate to.”
Erika Page of Richmond, Va., who founded and edits the vitiligo blog “Living Dappled,” told this news organization she was thrilled to see the new Lego character.
“Growing up I didn’t know anyone who looked like me, let alone a toy or a character,” she said. The message the representations send is important not just for the kids but for the parents of kids with vitiligo who want to help their kids in any way they can.
Ms. Page was diagnosed with vitiligo at age 7 and struggled emotionally in her high school and college years when she often looked in the mirror, saw “giraffe-like” spots, and cried. Over time she lost 100% of her pigment to the condition and today at age 33, lives with universal vitiligo or overall very pale skin.
She founded the Living Dappled blog 6 years ago to help people with the disease feel less alone. The Lego character will also help with that, she said.
“Growing up with vitiligo was so isolating and you felt so different,” Ms. Page said. “Today we see billboards and models and dolls and now Legos that look like us. I hope this is a first of many to come for Lego.”
Dr. Harris and Ms. Page declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The
The character appears with the customizable array of players to assemble for a table football team.
It’s the latest representation of the disease as toymakers diversify their lines.
In May 2022, Mattel released a Ken doll with vitiligo after a Barbie with vitiligo was released in 2020. Rainbow High and other toy makers also have character versions.
The Lego addition follows a big summer medically for vitiligo as the first treatment was approved for repigmentation. In July, a cream formulation of ruxolitinib (Opzelura), a Janus kinase inhibitor, became the first repigmentation treatment approved by the Food and Drug Administration for nonsegmental vitiligo, the most common form of the disease.
Vitiligo is estimated to affect 1.9 million–2.8 million adults in the United States and more than 100 million people worldwide. It cuts across races and genders and can be psychologically painful for many who live with it.
John E. Harris, MD, director of the Vitiligo Clinic and Research Center at the University of Massachusetts, Worcester, wrote about the Lego character in his blog “Speaking of Vitiligo ...” saying: “I could not be more excited. This new minifigure also serves as a way to educate both children and adults who are not familiar with vitiligo about the disease.”
He noted that until recently vitiligo representation in kids’ toys has been limited. “By adding diversity such as representations of vitiligo in toys, it can help remove stigmas associated with vitiligo and give children more options that they can relate to.”
Erika Page of Richmond, Va., who founded and edits the vitiligo blog “Living Dappled,” told this news organization she was thrilled to see the new Lego character.
“Growing up I didn’t know anyone who looked like me, let alone a toy or a character,” she said. The message the representations send is important not just for the kids but for the parents of kids with vitiligo who want to help their kids in any way they can.
Ms. Page was diagnosed with vitiligo at age 7 and struggled emotionally in her high school and college years when she often looked in the mirror, saw “giraffe-like” spots, and cried. Over time she lost 100% of her pigment to the condition and today at age 33, lives with universal vitiligo or overall very pale skin.
She founded the Living Dappled blog 6 years ago to help people with the disease feel less alone. The Lego character will also help with that, she said.
“Growing up with vitiligo was so isolating and you felt so different,” Ms. Page said. “Today we see billboards and models and dolls and now Legos that look like us. I hope this is a first of many to come for Lego.”
Dr. Harris and Ms. Page declared no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Practical pearls guide treatment of psoriasis in tricky areas
LAS VEGAS – With the right regimen, a majority of patients with psoriasis can achieve at least a Psoriasis Area and Severity Index (PASI) 75 score, Jennifer Soung, MD, said in a presentation at MedscapeLive’s annual Las Vegas Dermatology Seminar.
The array of treatment options includes mainstay topicals, new nonsteroidals, traditional oral systemics, new oral systemics, biologics, and light therapy, said Dr. Soung, director of clinical research at Harbor-UCLA Medical Center, Santa Ana, Calif. However, she said.
For these areas, make sure the diagnosis of psoriasis is correct, to avoid wasting time on the wrong course of treatment, Dr. Soung emphasized.
Scalp strategies
The scalp is often the first area of the body affected by psoriasis, and patients with severe scalp psoriasis may have minimal plaques on the body, Dr. Soung said. However, a differential diagnosis should include seborrheic dermatitis, she noted.
For most cases of scalp psoriasis, “start with localized topical treatment,” such as vitamin D and corticosteroid combination therapy, or excimer laser, Dr. Soung advised.
Systemic treatments with demonstrated effectiveness on scalp psoriasis in post hoc analyses of patients with moderate to severe plaque psoriasis include adalimumab, etanercept, ixekizumab, and secukinumab. Studies specifically focused on treatment of scalp psoriasis have shown success with secukinumab and apremilast, she noted.
Roflumilast foam, 0.3%, is in development and is an emerging option for scalp psoriasis. (A cream formulation of roflumilast, a topical phosphodiesterase 4 inhibitor, was approved for treatment of plaque psoriasis in July 2022.) A phase 2b study of roflumilast foam showed that approximately one-third of patients with scalp psoriasis achieved a status of clear based on scalp-investigator global assessment, compared with approximately 3% of those on vehicle, and similar results were seen in a recently completed phase 3 trial for scalp and body psoriasis, she added.
Facial psoriasis
Patients with facial psoriasis tend to be younger, and they may have more severe disease overall, Dr. Soung said. Given the sensitivity of facial skin, “it is nice to have a nonsteroidal option,” she noted. Current novel nonsteroidal therapies include a cream formulation of tapinarof, an aryl hydrocarbon receptor agonist, which was approved earlier this year for plaque psoriasis in adults, and roflumilast cream. Vitamin D and topical calcineurin inhibitors are options as well, she said.
Intertriginous tricks
Intertriginous (inverse) psoriasis is distinct from other areas in that the plaques are usually smooth and well-demarcated, with little or no scaling, Dr. Soung said. Erosions or signs of maceration may be present. The prevalence of inverse psoriasis is approximately 30%, but the prevalence on external genitalia is 80%, she noted. For inverse psoriasis, topical corticosteroids can result in adverse events such as poor wound healing and skin fragility, and some patients resist the idea of a steroid and don’t adhere to the medication, she added. Dr. Soung recommended topical corticosteroids for the short term, and topical calcineurin inhibitors or calcipotriol for the long term.
New topical options for inverse psoriasis include tapinarof and roflumilast, Dr. Soung said. For tapinarof, the phase 3 PSOARING program included assessment of tolerability in sensitive skin areas and found little to no irritation. Similarly, treatment with roflumilast cream was effective and well tolerated by patients with intertriginous plaque psoriasis in the DERMIS-1 and DERMIS-2 studies, she said.
Genital psoriasis
Ask patients with psoriasis about genital psoriasis, because they often are too embarrassed to provide that information on their own, said Dr. Soung. In fact, 63% of patients with psoriasis report ever experiencing genital psoriasis, but it often goes undiagnosed and undertreated, which has a significant impact on patient quality of life and sexual health.
A differential diagnosis of genital psoriasis should include dermatitis, tinea or candidiasis, and even squamous cell carcinoma, she noted. Other considerations include fixed drug eruption, lichen nitidus, lichen sclerosus, and scabies.
Dr. Soung’s first line of treatment for genital psoriasis is low-potency topical corticosteroids for 2-4 weeks. If long-term topical therapy is needed, alternatives include calcineurin inhibitors and vitamin D analogs, she said. The new topicals roflumilast and tapinarof are options as well, she said.
For those patients with severe and extensive genital psoriasis, consider systemic therapy, possibly with ixekizumab or secukinumab, she added. Patients with moderate to severe genital psoriasis treated with apremilast have shown improvement at week 16, in an ongoing clinical trial, she noted.
Palmoplantar involvement
For patients with palmar plantar psoriasis, “don’t underestimate the impact on quality of life,” said Dr. Soung. Approximately 12%-16% of patients with psoriasis report palmoplantar involvement, she noted.
Palmoplantar psoriasis can be stubborn, and many patients will need combination therapy with topicals and systemics, she said. “I am very curious about how well our new topical nonsteroidals will work in these areas,” she added.
Dr. Soung starts patients with palmoplantar psoriasis with a “potent to super-potent” twice daily topical corticosteroid, with or without occlusion. Her first-line systemic therapy is acitretin, 10-50 mg daily. However, keep in mind that acitretin is contraindicated in pregnancy, and also may cause side effects including cheilitis, alopecia, and peeling skin, she cautioned.
During the question and answer session, Dr. Soung was asked whether she routinely biopsies patients with palmoplantar psoriasis. “Not always,” was her answer. Instead, she looks for clues elsewhere on the body to confirm the diagnosis.
Nail know-how
Approximately 23%-27% of patients with psoriasis experience nail involvement, said Dr. Soung. Nail psoriasis can appear on the nail plate as pitting, onycholysis, or subungual hyperkeratosis, or in the nail bed as splinter hemorrhages or oil spots, she said.
For patients with psoriasis of the nails only, Dr. Soung described the use of high-potency topical corticosteroids, with or without calcipotriol. In her experience, she said that intralesional steroids for nail psoriasis are torturous to patients. For patients who have failed topical therapy or have psoriasis in other areas, with or without psoriatic arthritis, she advised the use of either IL-17 antagonists (secukinumab, ixekizumab, brodalumab) or IL-23 antagonists (risankizumab, guselkumab).
Dr. Soung disclosed serving as a consultant or advisor for Arcutis, Bristol Myers Squibb Company, Dermavant, and Novartis. She also disclosed serving as a speaker or member of the speakers’ bureau for AbbVie, Amgen, Arcutis, Bristol Myers Squibb Company, Celgene, Leo Pharma, Eli Lilly, Novartis, Ortho Dermatologics, Pfizer, Regeneron, and Sanofi, as well as research funding from AbbVie, Amgen, Arcutis, Castle Biosciences, Dermavant, KoBio, Kyowa Kirin, Leo Pharma, Eli Lilly, Novartis, Pfizer, and UCB.
MedscapeLive and this news organization are owned by the same parent company.
LAS VEGAS – With the right regimen, a majority of patients with psoriasis can achieve at least a Psoriasis Area and Severity Index (PASI) 75 score, Jennifer Soung, MD, said in a presentation at MedscapeLive’s annual Las Vegas Dermatology Seminar.
The array of treatment options includes mainstay topicals, new nonsteroidals, traditional oral systemics, new oral systemics, biologics, and light therapy, said Dr. Soung, director of clinical research at Harbor-UCLA Medical Center, Santa Ana, Calif. However, she said.
For these areas, make sure the diagnosis of psoriasis is correct, to avoid wasting time on the wrong course of treatment, Dr. Soung emphasized.
Scalp strategies
The scalp is often the first area of the body affected by psoriasis, and patients with severe scalp psoriasis may have minimal plaques on the body, Dr. Soung said. However, a differential diagnosis should include seborrheic dermatitis, she noted.
For most cases of scalp psoriasis, “start with localized topical treatment,” such as vitamin D and corticosteroid combination therapy, or excimer laser, Dr. Soung advised.
Systemic treatments with demonstrated effectiveness on scalp psoriasis in post hoc analyses of patients with moderate to severe plaque psoriasis include adalimumab, etanercept, ixekizumab, and secukinumab. Studies specifically focused on treatment of scalp psoriasis have shown success with secukinumab and apremilast, she noted.
Roflumilast foam, 0.3%, is in development and is an emerging option for scalp psoriasis. (A cream formulation of roflumilast, a topical phosphodiesterase 4 inhibitor, was approved for treatment of plaque psoriasis in July 2022.) A phase 2b study of roflumilast foam showed that approximately one-third of patients with scalp psoriasis achieved a status of clear based on scalp-investigator global assessment, compared with approximately 3% of those on vehicle, and similar results were seen in a recently completed phase 3 trial for scalp and body psoriasis, she added.
Facial psoriasis
Patients with facial psoriasis tend to be younger, and they may have more severe disease overall, Dr. Soung said. Given the sensitivity of facial skin, “it is nice to have a nonsteroidal option,” she noted. Current novel nonsteroidal therapies include a cream formulation of tapinarof, an aryl hydrocarbon receptor agonist, which was approved earlier this year for plaque psoriasis in adults, and roflumilast cream. Vitamin D and topical calcineurin inhibitors are options as well, she said.
Intertriginous tricks
Intertriginous (inverse) psoriasis is distinct from other areas in that the plaques are usually smooth and well-demarcated, with little or no scaling, Dr. Soung said. Erosions or signs of maceration may be present. The prevalence of inverse psoriasis is approximately 30%, but the prevalence on external genitalia is 80%, she noted. For inverse psoriasis, topical corticosteroids can result in adverse events such as poor wound healing and skin fragility, and some patients resist the idea of a steroid and don’t adhere to the medication, she added. Dr. Soung recommended topical corticosteroids for the short term, and topical calcineurin inhibitors or calcipotriol for the long term.
New topical options for inverse psoriasis include tapinarof and roflumilast, Dr. Soung said. For tapinarof, the phase 3 PSOARING program included assessment of tolerability in sensitive skin areas and found little to no irritation. Similarly, treatment with roflumilast cream was effective and well tolerated by patients with intertriginous plaque psoriasis in the DERMIS-1 and DERMIS-2 studies, she said.
Genital psoriasis
Ask patients with psoriasis about genital psoriasis, because they often are too embarrassed to provide that information on their own, said Dr. Soung. In fact, 63% of patients with psoriasis report ever experiencing genital psoriasis, but it often goes undiagnosed and undertreated, which has a significant impact on patient quality of life and sexual health.
A differential diagnosis of genital psoriasis should include dermatitis, tinea or candidiasis, and even squamous cell carcinoma, she noted. Other considerations include fixed drug eruption, lichen nitidus, lichen sclerosus, and scabies.
Dr. Soung’s first line of treatment for genital psoriasis is low-potency topical corticosteroids for 2-4 weeks. If long-term topical therapy is needed, alternatives include calcineurin inhibitors and vitamin D analogs, she said. The new topicals roflumilast and tapinarof are options as well, she said.
For those patients with severe and extensive genital psoriasis, consider systemic therapy, possibly with ixekizumab or secukinumab, she added. Patients with moderate to severe genital psoriasis treated with apremilast have shown improvement at week 16, in an ongoing clinical trial, she noted.
Palmoplantar involvement
For patients with palmar plantar psoriasis, “don’t underestimate the impact on quality of life,” said Dr. Soung. Approximately 12%-16% of patients with psoriasis report palmoplantar involvement, she noted.
Palmoplantar psoriasis can be stubborn, and many patients will need combination therapy with topicals and systemics, she said. “I am very curious about how well our new topical nonsteroidals will work in these areas,” she added.
Dr. Soung starts patients with palmoplantar psoriasis with a “potent to super-potent” twice daily topical corticosteroid, with or without occlusion. Her first-line systemic therapy is acitretin, 10-50 mg daily. However, keep in mind that acitretin is contraindicated in pregnancy, and also may cause side effects including cheilitis, alopecia, and peeling skin, she cautioned.
During the question and answer session, Dr. Soung was asked whether she routinely biopsies patients with palmoplantar psoriasis. “Not always,” was her answer. Instead, she looks for clues elsewhere on the body to confirm the diagnosis.
Nail know-how
Approximately 23%-27% of patients with psoriasis experience nail involvement, said Dr. Soung. Nail psoriasis can appear on the nail plate as pitting, onycholysis, or subungual hyperkeratosis, or in the nail bed as splinter hemorrhages or oil spots, she said.
For patients with psoriasis of the nails only, Dr. Soung described the use of high-potency topical corticosteroids, with or without calcipotriol. In her experience, she said that intralesional steroids for nail psoriasis are torturous to patients. For patients who have failed topical therapy or have psoriasis in other areas, with or without psoriatic arthritis, she advised the use of either IL-17 antagonists (secukinumab, ixekizumab, brodalumab) or IL-23 antagonists (risankizumab, guselkumab).
Dr. Soung disclosed serving as a consultant or advisor for Arcutis, Bristol Myers Squibb Company, Dermavant, and Novartis. She also disclosed serving as a speaker or member of the speakers’ bureau for AbbVie, Amgen, Arcutis, Bristol Myers Squibb Company, Celgene, Leo Pharma, Eli Lilly, Novartis, Ortho Dermatologics, Pfizer, Regeneron, and Sanofi, as well as research funding from AbbVie, Amgen, Arcutis, Castle Biosciences, Dermavant, KoBio, Kyowa Kirin, Leo Pharma, Eli Lilly, Novartis, Pfizer, and UCB.
MedscapeLive and this news organization are owned by the same parent company.
LAS VEGAS – With the right regimen, a majority of patients with psoriasis can achieve at least a Psoriasis Area and Severity Index (PASI) 75 score, Jennifer Soung, MD, said in a presentation at MedscapeLive’s annual Las Vegas Dermatology Seminar.
The array of treatment options includes mainstay topicals, new nonsteroidals, traditional oral systemics, new oral systemics, biologics, and light therapy, said Dr. Soung, director of clinical research at Harbor-UCLA Medical Center, Santa Ana, Calif. However, she said.
For these areas, make sure the diagnosis of psoriasis is correct, to avoid wasting time on the wrong course of treatment, Dr. Soung emphasized.
Scalp strategies
The scalp is often the first area of the body affected by psoriasis, and patients with severe scalp psoriasis may have minimal plaques on the body, Dr. Soung said. However, a differential diagnosis should include seborrheic dermatitis, she noted.
For most cases of scalp psoriasis, “start with localized topical treatment,” such as vitamin D and corticosteroid combination therapy, or excimer laser, Dr. Soung advised.
Systemic treatments with demonstrated effectiveness on scalp psoriasis in post hoc analyses of patients with moderate to severe plaque psoriasis include adalimumab, etanercept, ixekizumab, and secukinumab. Studies specifically focused on treatment of scalp psoriasis have shown success with secukinumab and apremilast, she noted.
Roflumilast foam, 0.3%, is in development and is an emerging option for scalp psoriasis. (A cream formulation of roflumilast, a topical phosphodiesterase 4 inhibitor, was approved for treatment of plaque psoriasis in July 2022.) A phase 2b study of roflumilast foam showed that approximately one-third of patients with scalp psoriasis achieved a status of clear based on scalp-investigator global assessment, compared with approximately 3% of those on vehicle, and similar results were seen in a recently completed phase 3 trial for scalp and body psoriasis, she added.
Facial psoriasis
Patients with facial psoriasis tend to be younger, and they may have more severe disease overall, Dr. Soung said. Given the sensitivity of facial skin, “it is nice to have a nonsteroidal option,” she noted. Current novel nonsteroidal therapies include a cream formulation of tapinarof, an aryl hydrocarbon receptor agonist, which was approved earlier this year for plaque psoriasis in adults, and roflumilast cream. Vitamin D and topical calcineurin inhibitors are options as well, she said.
Intertriginous tricks
Intertriginous (inverse) psoriasis is distinct from other areas in that the plaques are usually smooth and well-demarcated, with little or no scaling, Dr. Soung said. Erosions or signs of maceration may be present. The prevalence of inverse psoriasis is approximately 30%, but the prevalence on external genitalia is 80%, she noted. For inverse psoriasis, topical corticosteroids can result in adverse events such as poor wound healing and skin fragility, and some patients resist the idea of a steroid and don’t adhere to the medication, she added. Dr. Soung recommended topical corticosteroids for the short term, and topical calcineurin inhibitors or calcipotriol for the long term.
New topical options for inverse psoriasis include tapinarof and roflumilast, Dr. Soung said. For tapinarof, the phase 3 PSOARING program included assessment of tolerability in sensitive skin areas and found little to no irritation. Similarly, treatment with roflumilast cream was effective and well tolerated by patients with intertriginous plaque psoriasis in the DERMIS-1 and DERMIS-2 studies, she said.
Genital psoriasis
Ask patients with psoriasis about genital psoriasis, because they often are too embarrassed to provide that information on their own, said Dr. Soung. In fact, 63% of patients with psoriasis report ever experiencing genital psoriasis, but it often goes undiagnosed and undertreated, which has a significant impact on patient quality of life and sexual health.
A differential diagnosis of genital psoriasis should include dermatitis, tinea or candidiasis, and even squamous cell carcinoma, she noted. Other considerations include fixed drug eruption, lichen nitidus, lichen sclerosus, and scabies.
Dr. Soung’s first line of treatment for genital psoriasis is low-potency topical corticosteroids for 2-4 weeks. If long-term topical therapy is needed, alternatives include calcineurin inhibitors and vitamin D analogs, she said. The new topicals roflumilast and tapinarof are options as well, she said.
For those patients with severe and extensive genital psoriasis, consider systemic therapy, possibly with ixekizumab or secukinumab, she added. Patients with moderate to severe genital psoriasis treated with apremilast have shown improvement at week 16, in an ongoing clinical trial, she noted.
Palmoplantar involvement
For patients with palmar plantar psoriasis, “don’t underestimate the impact on quality of life,” said Dr. Soung. Approximately 12%-16% of patients with psoriasis report palmoplantar involvement, she noted.
Palmoplantar psoriasis can be stubborn, and many patients will need combination therapy with topicals and systemics, she said. “I am very curious about how well our new topical nonsteroidals will work in these areas,” she added.
Dr. Soung starts patients with palmoplantar psoriasis with a “potent to super-potent” twice daily topical corticosteroid, with or without occlusion. Her first-line systemic therapy is acitretin, 10-50 mg daily. However, keep in mind that acitretin is contraindicated in pregnancy, and also may cause side effects including cheilitis, alopecia, and peeling skin, she cautioned.
During the question and answer session, Dr. Soung was asked whether she routinely biopsies patients with palmoplantar psoriasis. “Not always,” was her answer. Instead, she looks for clues elsewhere on the body to confirm the diagnosis.
Nail know-how
Approximately 23%-27% of patients with psoriasis experience nail involvement, said Dr. Soung. Nail psoriasis can appear on the nail plate as pitting, onycholysis, or subungual hyperkeratosis, or in the nail bed as splinter hemorrhages or oil spots, she said.
For patients with psoriasis of the nails only, Dr. Soung described the use of high-potency topical corticosteroids, with or without calcipotriol. In her experience, she said that intralesional steroids for nail psoriasis are torturous to patients. For patients who have failed topical therapy or have psoriasis in other areas, with or without psoriatic arthritis, she advised the use of either IL-17 antagonists (secukinumab, ixekizumab, brodalumab) or IL-23 antagonists (risankizumab, guselkumab).
Dr. Soung disclosed serving as a consultant or advisor for Arcutis, Bristol Myers Squibb Company, Dermavant, and Novartis. She also disclosed serving as a speaker or member of the speakers’ bureau for AbbVie, Amgen, Arcutis, Bristol Myers Squibb Company, Celgene, Leo Pharma, Eli Lilly, Novartis, Ortho Dermatologics, Pfizer, Regeneron, and Sanofi, as well as research funding from AbbVie, Amgen, Arcutis, Castle Biosciences, Dermavant, KoBio, Kyowa Kirin, Leo Pharma, Eli Lilly, Novartis, Pfizer, and UCB.
MedscapeLive and this news organization are owned by the same parent company.
AT INNOVATIONS IN DERMATOLOGY
Botanical Briefs: Toxicodendron Dermatitis
Reactions to poison ivy, poison oak, and poison sumac, which affect 10 to 50 million Americans a year,1 are classified as Toxicodendron dermatitis; 50% to 75% of US adults are clinically sensitive to these plants.2 Furthermore, people of all ethnicities, skin types, and ages residing in most US geographical regions are at risk.3 Allergenicity is caused by urushiol, which is found in members of the Anacardiaceae family.4 Once absorbed, urushiol causes a type IV hypersensitivity reaction in those who are susceptible.5
Cutaneous Manifestations
Toxicodendron dermatitis presents with an acute eczematous eruption characterized by streaks of intensely pruritic and erythematous papules and vesicles (Figure 1). Areas of involvement are characterized by sharp margins that follow the pattern of contact made by the plant’s leaves, berries, stems, and vines.6 The fluid content of the vesicles is not antigenic and cannot cause subsequent transmission to oneself or others.3 A person with prior contact to the plant who becomes sensitized develops an eruption 24 to 48 hours after subsequent contact with the plant; peak severity manifests 1 to 14 days later.7
When left untreated, the eruption can last 3 weeks. If the plant is burned, urushiol can be aerosolized in smoke, causing respiratory tract inflammation and generalized dermatitis, which has been reported among wildland firefighters.2 Long-term complications from an outbreak are limited but can include postinflammatory hyperpigmentation and secondary bacterial infection.8 Rare reports of nephrotic syndrome also have appeared in the literature.9 Toxicodendron dermatitis can present distinctively as so-called black dot dermatitis.6
Nomenclature
Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and genus Toxicodendron,6 derived from the Greek words toxikos (poison) and dendron (tree).10
Distribution
Toxicodendron plants characteristically are found in various regions of the United States. Poison ivy is the most common and is comprised of 2 species: Toxicodendron rydbergii and Toxicodendron radicans. Toxicodendron rydbergii is a nonclimbing dwarf shrub typically found in the northern and western United States. Toxicodendron radicans is a climbing vine found in the eastern United States. Poison oak also is comprised of 2 species—Toxicodendron toxicarium and Toxicodendron diversilobum—and is more common in the western United States. Poison sumac (also known as Toxicodendron vernix) is a small shrub that grows in moist swampy areas. It has a predilection for marshes of the eastern and southeastern United States.6,11
Identifying Features
Educating patients on how to identify poison ivy can play a key role in avoidance, which is the most important step in preventing Toxicodendron dermatitis. A challenge in identification of poison ivy is the plant’s variable appearance; it grows as a small shrub, low-lying vine, or vine that climbs other trees.
As the vine matures, it develops tiny, rough, “hairy” rootlets—hence the saying, “Hairy vine, no friend of mine!” Rootlets help the plant attach to trees growing near a water source. Vines can reach a diameter of 3 inches. From mature vines, solitary stems extend 1 to 2 inches with 3 characteristic leaves at the terminus (Figure 2), prompting another classic saying, “Leaves of 3, let it be!”12
Poison oak is characterized by 3 to 5 leaflets. Poison sumac has 7 to 13 pointed, smooth-edged leaves.6
Dermatitis-Inducing Plant Parts
The primary allergenic component of Toxicodendron plants is urushiol, a resinous sap found in stems, roots, leaves, and skins of the fruits. These components must be damaged or bruised to release the allergen; slight contact with an uninjured plant part might not lead to harm.2,13 Some common forms of transmission include skin contact, ingestion, inhalation of smoke from burning plants, and contact with skin through contaminated items, such as clothing, animals, and tools.14
Allergens
The catecholic ring and aliphatic chain of the urushiol molecule are allergenic.15 The degree of saturation and length of the side chains vary with different catechols. Urushiol displays cross-reactivity with poison ivy, poison oak, and poison sumac. Urushiol from these plants differs only slightly in structure; therefore, sensitization to one causes sensitization to all. There also is cross-reactivity between different members of the Anacardiaceae family, including Anacardium occidentale (tropical cashew nut), Mangifera indica (tropical mango tree), Ginkgo biloba (ginkgo tree), and Semecarpus anacardium (Indian marking nut tree).12
Poison ivy, poison oak, and poison sumac cause allergic contact dermatitis as a type IV hypersensitivity reaction. First, urushiol binds and penetrates the skin, where it is oxidized to quinone intermediates and bound to haptens. Then, the intermediates bind surface proteins on antigen-presenting cells, specifically Langerhans cells in the epidermis and dermis.5
Presentation of nonpeptide antigens, such as urushiol, to T cells requires expression of langerin (also known as CD207) and CD1a.16 Langerin is a C-type lectin that causes formation of Birbeck granules; CD1a is a major histocompatibility complex class I molecule found in Birbeck granules.5,17 After Langerhans cells internalize and process the urushiol self-hapten neoantigen, it is presented to CD4+ T cells.6 These cells then expand to form circulating activated T-effector and T-memory lymphocytes.18
The molecular link that occurs between the hapten and carrier protein determines the response. When linked by an amino nucleophile, selective induction of T-effector cells ensues, resulting in allergic contact dermatitis. When linked by a sulfhydryl bond, selective induction of suppressor cells occurs, resulting in a reduced allergic contact dermatitis response.19 In the case of activation of T-effector cells, a cell-mediated cytotoxic immune response is generated that destroys epidermal cells and dermal vasculature.2 The incidence and intensity of poison ivy sensitivity decline proportionally with age and the absence of continued exposure.20
Preventive Action—Patients should be counseled that if contact between plant and skin occurs, it is important to remove contaminated clothing or objects and wash them with soap to prevent additional exposure.14,21 Areas of the skin that made contact with the plant should be washed with water as soon as possible; after 30 minutes, urushiol has sufficiently penetrated to cause a reaction.2 Forceful unidirectional washing with a damp washcloth and liquid dishwashing soap is recommended.22
Several barrier creams are commercially available to help prevent absorption or to deactivate the urushiol antigen. These products are used widely by forestry workers and wildland firefighters.23 One such barrier cream is bentoquatam (sold as various trade names), an organoclay compound made of quaternium-18 bentonite that interferes with absorption of the allergen by acting as a physical blocker.24
Treatment
After Toxicodendron dermatitis develops, several treatments are available to help manage symptoms. Calamine lotion can be used to help dry weeping lesions.25,26 Topical steroids can be used to help control pruritus and alleviate inflammation. High-potency topical corticosteroids such as clobetasol and mid-potency steroids such as triamcinolone can be used. Topical anesthetics (eg, benzocaine, pramoxine, benzyl alcohol) might provide symptomatic relief.27,28
Oral antihistamines can allow for better sleep by providing sedation but do not target the pruritus of poison ivy dermatitis, which is not histamine mediated.29,30 Systemic corticosteroids usually are considered in more severe dermatitis—when 20% or more of the body surface area is involved; blistering and itching are severe; or the face, hands, or genitalia are involved.31,32
Clinical Uses
Therapeutic uses for poison ivy have been explored extensively. In 1892, Dakin33 reported that ingestion of leaves by Native Americans reduced the incidence and severity of skin lesions after contact with poison ivy. Consumption of poison ivy was further studied by Epstein and colleagues34 in 1974; they concluded that ingestion of a large amount of urushiol over a period of 3 months or longer may help with hyposensitization—but not complete desensitization—to contact with poison ivy. However, the risk for adverse effects is thought to outweigh benefits because ingestion can cause perianal dermatitis, mucocutaneous sequelae, and systemic contact dermatitis.2
Although the use of Toxicodendron plants in modern-day medicine is limited, development of a vaccine (immunotherapy) against Toxicodendron dermatitis offers an exciting opportunity for further research.
- Pariser DM, Ceilley RI, Lefkovits AM, et al. Poison ivy, oak and sumac. Derm Insights. 2003;4:26-28.
- Gladman AC. Toxicodendron dermatitis: poison ivy, oak, and sumac. Wilderness Environ Med. 2006;17:120-128. doi:10.1580/pr31-05.1
- Fisher AA. Poison ivy/oak/sumac. part II: specific features. Cutis. 1996;58:22-24.
- Cruse JM, Lewis RE. Atlas of Immunology. CRC Press; 2004.
- Valladeau J, Ravel O, Dezutter-Dambuyant C, et al. Langerin, a novel C-type lectin specific to Langerhans cells, is an endocytic receptor that induces the formation of Birbeck granules. Immunity. 2000;12:71-81. doi:10.1016/s1074-7613(00)80160-0
- Marks JG. Poison ivy and poison oak allergic contact dermatitis. J Allergy Clin Immunol. 1989;9:497-506.
- Williams JV, Light J, Marks JG Jr. Individual variations in allergic contact dermatitis from urushiol. Arch Dermatol. 1999;135:1002-1003. doi:10.1001/archderm.135.8.1002
- Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis. Br J Dermatol. 2000;142:943-946. doi:10.1046/j.1365-2133.2000.03475.x
- Rytand DA. Fatal anuria, the nephrotic syndrome and glomerular nephritis as sequels of the dermatitis of poison oak. Am J Med. 1948;5:548-560. doi:10.1016/0002-9343(48)90105-3
- Gledhill D. The Names of Plants. Cambridge University Press; 2008.
- American Academy of Dermatology Association. Poison ivy, oak, and sumac: how to treat the rash. Accessed October 19, 2022. https://www.aad.org/public/everyday-care/itchy-skin/poison-ivy/treat-rash
- Monroe J. Toxicodendron contact dermatitis: a case report and brief review. J Clin Aesthet Dermatol. 2020;13(9 suppl 1):S29-S34.
- Marks JG Jr, Anderson BE, DeLeo VA. Contact & Occupational Dermatology. 4th ed. Jaypee Brothers Medical Publishers; 2016.
- Fisher AA, Mitchell JC. Toxicodendron plants and spices. In: Rietschel RL, Fowler JF Jr, eds. Fisher’s Contact Dermatitis. 4th ed. Williams and Wilkins; 1995:461-523.
- Dawson CR. The chemistry of poison ivy. Trans N Y Acad Sci. 1956;18:427-443. doi:10.1111/j.2164-0947.1956.tb00465.x
- Hunger RE, Sieling PA, Ochoa MT, et al. Langerhans cells utilize CD1a and langerin to efficiently present nonpeptide antigens to T cells. J Clin Invest. 2004;113:701-708. doi:10.1172/JCI19655
- Hanau D, Fabre M, Schmitt DA, et al. Human epidermal Langerhans cells cointernalize by receptor-mediated endocytosis “non-classical” major histocompatibility complex class Imolecules (T6 antigens) and class II molecules (HLA-DR antigens). Proc Natl Acad Sci U S A. 1987;84:2901-2905. doi:10.1073/pnas.84.9.2901
- Gayer KD, Burnett JW. Toxicodendron dermatitis. Cutis. 1988;42:99-100.
- Dunn IS, Liberato DJ, Castagnoli N, et al. Contact sensitivity to urushiol: role of covalent bond formation. Cell Immunol. 1982;74:220-233. doi:10.1016/0008-8749(82)90023-5
- Kligman AM. Poison ivy (Rhus) dermatitis; an experimental study. AMA Arch Derm. 1958;77:149-180. doi:10.1001/archderm.1958.01560020001001
- Derraik JGB. Heracleum mantegazzianum and Toxicodendron succedaneum: plants of human health significance in New Zealand and the National Pest Plant Accord. N Z Med J. 2007;120:U2657.
- Neill BC, Neill JA, Brauker J, et al. Postexposure prevention of Toxicodendron dermatitis by early forceful unidirectional washing with liquid dishwashing soap. J Am Acad Dermatol. 2018;81:E25. doi:10.1016/j.jaad.2017.12.081
- Kim Y, Flamm A, ElSohly MA, et al. Poison ivy, oak, and sumac dermatitis: what is known and what is new? Dermatitis. 2019;30:183-190. doi:10.1097/DER.0000000000000472
- Marks JG Jr, Fowler JF Jr, Sheretz EF, et al. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite. J Am Acad Dermatol. 1995;33:212-216. doi:10.1016/0190-9622(95)90237-6
- Baer RL. Poison ivy dermatitis. Cutis. 1990;46:34-36.
- Williford PM, Sheretz EF. Poison ivy dermatitis. nuances in treatment. Arch Fam Med. 1995;3:184.
- Amrol D, Keitel D, Hagaman D, et al. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol. 2003;91:563-566. doi:10.1016/S1081-1206(10)61535-9
- Stephanides SL, Moore C. Toxicodendron poisoning treatment & management. Medscape. Updated June 13, 2022. Accessed October 19, 2022. https://emedicine.medscape.com/article/817671-treatment#d11
- Munday J, Bloomfield R, Goldman M, et al. Chlorpheniramine is no more effective than placebo in relieving the symptoms of childhood atopic dermatitis with a nocturnal itching and scratching component. Dermatology. 2002;205:40-45. doi:10.1159/000063138
- Yosipovitch G, Fleischer A. Itch associated with skin disease: advances in pathophysiology and emerging therapies. Am J Clin Dermatol. 2003;4:617-622. doi:10.2165/00128071-200304090-00004
- Li LY, Cruz PD Jr. Allergic contact dermatitis: pathophysiology applied to future therapy. Dermatol Ther. 2004;17:219-223. doi:10.1111/j.1396-0296.2004.04023.x
- Craig K, Meadows SE. What is the best duration of steroid therapy for contact dermatitis (Rhus)? J Fam Pract. 2006;55:166-167.
- Dakin R. Remarks on a cutaneous affection, produced by certain poisonous vegetables. Am J Med Sci. 1829;4:98-100.
- Epstein WL, Baer H, Dawson CR, et al. Poison oak hyposensitization. evaluation of purified urushiol. Arch Dermatol. 1974;109:356-360.
Reactions to poison ivy, poison oak, and poison sumac, which affect 10 to 50 million Americans a year,1 are classified as Toxicodendron dermatitis; 50% to 75% of US adults are clinically sensitive to these plants.2 Furthermore, people of all ethnicities, skin types, and ages residing in most US geographical regions are at risk.3 Allergenicity is caused by urushiol, which is found in members of the Anacardiaceae family.4 Once absorbed, urushiol causes a type IV hypersensitivity reaction in those who are susceptible.5
Cutaneous Manifestations
Toxicodendron dermatitis presents with an acute eczematous eruption characterized by streaks of intensely pruritic and erythematous papules and vesicles (Figure 1). Areas of involvement are characterized by sharp margins that follow the pattern of contact made by the plant’s leaves, berries, stems, and vines.6 The fluid content of the vesicles is not antigenic and cannot cause subsequent transmission to oneself or others.3 A person with prior contact to the plant who becomes sensitized develops an eruption 24 to 48 hours after subsequent contact with the plant; peak severity manifests 1 to 14 days later.7
When left untreated, the eruption can last 3 weeks. If the plant is burned, urushiol can be aerosolized in smoke, causing respiratory tract inflammation and generalized dermatitis, which has been reported among wildland firefighters.2 Long-term complications from an outbreak are limited but can include postinflammatory hyperpigmentation and secondary bacterial infection.8 Rare reports of nephrotic syndrome also have appeared in the literature.9 Toxicodendron dermatitis can present distinctively as so-called black dot dermatitis.6
Nomenclature
Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and genus Toxicodendron,6 derived from the Greek words toxikos (poison) and dendron (tree).10
Distribution
Toxicodendron plants characteristically are found in various regions of the United States. Poison ivy is the most common and is comprised of 2 species: Toxicodendron rydbergii and Toxicodendron radicans. Toxicodendron rydbergii is a nonclimbing dwarf shrub typically found in the northern and western United States. Toxicodendron radicans is a climbing vine found in the eastern United States. Poison oak also is comprised of 2 species—Toxicodendron toxicarium and Toxicodendron diversilobum—and is more common in the western United States. Poison sumac (also known as Toxicodendron vernix) is a small shrub that grows in moist swampy areas. It has a predilection for marshes of the eastern and southeastern United States.6,11
Identifying Features
Educating patients on how to identify poison ivy can play a key role in avoidance, which is the most important step in preventing Toxicodendron dermatitis. A challenge in identification of poison ivy is the plant’s variable appearance; it grows as a small shrub, low-lying vine, or vine that climbs other trees.
As the vine matures, it develops tiny, rough, “hairy” rootlets—hence the saying, “Hairy vine, no friend of mine!” Rootlets help the plant attach to trees growing near a water source. Vines can reach a diameter of 3 inches. From mature vines, solitary stems extend 1 to 2 inches with 3 characteristic leaves at the terminus (Figure 2), prompting another classic saying, “Leaves of 3, let it be!”12
Poison oak is characterized by 3 to 5 leaflets. Poison sumac has 7 to 13 pointed, smooth-edged leaves.6
Dermatitis-Inducing Plant Parts
The primary allergenic component of Toxicodendron plants is urushiol, a resinous sap found in stems, roots, leaves, and skins of the fruits. These components must be damaged or bruised to release the allergen; slight contact with an uninjured plant part might not lead to harm.2,13 Some common forms of transmission include skin contact, ingestion, inhalation of smoke from burning plants, and contact with skin through contaminated items, such as clothing, animals, and tools.14
Allergens
The catecholic ring and aliphatic chain of the urushiol molecule are allergenic.15 The degree of saturation and length of the side chains vary with different catechols. Urushiol displays cross-reactivity with poison ivy, poison oak, and poison sumac. Urushiol from these plants differs only slightly in structure; therefore, sensitization to one causes sensitization to all. There also is cross-reactivity between different members of the Anacardiaceae family, including Anacardium occidentale (tropical cashew nut), Mangifera indica (tropical mango tree), Ginkgo biloba (ginkgo tree), and Semecarpus anacardium (Indian marking nut tree).12
Poison ivy, poison oak, and poison sumac cause allergic contact dermatitis as a type IV hypersensitivity reaction. First, urushiol binds and penetrates the skin, where it is oxidized to quinone intermediates and bound to haptens. Then, the intermediates bind surface proteins on antigen-presenting cells, specifically Langerhans cells in the epidermis and dermis.5
Presentation of nonpeptide antigens, such as urushiol, to T cells requires expression of langerin (also known as CD207) and CD1a.16 Langerin is a C-type lectin that causes formation of Birbeck granules; CD1a is a major histocompatibility complex class I molecule found in Birbeck granules.5,17 After Langerhans cells internalize and process the urushiol self-hapten neoantigen, it is presented to CD4+ T cells.6 These cells then expand to form circulating activated T-effector and T-memory lymphocytes.18
The molecular link that occurs between the hapten and carrier protein determines the response. When linked by an amino nucleophile, selective induction of T-effector cells ensues, resulting in allergic contact dermatitis. When linked by a sulfhydryl bond, selective induction of suppressor cells occurs, resulting in a reduced allergic contact dermatitis response.19 In the case of activation of T-effector cells, a cell-mediated cytotoxic immune response is generated that destroys epidermal cells and dermal vasculature.2 The incidence and intensity of poison ivy sensitivity decline proportionally with age and the absence of continued exposure.20
Preventive Action—Patients should be counseled that if contact between plant and skin occurs, it is important to remove contaminated clothing or objects and wash them with soap to prevent additional exposure.14,21 Areas of the skin that made contact with the plant should be washed with water as soon as possible; after 30 minutes, urushiol has sufficiently penetrated to cause a reaction.2 Forceful unidirectional washing with a damp washcloth and liquid dishwashing soap is recommended.22
Several barrier creams are commercially available to help prevent absorption or to deactivate the urushiol antigen. These products are used widely by forestry workers and wildland firefighters.23 One such barrier cream is bentoquatam (sold as various trade names), an organoclay compound made of quaternium-18 bentonite that interferes with absorption of the allergen by acting as a physical blocker.24
Treatment
After Toxicodendron dermatitis develops, several treatments are available to help manage symptoms. Calamine lotion can be used to help dry weeping lesions.25,26 Topical steroids can be used to help control pruritus and alleviate inflammation. High-potency topical corticosteroids such as clobetasol and mid-potency steroids such as triamcinolone can be used. Topical anesthetics (eg, benzocaine, pramoxine, benzyl alcohol) might provide symptomatic relief.27,28
Oral antihistamines can allow for better sleep by providing sedation but do not target the pruritus of poison ivy dermatitis, which is not histamine mediated.29,30 Systemic corticosteroids usually are considered in more severe dermatitis—when 20% or more of the body surface area is involved; blistering and itching are severe; or the face, hands, or genitalia are involved.31,32
Clinical Uses
Therapeutic uses for poison ivy have been explored extensively. In 1892, Dakin33 reported that ingestion of leaves by Native Americans reduced the incidence and severity of skin lesions after contact with poison ivy. Consumption of poison ivy was further studied by Epstein and colleagues34 in 1974; they concluded that ingestion of a large amount of urushiol over a period of 3 months or longer may help with hyposensitization—but not complete desensitization—to contact with poison ivy. However, the risk for adverse effects is thought to outweigh benefits because ingestion can cause perianal dermatitis, mucocutaneous sequelae, and systemic contact dermatitis.2
Although the use of Toxicodendron plants in modern-day medicine is limited, development of a vaccine (immunotherapy) against Toxicodendron dermatitis offers an exciting opportunity for further research.
Reactions to poison ivy, poison oak, and poison sumac, which affect 10 to 50 million Americans a year,1 are classified as Toxicodendron dermatitis; 50% to 75% of US adults are clinically sensitive to these plants.2 Furthermore, people of all ethnicities, skin types, and ages residing in most US geographical regions are at risk.3 Allergenicity is caused by urushiol, which is found in members of the Anacardiaceae family.4 Once absorbed, urushiol causes a type IV hypersensitivity reaction in those who are susceptible.5
Cutaneous Manifestations
Toxicodendron dermatitis presents with an acute eczematous eruption characterized by streaks of intensely pruritic and erythematous papules and vesicles (Figure 1). Areas of involvement are characterized by sharp margins that follow the pattern of contact made by the plant’s leaves, berries, stems, and vines.6 The fluid content of the vesicles is not antigenic and cannot cause subsequent transmission to oneself or others.3 A person with prior contact to the plant who becomes sensitized develops an eruption 24 to 48 hours after subsequent contact with the plant; peak severity manifests 1 to 14 days later.7
When left untreated, the eruption can last 3 weeks. If the plant is burned, urushiol can be aerosolized in smoke, causing respiratory tract inflammation and generalized dermatitis, which has been reported among wildland firefighters.2 Long-term complications from an outbreak are limited but can include postinflammatory hyperpigmentation and secondary bacterial infection.8 Rare reports of nephrotic syndrome also have appeared in the literature.9 Toxicodendron dermatitis can present distinctively as so-called black dot dermatitis.6
Nomenclature
Poison ivy, poison oak, and poison sumac are members of the family Anacardiaceae and genus Toxicodendron,6 derived from the Greek words toxikos (poison) and dendron (tree).10
Distribution
Toxicodendron plants characteristically are found in various regions of the United States. Poison ivy is the most common and is comprised of 2 species: Toxicodendron rydbergii and Toxicodendron radicans. Toxicodendron rydbergii is a nonclimbing dwarf shrub typically found in the northern and western United States. Toxicodendron radicans is a climbing vine found in the eastern United States. Poison oak also is comprised of 2 species—Toxicodendron toxicarium and Toxicodendron diversilobum—and is more common in the western United States. Poison sumac (also known as Toxicodendron vernix) is a small shrub that grows in moist swampy areas. It has a predilection for marshes of the eastern and southeastern United States.6,11
Identifying Features
Educating patients on how to identify poison ivy can play a key role in avoidance, which is the most important step in preventing Toxicodendron dermatitis. A challenge in identification of poison ivy is the plant’s variable appearance; it grows as a small shrub, low-lying vine, or vine that climbs other trees.
As the vine matures, it develops tiny, rough, “hairy” rootlets—hence the saying, “Hairy vine, no friend of mine!” Rootlets help the plant attach to trees growing near a water source. Vines can reach a diameter of 3 inches. From mature vines, solitary stems extend 1 to 2 inches with 3 characteristic leaves at the terminus (Figure 2), prompting another classic saying, “Leaves of 3, let it be!”12
Poison oak is characterized by 3 to 5 leaflets. Poison sumac has 7 to 13 pointed, smooth-edged leaves.6
Dermatitis-Inducing Plant Parts
The primary allergenic component of Toxicodendron plants is urushiol, a resinous sap found in stems, roots, leaves, and skins of the fruits. These components must be damaged or bruised to release the allergen; slight contact with an uninjured plant part might not lead to harm.2,13 Some common forms of transmission include skin contact, ingestion, inhalation of smoke from burning plants, and contact with skin through contaminated items, such as clothing, animals, and tools.14
Allergens
The catecholic ring and aliphatic chain of the urushiol molecule are allergenic.15 The degree of saturation and length of the side chains vary with different catechols. Urushiol displays cross-reactivity with poison ivy, poison oak, and poison sumac. Urushiol from these plants differs only slightly in structure; therefore, sensitization to one causes sensitization to all. There also is cross-reactivity between different members of the Anacardiaceae family, including Anacardium occidentale (tropical cashew nut), Mangifera indica (tropical mango tree), Ginkgo biloba (ginkgo tree), and Semecarpus anacardium (Indian marking nut tree).12
Poison ivy, poison oak, and poison sumac cause allergic contact dermatitis as a type IV hypersensitivity reaction. First, urushiol binds and penetrates the skin, where it is oxidized to quinone intermediates and bound to haptens. Then, the intermediates bind surface proteins on antigen-presenting cells, specifically Langerhans cells in the epidermis and dermis.5
Presentation of nonpeptide antigens, such as urushiol, to T cells requires expression of langerin (also known as CD207) and CD1a.16 Langerin is a C-type lectin that causes formation of Birbeck granules; CD1a is a major histocompatibility complex class I molecule found in Birbeck granules.5,17 After Langerhans cells internalize and process the urushiol self-hapten neoantigen, it is presented to CD4+ T cells.6 These cells then expand to form circulating activated T-effector and T-memory lymphocytes.18
The molecular link that occurs between the hapten and carrier protein determines the response. When linked by an amino nucleophile, selective induction of T-effector cells ensues, resulting in allergic contact dermatitis. When linked by a sulfhydryl bond, selective induction of suppressor cells occurs, resulting in a reduced allergic contact dermatitis response.19 In the case of activation of T-effector cells, a cell-mediated cytotoxic immune response is generated that destroys epidermal cells and dermal vasculature.2 The incidence and intensity of poison ivy sensitivity decline proportionally with age and the absence of continued exposure.20
Preventive Action—Patients should be counseled that if contact between plant and skin occurs, it is important to remove contaminated clothing or objects and wash them with soap to prevent additional exposure.14,21 Areas of the skin that made contact with the plant should be washed with water as soon as possible; after 30 minutes, urushiol has sufficiently penetrated to cause a reaction.2 Forceful unidirectional washing with a damp washcloth and liquid dishwashing soap is recommended.22
Several barrier creams are commercially available to help prevent absorption or to deactivate the urushiol antigen. These products are used widely by forestry workers and wildland firefighters.23 One such barrier cream is bentoquatam (sold as various trade names), an organoclay compound made of quaternium-18 bentonite that interferes with absorption of the allergen by acting as a physical blocker.24
Treatment
After Toxicodendron dermatitis develops, several treatments are available to help manage symptoms. Calamine lotion can be used to help dry weeping lesions.25,26 Topical steroids can be used to help control pruritus and alleviate inflammation. High-potency topical corticosteroids such as clobetasol and mid-potency steroids such as triamcinolone can be used. Topical anesthetics (eg, benzocaine, pramoxine, benzyl alcohol) might provide symptomatic relief.27,28
Oral antihistamines can allow for better sleep by providing sedation but do not target the pruritus of poison ivy dermatitis, which is not histamine mediated.29,30 Systemic corticosteroids usually are considered in more severe dermatitis—when 20% or more of the body surface area is involved; blistering and itching are severe; or the face, hands, or genitalia are involved.31,32
Clinical Uses
Therapeutic uses for poison ivy have been explored extensively. In 1892, Dakin33 reported that ingestion of leaves by Native Americans reduced the incidence and severity of skin lesions after contact with poison ivy. Consumption of poison ivy was further studied by Epstein and colleagues34 in 1974; they concluded that ingestion of a large amount of urushiol over a period of 3 months or longer may help with hyposensitization—but not complete desensitization—to contact with poison ivy. However, the risk for adverse effects is thought to outweigh benefits because ingestion can cause perianal dermatitis, mucocutaneous sequelae, and systemic contact dermatitis.2
Although the use of Toxicodendron plants in modern-day medicine is limited, development of a vaccine (immunotherapy) against Toxicodendron dermatitis offers an exciting opportunity for further research.
- Pariser DM, Ceilley RI, Lefkovits AM, et al. Poison ivy, oak and sumac. Derm Insights. 2003;4:26-28.
- Gladman AC. Toxicodendron dermatitis: poison ivy, oak, and sumac. Wilderness Environ Med. 2006;17:120-128. doi:10.1580/pr31-05.1
- Fisher AA. Poison ivy/oak/sumac. part II: specific features. Cutis. 1996;58:22-24.
- Cruse JM, Lewis RE. Atlas of Immunology. CRC Press; 2004.
- Valladeau J, Ravel O, Dezutter-Dambuyant C, et al. Langerin, a novel C-type lectin specific to Langerhans cells, is an endocytic receptor that induces the formation of Birbeck granules. Immunity. 2000;12:71-81. doi:10.1016/s1074-7613(00)80160-0
- Marks JG. Poison ivy and poison oak allergic contact dermatitis. J Allergy Clin Immunol. 1989;9:497-506.
- Williams JV, Light J, Marks JG Jr. Individual variations in allergic contact dermatitis from urushiol. Arch Dermatol. 1999;135:1002-1003. doi:10.1001/archderm.135.8.1002
- Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis. Br J Dermatol. 2000;142:943-946. doi:10.1046/j.1365-2133.2000.03475.x
- Rytand DA. Fatal anuria, the nephrotic syndrome and glomerular nephritis as sequels of the dermatitis of poison oak. Am J Med. 1948;5:548-560. doi:10.1016/0002-9343(48)90105-3
- Gledhill D. The Names of Plants. Cambridge University Press; 2008.
- American Academy of Dermatology Association. Poison ivy, oak, and sumac: how to treat the rash. Accessed October 19, 2022. https://www.aad.org/public/everyday-care/itchy-skin/poison-ivy/treat-rash
- Monroe J. Toxicodendron contact dermatitis: a case report and brief review. J Clin Aesthet Dermatol. 2020;13(9 suppl 1):S29-S34.
- Marks JG Jr, Anderson BE, DeLeo VA. Contact & Occupational Dermatology. 4th ed. Jaypee Brothers Medical Publishers; 2016.
- Fisher AA, Mitchell JC. Toxicodendron plants and spices. In: Rietschel RL, Fowler JF Jr, eds. Fisher’s Contact Dermatitis. 4th ed. Williams and Wilkins; 1995:461-523.
- Dawson CR. The chemistry of poison ivy. Trans N Y Acad Sci. 1956;18:427-443. doi:10.1111/j.2164-0947.1956.tb00465.x
- Hunger RE, Sieling PA, Ochoa MT, et al. Langerhans cells utilize CD1a and langerin to efficiently present nonpeptide antigens to T cells. J Clin Invest. 2004;113:701-708. doi:10.1172/JCI19655
- Hanau D, Fabre M, Schmitt DA, et al. Human epidermal Langerhans cells cointernalize by receptor-mediated endocytosis “non-classical” major histocompatibility complex class Imolecules (T6 antigens) and class II molecules (HLA-DR antigens). Proc Natl Acad Sci U S A. 1987;84:2901-2905. doi:10.1073/pnas.84.9.2901
- Gayer KD, Burnett JW. Toxicodendron dermatitis. Cutis. 1988;42:99-100.
- Dunn IS, Liberato DJ, Castagnoli N, et al. Contact sensitivity to urushiol: role of covalent bond formation. Cell Immunol. 1982;74:220-233. doi:10.1016/0008-8749(82)90023-5
- Kligman AM. Poison ivy (Rhus) dermatitis; an experimental study. AMA Arch Derm. 1958;77:149-180. doi:10.1001/archderm.1958.01560020001001
- Derraik JGB. Heracleum mantegazzianum and Toxicodendron succedaneum: plants of human health significance in New Zealand and the National Pest Plant Accord. N Z Med J. 2007;120:U2657.
- Neill BC, Neill JA, Brauker J, et al. Postexposure prevention of Toxicodendron dermatitis by early forceful unidirectional washing with liquid dishwashing soap. J Am Acad Dermatol. 2018;81:E25. doi:10.1016/j.jaad.2017.12.081
- Kim Y, Flamm A, ElSohly MA, et al. Poison ivy, oak, and sumac dermatitis: what is known and what is new? Dermatitis. 2019;30:183-190. doi:10.1097/DER.0000000000000472
- Marks JG Jr, Fowler JF Jr, Sheretz EF, et al. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite. J Am Acad Dermatol. 1995;33:212-216. doi:10.1016/0190-9622(95)90237-6
- Baer RL. Poison ivy dermatitis. Cutis. 1990;46:34-36.
- Williford PM, Sheretz EF. Poison ivy dermatitis. nuances in treatment. Arch Fam Med. 1995;3:184.
- Amrol D, Keitel D, Hagaman D, et al. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol. 2003;91:563-566. doi:10.1016/S1081-1206(10)61535-9
- Stephanides SL, Moore C. Toxicodendron poisoning treatment & management. Medscape. Updated June 13, 2022. Accessed October 19, 2022. https://emedicine.medscape.com/article/817671-treatment#d11
- Munday J, Bloomfield R, Goldman M, et al. Chlorpheniramine is no more effective than placebo in relieving the symptoms of childhood atopic dermatitis with a nocturnal itching and scratching component. Dermatology. 2002;205:40-45. doi:10.1159/000063138
- Yosipovitch G, Fleischer A. Itch associated with skin disease: advances in pathophysiology and emerging therapies. Am J Clin Dermatol. 2003;4:617-622. doi:10.2165/00128071-200304090-00004
- Li LY, Cruz PD Jr. Allergic contact dermatitis: pathophysiology applied to future therapy. Dermatol Ther. 2004;17:219-223. doi:10.1111/j.1396-0296.2004.04023.x
- Craig K, Meadows SE. What is the best duration of steroid therapy for contact dermatitis (Rhus)? J Fam Pract. 2006;55:166-167.
- Dakin R. Remarks on a cutaneous affection, produced by certain poisonous vegetables. Am J Med Sci. 1829;4:98-100.
- Epstein WL, Baer H, Dawson CR, et al. Poison oak hyposensitization. evaluation of purified urushiol. Arch Dermatol. 1974;109:356-360.
- Pariser DM, Ceilley RI, Lefkovits AM, et al. Poison ivy, oak and sumac. Derm Insights. 2003;4:26-28.
- Gladman AC. Toxicodendron dermatitis: poison ivy, oak, and sumac. Wilderness Environ Med. 2006;17:120-128. doi:10.1580/pr31-05.1
- Fisher AA. Poison ivy/oak/sumac. part II: specific features. Cutis. 1996;58:22-24.
- Cruse JM, Lewis RE. Atlas of Immunology. CRC Press; 2004.
- Valladeau J, Ravel O, Dezutter-Dambuyant C, et al. Langerin, a novel C-type lectin specific to Langerhans cells, is an endocytic receptor that induces the formation of Birbeck granules. Immunity. 2000;12:71-81. doi:10.1016/s1074-7613(00)80160-0
- Marks JG. Poison ivy and poison oak allergic contact dermatitis. J Allergy Clin Immunol. 1989;9:497-506.
- Williams JV, Light J, Marks JG Jr. Individual variations in allergic contact dermatitis from urushiol. Arch Dermatol. 1999;135:1002-1003. doi:10.1001/archderm.135.8.1002
- Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis. Br J Dermatol. 2000;142:943-946. doi:10.1046/j.1365-2133.2000.03475.x
- Rytand DA. Fatal anuria, the nephrotic syndrome and glomerular nephritis as sequels of the dermatitis of poison oak. Am J Med. 1948;5:548-560. doi:10.1016/0002-9343(48)90105-3
- Gledhill D. The Names of Plants. Cambridge University Press; 2008.
- American Academy of Dermatology Association. Poison ivy, oak, and sumac: how to treat the rash. Accessed October 19, 2022. https://www.aad.org/public/everyday-care/itchy-skin/poison-ivy/treat-rash
- Monroe J. Toxicodendron contact dermatitis: a case report and brief review. J Clin Aesthet Dermatol. 2020;13(9 suppl 1):S29-S34.
- Marks JG Jr, Anderson BE, DeLeo VA. Contact & Occupational Dermatology. 4th ed. Jaypee Brothers Medical Publishers; 2016.
- Fisher AA, Mitchell JC. Toxicodendron plants and spices. In: Rietschel RL, Fowler JF Jr, eds. Fisher’s Contact Dermatitis. 4th ed. Williams and Wilkins; 1995:461-523.
- Dawson CR. The chemistry of poison ivy. Trans N Y Acad Sci. 1956;18:427-443. doi:10.1111/j.2164-0947.1956.tb00465.x
- Hunger RE, Sieling PA, Ochoa MT, et al. Langerhans cells utilize CD1a and langerin to efficiently present nonpeptide antigens to T cells. J Clin Invest. 2004;113:701-708. doi:10.1172/JCI19655
- Hanau D, Fabre M, Schmitt DA, et al. Human epidermal Langerhans cells cointernalize by receptor-mediated endocytosis “non-classical” major histocompatibility complex class Imolecules (T6 antigens) and class II molecules (HLA-DR antigens). Proc Natl Acad Sci U S A. 1987;84:2901-2905. doi:10.1073/pnas.84.9.2901
- Gayer KD, Burnett JW. Toxicodendron dermatitis. Cutis. 1988;42:99-100.
- Dunn IS, Liberato DJ, Castagnoli N, et al. Contact sensitivity to urushiol: role of covalent bond formation. Cell Immunol. 1982;74:220-233. doi:10.1016/0008-8749(82)90023-5
- Kligman AM. Poison ivy (Rhus) dermatitis; an experimental study. AMA Arch Derm. 1958;77:149-180. doi:10.1001/archderm.1958.01560020001001
- Derraik JGB. Heracleum mantegazzianum and Toxicodendron succedaneum: plants of human health significance in New Zealand and the National Pest Plant Accord. N Z Med J. 2007;120:U2657.
- Neill BC, Neill JA, Brauker J, et al. Postexposure prevention of Toxicodendron dermatitis by early forceful unidirectional washing with liquid dishwashing soap. J Am Acad Dermatol. 2018;81:E25. doi:10.1016/j.jaad.2017.12.081
- Kim Y, Flamm A, ElSohly MA, et al. Poison ivy, oak, and sumac dermatitis: what is known and what is new? Dermatitis. 2019;30:183-190. doi:10.1097/DER.0000000000000472
- Marks JG Jr, Fowler JF Jr, Sheretz EF, et al. Prevention of poison ivy and poison oak allergic contact dermatitis by quaternium-18 bentonite. J Am Acad Dermatol. 1995;33:212-216. doi:10.1016/0190-9622(95)90237-6
- Baer RL. Poison ivy dermatitis. Cutis. 1990;46:34-36.
- Williford PM, Sheretz EF. Poison ivy dermatitis. nuances in treatment. Arch Fam Med. 1995;3:184.
- Amrol D, Keitel D, Hagaman D, et al. Topical pimecrolimus in the treatment of human allergic contact dermatitis. Ann Allergy Asthma Immunol. 2003;91:563-566. doi:10.1016/S1081-1206(10)61535-9
- Stephanides SL, Moore C. Toxicodendron poisoning treatment & management. Medscape. Updated June 13, 2022. Accessed October 19, 2022. https://emedicine.medscape.com/article/817671-treatment#d11
- Munday J, Bloomfield R, Goldman M, et al. Chlorpheniramine is no more effective than placebo in relieving the symptoms of childhood atopic dermatitis with a nocturnal itching and scratching component. Dermatology. 2002;205:40-45. doi:10.1159/000063138
- Yosipovitch G, Fleischer A. Itch associated with skin disease: advances in pathophysiology and emerging therapies. Am J Clin Dermatol. 2003;4:617-622. doi:10.2165/00128071-200304090-00004
- Li LY, Cruz PD Jr. Allergic contact dermatitis: pathophysiology applied to future therapy. Dermatol Ther. 2004;17:219-223. doi:10.1111/j.1396-0296.2004.04023.x
- Craig K, Meadows SE. What is the best duration of steroid therapy for contact dermatitis (Rhus)? J Fam Pract. 2006;55:166-167.
- Dakin R. Remarks on a cutaneous affection, produced by certain poisonous vegetables. Am J Med Sci. 1829;4:98-100.
- Epstein WL, Baer H, Dawson CR, et al. Poison oak hyposensitization. evaluation of purified urushiol. Arch Dermatol. 1974;109:356-360.
Practice Points
- Toxicodendron dermatitis is a pruritic vesicular eruption in areas of contact with the plant.
- Identification and avoidance are primary methods of preventing Toxicodendron dermatitis.
Dietary Triggers for Atopic Dermatitis in Children
It is unsurprising that food frequently is thought to be the culprit behind an eczema flare, especially in infants. Indeed, it often is said that infants do only 3 things: eat, sleep, and poop.1 For those unfortunate enough to develop the signs and symptoms of atopic dermatitis (AD), food quickly emerges as a potential culprit from the tiny pool of suspects, which is against a cultural backdrop of unprecedented focus on foods and food reactions.2 The prevalence of food allergies in children, though admittedly fraught with methodological difficulties, is estimated to have more than doubled from 3.4% in 1999 to 7.6% in 2018.3 As expected, prevalence rates were higher among children with other atopic comorbidities including AD, with up to 50% of children with AD demonstrating convincing food allergy.4 It is easy to imagine a patient conflating these 2 entities and mistaking their correlation for causation. Thus, it follows that more than 90% of parents/guardians have reported that their children have had food-induced AD, and understandably—at least according to one study—75% of parents/guardians were found to have manipulated the diet in an attempt to manage the disease.5,6
Patients and parents/guardians are not the only ones who have suspected food as a driving force in AD. An article in the British Medical Journal from the 1800s beautifully encapsulated the depth and duration of this quandary: “There is probably no subject in which more deeply rooted convictions have been held, not only in the profession but by the laity, than the connection between diet and disease, both as regards the causation and treatment of the latter.”7 Herein, a wide range of food reactions is examined to highlight evidence for the role of diet in AD, which may contradict what patients—and even some clinicians—believe.
No Easy Answers
A definitive statement that food allergy is not the root cause of AD would put this issue to rest, but such simplicity does not reflect the complex reality. First, we must agree on definitions for certain terms. What do we mean by food allergy? A broader category—adverse food reactions—covers a wide range of entities, some immune mediated and some not, including lactose intolerance, irritant contact dermatitis around the mouth, and even dermatitis herpetiformis (the cutaneous manifestation of celiac disease).8 Although the term food allergy often is used synonymously with adverse food reactions, the exact definition of a food allergy is specific: “adverse immune responses to food proteins that result in typical clinical symptoms.”8 The fact that many patients and even health care practitioners seem to frequently misapply this term makes it even more confusing.
The current focus is on foods that could trigger a flare of AD, which clearly is a broader question than food allergy sensu stricto. It seems self-evident, for example, that if an infant with AD were to (messily) eat an acidic food such as an orange, a flare-up of AD around the mouth and on the cheeks and hands would be a forgone conclusion. Similar nonimmunologic scenarios unambiguously can occur with many foods, including citrus; corn; radish; mustard; garlic; onion; pineapple; and many spices, food additives, and preservatives.9 Clearly there are some scenarios whereby food could trigger an AD flare, and yet this more limited vignette generally is not what patients are referring to when suggesting that food is the root cause of their AD.
The Labyrinth of Testing for Food Allergies
Although there is no reliable method for testing for irritant dermatitis, understanding the other types of tests may help guide our thinking. Testing for IgE-mediated food allergies generally is done via an immunoenzymatic serum assay that can document sensitization to a food protein; however, this testing by itself is not sufficient to diagnose a clinical food allergy.10 Similarly, skin prick testing allows for intradermal administration of a food extract to evaluate for an urticarial reaction within 10 to 15 minutes. Although the sensitivity and specificity vary by age, population, and the specific allergen being tested, these are limited to immediate-type reactions and do not reflect the potential to drive an eczematous flare.
The gold standard, if there is one, is likely the double-blind, placebo-controlled food challenge (DBPCFC), ideally with a long enough observation period to capture later-occurring reactions such as an AD flare. However, given the nature of the test—having patients eat the foods of concern and then carefully following them for reactions—it remains time consuming, expensive, and labor intensive.11
To further complicate matters, several unvalidated tests exist such as IgG testing, atopy patch testing, kinesiology, and hair and gastric juice analysis, which remain investigational but continue to be used and may further confuse patients and clinicians.12
Classification of Food Allergies
It is useful to first separate out the classic IgE-mediated food allergy reactions that are common. In these immediate-type reactions, a person sensitized to a food protein will develop characteristic cutaneous and/or extracutaneous reactions such as urticaria, angioedema, and even anaphylaxis, usually within minutes of exposure. Although it is possible that an IgE-mediated reaction could trigger an AD flare—perhaps simply by causing pruritus, which could initiate the itch-scratch cycle—because of the near simultaneity with ingestion of the offending food and the often dramatic clinical presentations, such foods clearly do not represent “hidden” triggers for AD flares.3 The concept of food-triggered AD (FTAD) is crucial for thinking about foods that could result in true eczematous flares, which historically have been classified as early-type (<2 hours after food challenge) and late-type (≥2 hours after food challenge) reactions.13,14
A study of more than 1000 DBPCFCs performed in patients with AD was illustrative.15 Immediate reactions other than AD were fairly common and were observed in 40% of the food challenges compared to only 9% in the placebo group. These reactions included urticaria, angioedema, and gastrointestinal and respiratory tract symptoms. Immediate reactions of AD alone were exceedingly rare at only 0.7% and not significantly elevated compared to placebo. Just over 4% experienced both an immediate AD exacerbation along with other non-AD findings, which was significantly greater than placebo (P<.01). Although intermediate and late reactions manifesting as AD exacerbations did occur after food ingestion, they were rare (2.2% or less) and not significantly different from placebo. The authors concluded that an exacerbation of AD in the absence of other allergic symptoms in children was unlikely to be due to food,15 which is an important finding.
A recent retrospective review of 372 children with AD reported similar results.4 The authors defined FTAD in a different way; instead of showing a flare after a DBPCFC, they looked for “physician-noted sustained improvement in AD upon removal of a food (typically after 2–6-wk follow-up), to which the child was sensitized without any other changes in skin care.” Despite this fundamentally different approach, they similarly concluded that while food allergies were common, FTAD was relatively uncommon—found in 2% of those with mild AD, 6% of those with moderate AD, and 4% of those with severe AD.4
There are other ways that foods could contribute to disease flares, however, and one of the most compelling is that there may be broader concepts at play; perhaps some diets are not specifically driving the AD but rather are affecting inflammation in the body at large. Although somewhat speculative, there is evidence that some foods may simply be proinflammatory, working to exacerbate the disease outside of a specific mechanism, which has been seen in a variety of other conditions such as acne or rheumatoid arthritis.16,17 To speculate further, it is possible that there may be a threshold effect such that when the AD is poorly controlled, certain factors such as inflammatory foods could lead to a flare, while when under better control, these same factors may not cause an effect.
Finally, it is important to also consider the emotional and/or psychological aspects related to food and diet. The power of the placebo in dietary change has been documented in several diseases, though this certainly is not to be dismissive of the patient’s symptoms; it seems reasonable that the very act of changing such a fundamental aspect of daily life could result in a placebo effect.18,19 In the context of relapsing and remitting conditions such as AD, this effect may be magnified. A landmark study by Thompson and Hanifin20 illustrates this possibility. The authors found that in 80% of cases in which patients were convinced that food was a major contributing factor to their AD, such concerns diminished markedly once better control of the eczema was achieved.20
Navigating the Complexity of Dietary Restrictions
This brings us to what to do with an individual patient in the examination room. Because there is such widespread concern and discussion around this topic, it is important to at least briefly address it. If there are known food allergens that are being avoided, it is important to underscore the importance of continuing to avoid those foods, especially when there is actual evidence of true food allergy rather than sensitization alone. Historically, elimination diets often were recommended empirically, though more recent studies, meta-analyses, and guidance documents increasingly have recommended against them.3 In particular, there are major concerns for iatrogenic harm.
First, heavily restricted diets may result in nutritional and/or caloric deficiencies that can be dangerous and lead to poor growth.21 Practices such as drinking unpasteurized milk can expose children to dangerous infections, while feeding them exclusively rice milk can lead to severe malnutrition.22
Second, there is a dawning realization that children with AD placed on elimination diets may actually develop true IgE-mediated allergies, including fatal anaphylaxis, to the excluded foods. In fact, one retrospective review of 298 patients with a history of AD and no prior immediate reactions found that 19% of patients developed new immediate-type hypersensitivity reactions after starting an elimination diet, presumably due to the loss of tolerance to these foods. A striking one-third of these reactions were classified as anaphylaxis, with cow’s milk and egg being the most common offenders.23
It also is crucial to acknowledge that recommending sweeping lifestyle changes is not easy for patients, especially pediatric patients. Onerous dietary restrictions may add considerable stress, ironically a known trigger for AD itself.
Finally, dietary modifications can be a distraction from conventional therapy and may result in treatment delays while the patient continues to experience uncontrolled symptoms of AD.
Final Thoughts
Diet is intimately related to AD. Although the narrative continues to unfold in fascinating domains, such as the skin barrier and the microbiome, it is increasingly clear that these are intertwined and always have been. Despite the rarity of true food-triggered AD, the perception of dietary triggers is so widespread and addressing the topic is important and may help avoid unnecessary harm from unfounded extreme dietary changes. A recent multispecialty workgroup report on AD and food allergy succinctly summarized this as: “AD has many triggers and comorbidities, and food allergy is only one of the potential triggers and comorbid conditions. With regard to AD management, education and skin care are most important.”3 With proper testing, guidance, and both topical and systemic therapies, most AD can be brought under control, and for at least some patients, this may allay concerns about foods triggering their AD.
- Eat, sleep, poop—the top 3 things new parents need to know. John’s Hopkins All Children’s Hospital website. Published May 18, 2019. Accessed September 13, 2022. https://www.hopkinsallchildrens.org/ACH-News/General-News/Eat-Sleep-Poop-%E2%80%93-The-Top-3-Things-New-Parents-Ne
- Onyimba F, Crowe SE, Johnson S, et al. Food allergies and intolerances: a clinical approach to the diagnosis and management of adverse reactions to food. Clin Gastroenterol Hepatol. 2021;19:2230-2240.e1.
- Singh AM, Anvari S, Hauk P, et al. Atopic dermatitis and food allergy: best practices and knowledge gaps—a work group report from the AAAAI Allergic Skin Diseases Committee and Leadership Institute Project. J Allergy Clin Immunol Pract. 2022;10:697-706.
- Li JC, Arkin LM, Makhija MM, et al. Prevalence of food allergy diagnosis in pediatric patients with atopic dermatitis referred to allergy and/or dermatology subspecialty clinics. J Allergy Clin Immunol Pract. 2022;10:2469-2471.
- Thompson MM, Tofte SJ, Simpson EL, et al. Patterns of care and referral in children with atopic dermatitis and concern for food allergy. Dermatol Ther. 2006;19:91-96.
- Johnston GA, Bilbao RM, Graham-Brown RAC. The use of dietary manipulation by parents of children with atopic dermatitis. Br J Dermatol. 2004;150:1186-1189.
- Mackenzie S. The inaugural address on the advantages to be derived from the study of dermatology: delivered to the Reading Pathological Society. Br Med J. 1896;1:193-197.
- Anvari S, Miller J, Yeh CY, et al. IgE-mediated food allergy. Clin Rev Allergy Immunol. 2019;57:244-260.
- Brancaccio RR, Alvarez MS. Contact allergy to food. Dermatol Ther. 2004;17:302-313.
- Robison RG, Singh AM. Controversies in allergy: food testing and dietary avoidance in atopic dermatitis. J Allergy Clin Immunol Pract. 2019;7:35-39.
- Sicherer SH, Morrow EH, Sampson HA. Dose-response in double-blind, placebo-controlled oral food challenges in children with atopic dermatitis. J Allergy Clin Immunol. 2000;105:582-586.
- Kelso JM. Unproven diagnostic tests for adverse reactions to foods. J Allergy Clin Immunol Pract. 2018;6:362-365.
- Heratizadeh A, Wichmann K, Werfel T. Food allergy and atopic dermatitis: how are they connected? Curr Allergy Asthma Rep. 2011;11:284-291.
- Breuer K, Heratizadeh A, Wulf A, et al. Late eczematous reactions to food in children with atopic dermatitis. Clin Exp Allergy. 2004;34:817-824.
- Roerdink EM, Flokstra-de Blok BMJ, Blok JL, et al. Association of food allergy and atopic dermatitis exacerbations. Ann Allergy Asthma Immunol. 2016;116:334-338.
- Fuglsang G, Madsen G, Halken S, et al. Adverse reactions to food additives in children with atopic symptoms. Allergy. 1994;49:31-37.
- Ehlers I, Worm M, Sterry W, et al. Sugar is not an aggravating factor in atopic dermatitis. Acta Derm Venereol. 2001;81:282-284.
- Staudacher HM, Irving PM, Lomer MCE, et al. The challenges of control groups, placebos and blinding in clinical trials of dietary interventions. Proc Nutr Soc. 2017;76:203-212.
- Masi A, Lampit A, Glozier N, et al. Predictors of placebo response in pharmacological and dietary supplement treatment trials in pediatric autism spectrum disorder: a meta-analysis. Transl Psychiatry. 2015;5:E640.
- Thompson MM, Hanifin JM. Effective therapy of childhood atopic dermatitis allays food allergy concerns. J Am Acad Dermatol. 2005;53(2 suppl 2):S214-S219.
- Meyer R, De Koker C, Dziubak R, et al. The impact of the elimination diet on growth and nutrient intake in children with food protein induced gastrointestinal allergies. Clin Transl Allergy. 2016;6:25.
- Webber SA, Graham-Brown RA, Hutchinson PE, et al. Dietary manipulation in childhood atopic dermatitis. Br J Dermatol. 1989;121:91-98.
- Chang A, Robison R, Cai M, et al. Natural history of food-triggered atopic dermatitis and development of immediate reactions in children. J Allergy Clin Immunol Pract. 2016;4:229-236.e1.
It is unsurprising that food frequently is thought to be the culprit behind an eczema flare, especially in infants. Indeed, it often is said that infants do only 3 things: eat, sleep, and poop.1 For those unfortunate enough to develop the signs and symptoms of atopic dermatitis (AD), food quickly emerges as a potential culprit from the tiny pool of suspects, which is against a cultural backdrop of unprecedented focus on foods and food reactions.2 The prevalence of food allergies in children, though admittedly fraught with methodological difficulties, is estimated to have more than doubled from 3.4% in 1999 to 7.6% in 2018.3 As expected, prevalence rates were higher among children with other atopic comorbidities including AD, with up to 50% of children with AD demonstrating convincing food allergy.4 It is easy to imagine a patient conflating these 2 entities and mistaking their correlation for causation. Thus, it follows that more than 90% of parents/guardians have reported that their children have had food-induced AD, and understandably—at least according to one study—75% of parents/guardians were found to have manipulated the diet in an attempt to manage the disease.5,6
Patients and parents/guardians are not the only ones who have suspected food as a driving force in AD. An article in the British Medical Journal from the 1800s beautifully encapsulated the depth and duration of this quandary: “There is probably no subject in which more deeply rooted convictions have been held, not only in the profession but by the laity, than the connection between diet and disease, both as regards the causation and treatment of the latter.”7 Herein, a wide range of food reactions is examined to highlight evidence for the role of diet in AD, which may contradict what patients—and even some clinicians—believe.
No Easy Answers
A definitive statement that food allergy is not the root cause of AD would put this issue to rest, but such simplicity does not reflect the complex reality. First, we must agree on definitions for certain terms. What do we mean by food allergy? A broader category—adverse food reactions—covers a wide range of entities, some immune mediated and some not, including lactose intolerance, irritant contact dermatitis around the mouth, and even dermatitis herpetiformis (the cutaneous manifestation of celiac disease).8 Although the term food allergy often is used synonymously with adverse food reactions, the exact definition of a food allergy is specific: “adverse immune responses to food proteins that result in typical clinical symptoms.”8 The fact that many patients and even health care practitioners seem to frequently misapply this term makes it even more confusing.
The current focus is on foods that could trigger a flare of AD, which clearly is a broader question than food allergy sensu stricto. It seems self-evident, for example, that if an infant with AD were to (messily) eat an acidic food such as an orange, a flare-up of AD around the mouth and on the cheeks and hands would be a forgone conclusion. Similar nonimmunologic scenarios unambiguously can occur with many foods, including citrus; corn; radish; mustard; garlic; onion; pineapple; and many spices, food additives, and preservatives.9 Clearly there are some scenarios whereby food could trigger an AD flare, and yet this more limited vignette generally is not what patients are referring to when suggesting that food is the root cause of their AD.
The Labyrinth of Testing for Food Allergies
Although there is no reliable method for testing for irritant dermatitis, understanding the other types of tests may help guide our thinking. Testing for IgE-mediated food allergies generally is done via an immunoenzymatic serum assay that can document sensitization to a food protein; however, this testing by itself is not sufficient to diagnose a clinical food allergy.10 Similarly, skin prick testing allows for intradermal administration of a food extract to evaluate for an urticarial reaction within 10 to 15 minutes. Although the sensitivity and specificity vary by age, population, and the specific allergen being tested, these are limited to immediate-type reactions and do not reflect the potential to drive an eczematous flare.
The gold standard, if there is one, is likely the double-blind, placebo-controlled food challenge (DBPCFC), ideally with a long enough observation period to capture later-occurring reactions such as an AD flare. However, given the nature of the test—having patients eat the foods of concern and then carefully following them for reactions—it remains time consuming, expensive, and labor intensive.11
To further complicate matters, several unvalidated tests exist such as IgG testing, atopy patch testing, kinesiology, and hair and gastric juice analysis, which remain investigational but continue to be used and may further confuse patients and clinicians.12
Classification of Food Allergies
It is useful to first separate out the classic IgE-mediated food allergy reactions that are common. In these immediate-type reactions, a person sensitized to a food protein will develop characteristic cutaneous and/or extracutaneous reactions such as urticaria, angioedema, and even anaphylaxis, usually within minutes of exposure. Although it is possible that an IgE-mediated reaction could trigger an AD flare—perhaps simply by causing pruritus, which could initiate the itch-scratch cycle—because of the near simultaneity with ingestion of the offending food and the often dramatic clinical presentations, such foods clearly do not represent “hidden” triggers for AD flares.3 The concept of food-triggered AD (FTAD) is crucial for thinking about foods that could result in true eczematous flares, which historically have been classified as early-type (<2 hours after food challenge) and late-type (≥2 hours after food challenge) reactions.13,14
A study of more than 1000 DBPCFCs performed in patients with AD was illustrative.15 Immediate reactions other than AD were fairly common and were observed in 40% of the food challenges compared to only 9% in the placebo group. These reactions included urticaria, angioedema, and gastrointestinal and respiratory tract symptoms. Immediate reactions of AD alone were exceedingly rare at only 0.7% and not significantly elevated compared to placebo. Just over 4% experienced both an immediate AD exacerbation along with other non-AD findings, which was significantly greater than placebo (P<.01). Although intermediate and late reactions manifesting as AD exacerbations did occur after food ingestion, they were rare (2.2% or less) and not significantly different from placebo. The authors concluded that an exacerbation of AD in the absence of other allergic symptoms in children was unlikely to be due to food,15 which is an important finding.
A recent retrospective review of 372 children with AD reported similar results.4 The authors defined FTAD in a different way; instead of showing a flare after a DBPCFC, they looked for “physician-noted sustained improvement in AD upon removal of a food (typically after 2–6-wk follow-up), to which the child was sensitized without any other changes in skin care.” Despite this fundamentally different approach, they similarly concluded that while food allergies were common, FTAD was relatively uncommon—found in 2% of those with mild AD, 6% of those with moderate AD, and 4% of those with severe AD.4
There are other ways that foods could contribute to disease flares, however, and one of the most compelling is that there may be broader concepts at play; perhaps some diets are not specifically driving the AD but rather are affecting inflammation in the body at large. Although somewhat speculative, there is evidence that some foods may simply be proinflammatory, working to exacerbate the disease outside of a specific mechanism, which has been seen in a variety of other conditions such as acne or rheumatoid arthritis.16,17 To speculate further, it is possible that there may be a threshold effect such that when the AD is poorly controlled, certain factors such as inflammatory foods could lead to a flare, while when under better control, these same factors may not cause an effect.
Finally, it is important to also consider the emotional and/or psychological aspects related to food and diet. The power of the placebo in dietary change has been documented in several diseases, though this certainly is not to be dismissive of the patient’s symptoms; it seems reasonable that the very act of changing such a fundamental aspect of daily life could result in a placebo effect.18,19 In the context of relapsing and remitting conditions such as AD, this effect may be magnified. A landmark study by Thompson and Hanifin20 illustrates this possibility. The authors found that in 80% of cases in which patients were convinced that food was a major contributing factor to their AD, such concerns diminished markedly once better control of the eczema was achieved.20
Navigating the Complexity of Dietary Restrictions
This brings us to what to do with an individual patient in the examination room. Because there is such widespread concern and discussion around this topic, it is important to at least briefly address it. If there are known food allergens that are being avoided, it is important to underscore the importance of continuing to avoid those foods, especially when there is actual evidence of true food allergy rather than sensitization alone. Historically, elimination diets often were recommended empirically, though more recent studies, meta-analyses, and guidance documents increasingly have recommended against them.3 In particular, there are major concerns for iatrogenic harm.
First, heavily restricted diets may result in nutritional and/or caloric deficiencies that can be dangerous and lead to poor growth.21 Practices such as drinking unpasteurized milk can expose children to dangerous infections, while feeding them exclusively rice milk can lead to severe malnutrition.22
Second, there is a dawning realization that children with AD placed on elimination diets may actually develop true IgE-mediated allergies, including fatal anaphylaxis, to the excluded foods. In fact, one retrospective review of 298 patients with a history of AD and no prior immediate reactions found that 19% of patients developed new immediate-type hypersensitivity reactions after starting an elimination diet, presumably due to the loss of tolerance to these foods. A striking one-third of these reactions were classified as anaphylaxis, with cow’s milk and egg being the most common offenders.23
It also is crucial to acknowledge that recommending sweeping lifestyle changes is not easy for patients, especially pediatric patients. Onerous dietary restrictions may add considerable stress, ironically a known trigger for AD itself.
Finally, dietary modifications can be a distraction from conventional therapy and may result in treatment delays while the patient continues to experience uncontrolled symptoms of AD.
Final Thoughts
Diet is intimately related to AD. Although the narrative continues to unfold in fascinating domains, such as the skin barrier and the microbiome, it is increasingly clear that these are intertwined and always have been. Despite the rarity of true food-triggered AD, the perception of dietary triggers is so widespread and addressing the topic is important and may help avoid unnecessary harm from unfounded extreme dietary changes. A recent multispecialty workgroup report on AD and food allergy succinctly summarized this as: “AD has many triggers and comorbidities, and food allergy is only one of the potential triggers and comorbid conditions. With regard to AD management, education and skin care are most important.”3 With proper testing, guidance, and both topical and systemic therapies, most AD can be brought under control, and for at least some patients, this may allay concerns about foods triggering their AD.
It is unsurprising that food frequently is thought to be the culprit behind an eczema flare, especially in infants. Indeed, it often is said that infants do only 3 things: eat, sleep, and poop.1 For those unfortunate enough to develop the signs and symptoms of atopic dermatitis (AD), food quickly emerges as a potential culprit from the tiny pool of suspects, which is against a cultural backdrop of unprecedented focus on foods and food reactions.2 The prevalence of food allergies in children, though admittedly fraught with methodological difficulties, is estimated to have more than doubled from 3.4% in 1999 to 7.6% in 2018.3 As expected, prevalence rates were higher among children with other atopic comorbidities including AD, with up to 50% of children with AD demonstrating convincing food allergy.4 It is easy to imagine a patient conflating these 2 entities and mistaking their correlation for causation. Thus, it follows that more than 90% of parents/guardians have reported that their children have had food-induced AD, and understandably—at least according to one study—75% of parents/guardians were found to have manipulated the diet in an attempt to manage the disease.5,6
Patients and parents/guardians are not the only ones who have suspected food as a driving force in AD. An article in the British Medical Journal from the 1800s beautifully encapsulated the depth and duration of this quandary: “There is probably no subject in which more deeply rooted convictions have been held, not only in the profession but by the laity, than the connection between diet and disease, both as regards the causation and treatment of the latter.”7 Herein, a wide range of food reactions is examined to highlight evidence for the role of diet in AD, which may contradict what patients—and even some clinicians—believe.
No Easy Answers
A definitive statement that food allergy is not the root cause of AD would put this issue to rest, but such simplicity does not reflect the complex reality. First, we must agree on definitions for certain terms. What do we mean by food allergy? A broader category—adverse food reactions—covers a wide range of entities, some immune mediated and some not, including lactose intolerance, irritant contact dermatitis around the mouth, and even dermatitis herpetiformis (the cutaneous manifestation of celiac disease).8 Although the term food allergy often is used synonymously with adverse food reactions, the exact definition of a food allergy is specific: “adverse immune responses to food proteins that result in typical clinical symptoms.”8 The fact that many patients and even health care practitioners seem to frequently misapply this term makes it even more confusing.
The current focus is on foods that could trigger a flare of AD, which clearly is a broader question than food allergy sensu stricto. It seems self-evident, for example, that if an infant with AD were to (messily) eat an acidic food such as an orange, a flare-up of AD around the mouth and on the cheeks and hands would be a forgone conclusion. Similar nonimmunologic scenarios unambiguously can occur with many foods, including citrus; corn; radish; mustard; garlic; onion; pineapple; and many spices, food additives, and preservatives.9 Clearly there are some scenarios whereby food could trigger an AD flare, and yet this more limited vignette generally is not what patients are referring to when suggesting that food is the root cause of their AD.
The Labyrinth of Testing for Food Allergies
Although there is no reliable method for testing for irritant dermatitis, understanding the other types of tests may help guide our thinking. Testing for IgE-mediated food allergies generally is done via an immunoenzymatic serum assay that can document sensitization to a food protein; however, this testing by itself is not sufficient to diagnose a clinical food allergy.10 Similarly, skin prick testing allows for intradermal administration of a food extract to evaluate for an urticarial reaction within 10 to 15 minutes. Although the sensitivity and specificity vary by age, population, and the specific allergen being tested, these are limited to immediate-type reactions and do not reflect the potential to drive an eczematous flare.
The gold standard, if there is one, is likely the double-blind, placebo-controlled food challenge (DBPCFC), ideally with a long enough observation period to capture later-occurring reactions such as an AD flare. However, given the nature of the test—having patients eat the foods of concern and then carefully following them for reactions—it remains time consuming, expensive, and labor intensive.11
To further complicate matters, several unvalidated tests exist such as IgG testing, atopy patch testing, kinesiology, and hair and gastric juice analysis, which remain investigational but continue to be used and may further confuse patients and clinicians.12
Classification of Food Allergies
It is useful to first separate out the classic IgE-mediated food allergy reactions that are common. In these immediate-type reactions, a person sensitized to a food protein will develop characteristic cutaneous and/or extracutaneous reactions such as urticaria, angioedema, and even anaphylaxis, usually within minutes of exposure. Although it is possible that an IgE-mediated reaction could trigger an AD flare—perhaps simply by causing pruritus, which could initiate the itch-scratch cycle—because of the near simultaneity with ingestion of the offending food and the often dramatic clinical presentations, such foods clearly do not represent “hidden” triggers for AD flares.3 The concept of food-triggered AD (FTAD) is crucial for thinking about foods that could result in true eczematous flares, which historically have been classified as early-type (<2 hours after food challenge) and late-type (≥2 hours after food challenge) reactions.13,14
A study of more than 1000 DBPCFCs performed in patients with AD was illustrative.15 Immediate reactions other than AD were fairly common and were observed in 40% of the food challenges compared to only 9% in the placebo group. These reactions included urticaria, angioedema, and gastrointestinal and respiratory tract symptoms. Immediate reactions of AD alone were exceedingly rare at only 0.7% and not significantly elevated compared to placebo. Just over 4% experienced both an immediate AD exacerbation along with other non-AD findings, which was significantly greater than placebo (P<.01). Although intermediate and late reactions manifesting as AD exacerbations did occur after food ingestion, they were rare (2.2% or less) and not significantly different from placebo. The authors concluded that an exacerbation of AD in the absence of other allergic symptoms in children was unlikely to be due to food,15 which is an important finding.
A recent retrospective review of 372 children with AD reported similar results.4 The authors defined FTAD in a different way; instead of showing a flare after a DBPCFC, they looked for “physician-noted sustained improvement in AD upon removal of a food (typically after 2–6-wk follow-up), to which the child was sensitized without any other changes in skin care.” Despite this fundamentally different approach, they similarly concluded that while food allergies were common, FTAD was relatively uncommon—found in 2% of those with mild AD, 6% of those with moderate AD, and 4% of those with severe AD.4
There are other ways that foods could contribute to disease flares, however, and one of the most compelling is that there may be broader concepts at play; perhaps some diets are not specifically driving the AD but rather are affecting inflammation in the body at large. Although somewhat speculative, there is evidence that some foods may simply be proinflammatory, working to exacerbate the disease outside of a specific mechanism, which has been seen in a variety of other conditions such as acne or rheumatoid arthritis.16,17 To speculate further, it is possible that there may be a threshold effect such that when the AD is poorly controlled, certain factors such as inflammatory foods could lead to a flare, while when under better control, these same factors may not cause an effect.
Finally, it is important to also consider the emotional and/or psychological aspects related to food and diet. The power of the placebo in dietary change has been documented in several diseases, though this certainly is not to be dismissive of the patient’s symptoms; it seems reasonable that the very act of changing such a fundamental aspect of daily life could result in a placebo effect.18,19 In the context of relapsing and remitting conditions such as AD, this effect may be magnified. A landmark study by Thompson and Hanifin20 illustrates this possibility. The authors found that in 80% of cases in which patients were convinced that food was a major contributing factor to their AD, such concerns diminished markedly once better control of the eczema was achieved.20
Navigating the Complexity of Dietary Restrictions
This brings us to what to do with an individual patient in the examination room. Because there is such widespread concern and discussion around this topic, it is important to at least briefly address it. If there are known food allergens that are being avoided, it is important to underscore the importance of continuing to avoid those foods, especially when there is actual evidence of true food allergy rather than sensitization alone. Historically, elimination diets often were recommended empirically, though more recent studies, meta-analyses, and guidance documents increasingly have recommended against them.3 In particular, there are major concerns for iatrogenic harm.
First, heavily restricted diets may result in nutritional and/or caloric deficiencies that can be dangerous and lead to poor growth.21 Practices such as drinking unpasteurized milk can expose children to dangerous infections, while feeding them exclusively rice milk can lead to severe malnutrition.22
Second, there is a dawning realization that children with AD placed on elimination diets may actually develop true IgE-mediated allergies, including fatal anaphylaxis, to the excluded foods. In fact, one retrospective review of 298 patients with a history of AD and no prior immediate reactions found that 19% of patients developed new immediate-type hypersensitivity reactions after starting an elimination diet, presumably due to the loss of tolerance to these foods. A striking one-third of these reactions were classified as anaphylaxis, with cow’s milk and egg being the most common offenders.23
It also is crucial to acknowledge that recommending sweeping lifestyle changes is not easy for patients, especially pediatric patients. Onerous dietary restrictions may add considerable stress, ironically a known trigger for AD itself.
Finally, dietary modifications can be a distraction from conventional therapy and may result in treatment delays while the patient continues to experience uncontrolled symptoms of AD.
Final Thoughts
Diet is intimately related to AD. Although the narrative continues to unfold in fascinating domains, such as the skin barrier and the microbiome, it is increasingly clear that these are intertwined and always have been. Despite the rarity of true food-triggered AD, the perception of dietary triggers is so widespread and addressing the topic is important and may help avoid unnecessary harm from unfounded extreme dietary changes. A recent multispecialty workgroup report on AD and food allergy succinctly summarized this as: “AD has many triggers and comorbidities, and food allergy is only one of the potential triggers and comorbid conditions. With regard to AD management, education and skin care are most important.”3 With proper testing, guidance, and both topical and systemic therapies, most AD can be brought under control, and for at least some patients, this may allay concerns about foods triggering their AD.
- Eat, sleep, poop—the top 3 things new parents need to know. John’s Hopkins All Children’s Hospital website. Published May 18, 2019. Accessed September 13, 2022. https://www.hopkinsallchildrens.org/ACH-News/General-News/Eat-Sleep-Poop-%E2%80%93-The-Top-3-Things-New-Parents-Ne
- Onyimba F, Crowe SE, Johnson S, et al. Food allergies and intolerances: a clinical approach to the diagnosis and management of adverse reactions to food. Clin Gastroenterol Hepatol. 2021;19:2230-2240.e1.
- Singh AM, Anvari S, Hauk P, et al. Atopic dermatitis and food allergy: best practices and knowledge gaps—a work group report from the AAAAI Allergic Skin Diseases Committee and Leadership Institute Project. J Allergy Clin Immunol Pract. 2022;10:697-706.
- Li JC, Arkin LM, Makhija MM, et al. Prevalence of food allergy diagnosis in pediatric patients with atopic dermatitis referred to allergy and/or dermatology subspecialty clinics. J Allergy Clin Immunol Pract. 2022;10:2469-2471.
- Thompson MM, Tofte SJ, Simpson EL, et al. Patterns of care and referral in children with atopic dermatitis and concern for food allergy. Dermatol Ther. 2006;19:91-96.
- Johnston GA, Bilbao RM, Graham-Brown RAC. The use of dietary manipulation by parents of children with atopic dermatitis. Br J Dermatol. 2004;150:1186-1189.
- Mackenzie S. The inaugural address on the advantages to be derived from the study of dermatology: delivered to the Reading Pathological Society. Br Med J. 1896;1:193-197.
- Anvari S, Miller J, Yeh CY, et al. IgE-mediated food allergy. Clin Rev Allergy Immunol. 2019;57:244-260.
- Brancaccio RR, Alvarez MS. Contact allergy to food. Dermatol Ther. 2004;17:302-313.
- Robison RG, Singh AM. Controversies in allergy: food testing and dietary avoidance in atopic dermatitis. J Allergy Clin Immunol Pract. 2019;7:35-39.
- Sicherer SH, Morrow EH, Sampson HA. Dose-response in double-blind, placebo-controlled oral food challenges in children with atopic dermatitis. J Allergy Clin Immunol. 2000;105:582-586.
- Kelso JM. Unproven diagnostic tests for adverse reactions to foods. J Allergy Clin Immunol Pract. 2018;6:362-365.
- Heratizadeh A, Wichmann K, Werfel T. Food allergy and atopic dermatitis: how are they connected? Curr Allergy Asthma Rep. 2011;11:284-291.
- Breuer K, Heratizadeh A, Wulf A, et al. Late eczematous reactions to food in children with atopic dermatitis. Clin Exp Allergy. 2004;34:817-824.
- Roerdink EM, Flokstra-de Blok BMJ, Blok JL, et al. Association of food allergy and atopic dermatitis exacerbations. Ann Allergy Asthma Immunol. 2016;116:334-338.
- Fuglsang G, Madsen G, Halken S, et al. Adverse reactions to food additives in children with atopic symptoms. Allergy. 1994;49:31-37.
- Ehlers I, Worm M, Sterry W, et al. Sugar is not an aggravating factor in atopic dermatitis. Acta Derm Venereol. 2001;81:282-284.
- Staudacher HM, Irving PM, Lomer MCE, et al. The challenges of control groups, placebos and blinding in clinical trials of dietary interventions. Proc Nutr Soc. 2017;76:203-212.
- Masi A, Lampit A, Glozier N, et al. Predictors of placebo response in pharmacological and dietary supplement treatment trials in pediatric autism spectrum disorder: a meta-analysis. Transl Psychiatry. 2015;5:E640.
- Thompson MM, Hanifin JM. Effective therapy of childhood atopic dermatitis allays food allergy concerns. J Am Acad Dermatol. 2005;53(2 suppl 2):S214-S219.
- Meyer R, De Koker C, Dziubak R, et al. The impact of the elimination diet on growth and nutrient intake in children with food protein induced gastrointestinal allergies. Clin Transl Allergy. 2016;6:25.
- Webber SA, Graham-Brown RA, Hutchinson PE, et al. Dietary manipulation in childhood atopic dermatitis. Br J Dermatol. 1989;121:91-98.
- Chang A, Robison R, Cai M, et al. Natural history of food-triggered atopic dermatitis and development of immediate reactions in children. J Allergy Clin Immunol Pract. 2016;4:229-236.e1.
- Eat, sleep, poop—the top 3 things new parents need to know. John’s Hopkins All Children’s Hospital website. Published May 18, 2019. Accessed September 13, 2022. https://www.hopkinsallchildrens.org/ACH-News/General-News/Eat-Sleep-Poop-%E2%80%93-The-Top-3-Things-New-Parents-Ne
- Onyimba F, Crowe SE, Johnson S, et al. Food allergies and intolerances: a clinical approach to the diagnosis and management of adverse reactions to food. Clin Gastroenterol Hepatol. 2021;19:2230-2240.e1.
- Singh AM, Anvari S, Hauk P, et al. Atopic dermatitis and food allergy: best practices and knowledge gaps—a work group report from the AAAAI Allergic Skin Diseases Committee and Leadership Institute Project. J Allergy Clin Immunol Pract. 2022;10:697-706.
- Li JC, Arkin LM, Makhija MM, et al. Prevalence of food allergy diagnosis in pediatric patients with atopic dermatitis referred to allergy and/or dermatology subspecialty clinics. J Allergy Clin Immunol Pract. 2022;10:2469-2471.
- Thompson MM, Tofte SJ, Simpson EL, et al. Patterns of care and referral in children with atopic dermatitis and concern for food allergy. Dermatol Ther. 2006;19:91-96.
- Johnston GA, Bilbao RM, Graham-Brown RAC. The use of dietary manipulation by parents of children with atopic dermatitis. Br J Dermatol. 2004;150:1186-1189.
- Mackenzie S. The inaugural address on the advantages to be derived from the study of dermatology: delivered to the Reading Pathological Society. Br Med J. 1896;1:193-197.
- Anvari S, Miller J, Yeh CY, et al. IgE-mediated food allergy. Clin Rev Allergy Immunol. 2019;57:244-260.
- Brancaccio RR, Alvarez MS. Contact allergy to food. Dermatol Ther. 2004;17:302-313.
- Robison RG, Singh AM. Controversies in allergy: food testing and dietary avoidance in atopic dermatitis. J Allergy Clin Immunol Pract. 2019;7:35-39.
- Sicherer SH, Morrow EH, Sampson HA. Dose-response in double-blind, placebo-controlled oral food challenges in children with atopic dermatitis. J Allergy Clin Immunol. 2000;105:582-586.
- Kelso JM. Unproven diagnostic tests for adverse reactions to foods. J Allergy Clin Immunol Pract. 2018;6:362-365.
- Heratizadeh A, Wichmann K, Werfel T. Food allergy and atopic dermatitis: how are they connected? Curr Allergy Asthma Rep. 2011;11:284-291.
- Breuer K, Heratizadeh A, Wulf A, et al. Late eczematous reactions to food in children with atopic dermatitis. Clin Exp Allergy. 2004;34:817-824.
- Roerdink EM, Flokstra-de Blok BMJ, Blok JL, et al. Association of food allergy and atopic dermatitis exacerbations. Ann Allergy Asthma Immunol. 2016;116:334-338.
- Fuglsang G, Madsen G, Halken S, et al. Adverse reactions to food additives in children with atopic symptoms. Allergy. 1994;49:31-37.
- Ehlers I, Worm M, Sterry W, et al. Sugar is not an aggravating factor in atopic dermatitis. Acta Derm Venereol. 2001;81:282-284.
- Staudacher HM, Irving PM, Lomer MCE, et al. The challenges of control groups, placebos and blinding in clinical trials of dietary interventions. Proc Nutr Soc. 2017;76:203-212.
- Masi A, Lampit A, Glozier N, et al. Predictors of placebo response in pharmacological and dietary supplement treatment trials in pediatric autism spectrum disorder: a meta-analysis. Transl Psychiatry. 2015;5:E640.
- Thompson MM, Hanifin JM. Effective therapy of childhood atopic dermatitis allays food allergy concerns. J Am Acad Dermatol. 2005;53(2 suppl 2):S214-S219.
- Meyer R, De Koker C, Dziubak R, et al. The impact of the elimination diet on growth and nutrient intake in children with food protein induced gastrointestinal allergies. Clin Transl Allergy. 2016;6:25.
- Webber SA, Graham-Brown RA, Hutchinson PE, et al. Dietary manipulation in childhood atopic dermatitis. Br J Dermatol. 1989;121:91-98.
- Chang A, Robison R, Cai M, et al. Natural history of food-triggered atopic dermatitis and development of immediate reactions in children. J Allergy Clin Immunol Pract. 2016;4:229-236.e1.
Practice Points
- The perception of dietary triggers is so entrenched and widespread that it should be addressed even when thought to be irrelevant.
- It is important not to dismiss food as a factor in atopic dermatitis (AD), as it can play a number of roles in the condition.
- On the other hand, education about the wide range of food reactions and the relative rarity of true food-driven AD along with the potential risks of dietary modification may enhance both rapport and understanding between the clinician and patient.
Disaster Preparedness in Dermatology Residency Programs
In an age of changing climate and emerging global pandemics, the ability of residency programs to prepare for and adapt to potential disasters may be paramount in preserving the training of physicians. The current literature regarding residency program disaster preparedness, which focuses predominantly on hurricanes and COVID-19,1-8 is lacking in recommendations specific to dermatology residency programs. Likewise, the Accreditation Council for Graduate Medical Education (ACGME) guidelines9 do not address dermatology-specific concerns in disaster preparedness or response. Herein, we propose recommendations to mitigate the impact of various types of disasters on dermatology residency programs and their trainees with regard to resident safety and wellness, resident education, and patient care (Table).
Resident Safety and Wellness
Role of the Program Director—The role of the program director is critical, serving as a figure of structure and reassurance.4,7,10 Once concern of disaster arises, the program director should contact the Designated Institutional Official (DIO) to express concerns about possible disruptions to resident training. The DIO should then contact the ACGME within 10 days to report the disaster and submit a request for emergency (eg, pandemic) or extraordinary circumstances (eg, natural disaster) categorization.4,9 Program directors should promptly prepare plans for program reconfiguration and resident transfers in alignment with ACGME requirements to maintain evaluation and completion of core competencies of training during disasters.9 Program directors should prioritize the safety of trainees during the immediate threat with clear guidelines on sheltering, evacuations, or quarantines; a timeline of program recovery based on communication with residents, faculty, and administration should then be established.10,11
Communication—Establishing a strong line of communication between program directors and residents is paramount. Collection of emergency noninstitutional contact information, establishment of a centralized website for information dissemination, use of noninstitutional email and proxy servers outside of the location of impact, social media updates, on-site use of 2-way radios, and program-wide conference calls when possible should be strongly considered as part of the disaster response.2-4,12,13
Resident Accommodations and Mental Health—If training is disrupted, residents should be reassured of continued access to salary, housing, food, or other resources as necessary.3,4,11 There should be clear contingency plans if residents need to leave the program for extended periods of time due to injury, illness, or personal circumstances. Although relevant in all types of disasters, resident mental health and response to trauma also must be addressed. Access to counseling, morale-building opportunities (eg, resident social events), and screening for depression or posttraumatic stress disorder may help promote well-being among residents following traumatic events.14
Resident Education
Participation in Disaster Relief—Residents may seek to aid in the disaster response, which may prove challenging in the setting of programs with high patient volume.4 In coordination with the ACGME and graduate medical education governing bodies, program directors should consider how residents may fulfill dermatology training requirements in conjunction with disaster relief efforts, such as working in an inpatient setting or providing wound care.10
Continued Didactic Education—The use of online learning and conference calls for continuing the dermatology curriculum is an efficient means to maintaining resident education when meeting in person poses risks to residents.15 Projections of microscopy images, clinical photographs, or other instructional materials allow for continued instruction on resident examination, histopathology, and diagnostic skills.
Continued Clinical Training—If the home institution cannot support the operation of dermatology clinics, residents should be guaranteed continued training at other institutions. Agreements with other dermatology programs, community hospitals, or private dermatology practices should be established in advance, with consideration given to the number of residents a program can support, funding transfers, and credentialing requirements.2,4,5
Prolonged Disruptions—Nonessential departments of medical institutions may cease to function during war or mass casualty disasters, and it may be unsafe to send dermatology residents to other institutions or clinical areas. If the threat is prolonged, programs may need to consider allowing current residents a longer duration of training despite potential overlap with incoming dermatology residents.7
Patient Care
Disruptions to Clinic Operations—Regarding threats of violence, dangerous exposures, or natural disasters, there should be clear guidelines on sheltering in the clinical setting or stabilizing patients during a procedure.11 Equipment used by residents such as laptops, microscopes, and treatment devices (eg, lasers) should be stored in weather-safe locations that would not be notably impacted by moisture or structural damage to the clinic building. If electricity or internet access are compromised, paper medical records should be available to residents to continue clinical operations. Electronic health records used by residents should regularly be backed up on remote servers or cloud storage to allow continued access to patient health information if on-site servers are not functional.12 If disruptions are prolonged, residency program administration should coordinate with the institution to ensure there is adequate supply and storage of medications (eg, lidocaine, botulinum toxin) as well as a continued means of delivering biologic medications to patients and an ability to obtain laboratory or dermatopathology services.
In-Person Appointments vs Telemedicine—There are benefits to both residency training and patient care when physicians are able to perform in-person examinations, biopsies, and in-office treatments.16 Programs should ensure an adequate supply of personal protective equipment to continue in-office appointments, vaccinations, and medical care if a resident or other members of the team are exposed to an infectious disease.7 If in-person appointments are limited or impossible, telemedicine capabilities may still allow residents to meet program requirements.7,10,15 However, reduced patient volume due to decreased elective visits or procedures may complicate the fulfillment of clinical requirements, which may need to be adjusted in the wake of a disaster.7
Use of Immunosuppressive Therapies—Residency programs should address the risks of prescribing immunosuppressive therapies (eg, biologics) during an infectious threat with their residents and encourage trainees to counsel patients on the importance of preventative measures to reduce risks for severe infection.17
Final Thoughts
- Davis W. Hurricane Katrina: the challenge to graduate medical education. Ochsner J. 2006;6:39.
- Cefalu CA, Schwartz RS. Salvaging a geriatric medicine academic program in disaster mode—the LSU training program post-Katrina.J Natl Med Assoc. 2007;99:590-596.
- Ayyala R. Lessons from Katrina: a program director’s perspective. Ophthalmology. 2007;114:1425-1426.
- Wiese JG. Leadership in graduate medical education: eleven steps instrumental in recovering residency programs after a disaster. Am J Med Sci. 2008;336:168-173.
- Griffies WS. Post-Katrina stabilization of the LSU/Ochsner Psychiatry Residency Program: caveats for disaster preparedness. Acad Psychiatry. 2009;33:418-422.
- Kearns DG, Chat VS, Uppal S, et al. Applying to dermatology residency during the COVID-19 pandemic. J Am Acad Dermatol. 2020;83:1214-1215.
- Matthews JB, Blair PG, Ellison EC, et al. Checklist framework for surgical education disaster plans. J Am Coll Surg. 2021;233:557-563.
- Litchman GH, Marson JW, Rigel DS. The continuing impact of COVID-19 on dermatology practice: office workflow, economics, and future implications. J Am Acad Dermatol. 2021;84:576-579.
- Accreditation Council for Graduate Medical Education. Sponsoring institution emergency categorization. Accessed October 20, 2022. https://www.acgme.org/covid-19/sponsoring-institution-emergency-categorization/
- Li YM, Galimberti F, Abrouk M, et al. US dermatology resident responses about the COVID-19 pandemic: results from a nationwide survey. South Med J. 2020;113:462-465.
- Newman B, Gallion C. Hurricane Harvey: firsthand perspectives for disaster preparedness in graduate medical education. Acad Med. 2019;94:1267-1269.
- Pero CD, Pou AM, Arriaga MA, et al. Post-Katrina: study in crisis-related program adaptability. Otolaryngol Head Neck Surg. 2008;138:394-397.
- Hattaway R, Singh N, Rais-Bahrami S, et al. Adaptations of dermatology residency programs to changes in medical education amid the COVID-19 pandemic: virtual opportunities and social media. SKIN. 2021;5:94-100.
- Hillier K, Paskaradevan J, Wilkes JK, et al. Disaster plans: resident involvement and well-being during Hurricane Harvey. J Grad Med Educ. 2019;11:129-131.
- Samimi S, Choi J, Rosman IS, et al. Impact of COVID-19 on dermatology residency. Dermatol Clin. 2021;39:609-618.
- Bastola M, Locatis C, Fontelo P. Diagnostic reliability of in-person versus remote dermatology: a meta-analysis. Telemed J E Health. 2021;27:247-250.
- Bashyam AM, Feldman SR. Should patients stop their biologic treatment during the COVID-19 pandemic? J Dermatolog Treat. 2020;31:317-318.
In an age of changing climate and emerging global pandemics, the ability of residency programs to prepare for and adapt to potential disasters may be paramount in preserving the training of physicians. The current literature regarding residency program disaster preparedness, which focuses predominantly on hurricanes and COVID-19,1-8 is lacking in recommendations specific to dermatology residency programs. Likewise, the Accreditation Council for Graduate Medical Education (ACGME) guidelines9 do not address dermatology-specific concerns in disaster preparedness or response. Herein, we propose recommendations to mitigate the impact of various types of disasters on dermatology residency programs and their trainees with regard to resident safety and wellness, resident education, and patient care (Table).
Resident Safety and Wellness
Role of the Program Director—The role of the program director is critical, serving as a figure of structure and reassurance.4,7,10 Once concern of disaster arises, the program director should contact the Designated Institutional Official (DIO) to express concerns about possible disruptions to resident training. The DIO should then contact the ACGME within 10 days to report the disaster and submit a request for emergency (eg, pandemic) or extraordinary circumstances (eg, natural disaster) categorization.4,9 Program directors should promptly prepare plans for program reconfiguration and resident transfers in alignment with ACGME requirements to maintain evaluation and completion of core competencies of training during disasters.9 Program directors should prioritize the safety of trainees during the immediate threat with clear guidelines on sheltering, evacuations, or quarantines; a timeline of program recovery based on communication with residents, faculty, and administration should then be established.10,11
Communication—Establishing a strong line of communication between program directors and residents is paramount. Collection of emergency noninstitutional contact information, establishment of a centralized website for information dissemination, use of noninstitutional email and proxy servers outside of the location of impact, social media updates, on-site use of 2-way radios, and program-wide conference calls when possible should be strongly considered as part of the disaster response.2-4,12,13
Resident Accommodations and Mental Health—If training is disrupted, residents should be reassured of continued access to salary, housing, food, or other resources as necessary.3,4,11 There should be clear contingency plans if residents need to leave the program for extended periods of time due to injury, illness, or personal circumstances. Although relevant in all types of disasters, resident mental health and response to trauma also must be addressed. Access to counseling, morale-building opportunities (eg, resident social events), and screening for depression or posttraumatic stress disorder may help promote well-being among residents following traumatic events.14
Resident Education
Participation in Disaster Relief—Residents may seek to aid in the disaster response, which may prove challenging in the setting of programs with high patient volume.4 In coordination with the ACGME and graduate medical education governing bodies, program directors should consider how residents may fulfill dermatology training requirements in conjunction with disaster relief efforts, such as working in an inpatient setting or providing wound care.10
Continued Didactic Education—The use of online learning and conference calls for continuing the dermatology curriculum is an efficient means to maintaining resident education when meeting in person poses risks to residents.15 Projections of microscopy images, clinical photographs, or other instructional materials allow for continued instruction on resident examination, histopathology, and diagnostic skills.
Continued Clinical Training—If the home institution cannot support the operation of dermatology clinics, residents should be guaranteed continued training at other institutions. Agreements with other dermatology programs, community hospitals, or private dermatology practices should be established in advance, with consideration given to the number of residents a program can support, funding transfers, and credentialing requirements.2,4,5
Prolonged Disruptions—Nonessential departments of medical institutions may cease to function during war or mass casualty disasters, and it may be unsafe to send dermatology residents to other institutions or clinical areas. If the threat is prolonged, programs may need to consider allowing current residents a longer duration of training despite potential overlap with incoming dermatology residents.7
Patient Care
Disruptions to Clinic Operations—Regarding threats of violence, dangerous exposures, or natural disasters, there should be clear guidelines on sheltering in the clinical setting or stabilizing patients during a procedure.11 Equipment used by residents such as laptops, microscopes, and treatment devices (eg, lasers) should be stored in weather-safe locations that would not be notably impacted by moisture or structural damage to the clinic building. If electricity or internet access are compromised, paper medical records should be available to residents to continue clinical operations. Electronic health records used by residents should regularly be backed up on remote servers or cloud storage to allow continued access to patient health information if on-site servers are not functional.12 If disruptions are prolonged, residency program administration should coordinate with the institution to ensure there is adequate supply and storage of medications (eg, lidocaine, botulinum toxin) as well as a continued means of delivering biologic medications to patients and an ability to obtain laboratory or dermatopathology services.
In-Person Appointments vs Telemedicine—There are benefits to both residency training and patient care when physicians are able to perform in-person examinations, biopsies, and in-office treatments.16 Programs should ensure an adequate supply of personal protective equipment to continue in-office appointments, vaccinations, and medical care if a resident or other members of the team are exposed to an infectious disease.7 If in-person appointments are limited or impossible, telemedicine capabilities may still allow residents to meet program requirements.7,10,15 However, reduced patient volume due to decreased elective visits or procedures may complicate the fulfillment of clinical requirements, which may need to be adjusted in the wake of a disaster.7
Use of Immunosuppressive Therapies—Residency programs should address the risks of prescribing immunosuppressive therapies (eg, biologics) during an infectious threat with their residents and encourage trainees to counsel patients on the importance of preventative measures to reduce risks for severe infection.17
Final Thoughts
In an age of changing climate and emerging global pandemics, the ability of residency programs to prepare for and adapt to potential disasters may be paramount in preserving the training of physicians. The current literature regarding residency program disaster preparedness, which focuses predominantly on hurricanes and COVID-19,1-8 is lacking in recommendations specific to dermatology residency programs. Likewise, the Accreditation Council for Graduate Medical Education (ACGME) guidelines9 do not address dermatology-specific concerns in disaster preparedness or response. Herein, we propose recommendations to mitigate the impact of various types of disasters on dermatology residency programs and their trainees with regard to resident safety and wellness, resident education, and patient care (Table).
Resident Safety and Wellness
Role of the Program Director—The role of the program director is critical, serving as a figure of structure and reassurance.4,7,10 Once concern of disaster arises, the program director should contact the Designated Institutional Official (DIO) to express concerns about possible disruptions to resident training. The DIO should then contact the ACGME within 10 days to report the disaster and submit a request for emergency (eg, pandemic) or extraordinary circumstances (eg, natural disaster) categorization.4,9 Program directors should promptly prepare plans for program reconfiguration and resident transfers in alignment with ACGME requirements to maintain evaluation and completion of core competencies of training during disasters.9 Program directors should prioritize the safety of trainees during the immediate threat with clear guidelines on sheltering, evacuations, or quarantines; a timeline of program recovery based on communication with residents, faculty, and administration should then be established.10,11
Communication—Establishing a strong line of communication between program directors and residents is paramount. Collection of emergency noninstitutional contact information, establishment of a centralized website for information dissemination, use of noninstitutional email and proxy servers outside of the location of impact, social media updates, on-site use of 2-way radios, and program-wide conference calls when possible should be strongly considered as part of the disaster response.2-4,12,13
Resident Accommodations and Mental Health—If training is disrupted, residents should be reassured of continued access to salary, housing, food, or other resources as necessary.3,4,11 There should be clear contingency plans if residents need to leave the program for extended periods of time due to injury, illness, or personal circumstances. Although relevant in all types of disasters, resident mental health and response to trauma also must be addressed. Access to counseling, morale-building opportunities (eg, resident social events), and screening for depression or posttraumatic stress disorder may help promote well-being among residents following traumatic events.14
Resident Education
Participation in Disaster Relief—Residents may seek to aid in the disaster response, which may prove challenging in the setting of programs with high patient volume.4 In coordination with the ACGME and graduate medical education governing bodies, program directors should consider how residents may fulfill dermatology training requirements in conjunction with disaster relief efforts, such as working in an inpatient setting or providing wound care.10
Continued Didactic Education—The use of online learning and conference calls for continuing the dermatology curriculum is an efficient means to maintaining resident education when meeting in person poses risks to residents.15 Projections of microscopy images, clinical photographs, or other instructional materials allow for continued instruction on resident examination, histopathology, and diagnostic skills.
Continued Clinical Training—If the home institution cannot support the operation of dermatology clinics, residents should be guaranteed continued training at other institutions. Agreements with other dermatology programs, community hospitals, or private dermatology practices should be established in advance, with consideration given to the number of residents a program can support, funding transfers, and credentialing requirements.2,4,5
Prolonged Disruptions—Nonessential departments of medical institutions may cease to function during war or mass casualty disasters, and it may be unsafe to send dermatology residents to other institutions or clinical areas. If the threat is prolonged, programs may need to consider allowing current residents a longer duration of training despite potential overlap with incoming dermatology residents.7
Patient Care
Disruptions to Clinic Operations—Regarding threats of violence, dangerous exposures, or natural disasters, there should be clear guidelines on sheltering in the clinical setting or stabilizing patients during a procedure.11 Equipment used by residents such as laptops, microscopes, and treatment devices (eg, lasers) should be stored in weather-safe locations that would not be notably impacted by moisture or structural damage to the clinic building. If electricity or internet access are compromised, paper medical records should be available to residents to continue clinical operations. Electronic health records used by residents should regularly be backed up on remote servers or cloud storage to allow continued access to patient health information if on-site servers are not functional.12 If disruptions are prolonged, residency program administration should coordinate with the institution to ensure there is adequate supply and storage of medications (eg, lidocaine, botulinum toxin) as well as a continued means of delivering biologic medications to patients and an ability to obtain laboratory or dermatopathology services.
In-Person Appointments vs Telemedicine—There are benefits to both residency training and patient care when physicians are able to perform in-person examinations, biopsies, and in-office treatments.16 Programs should ensure an adequate supply of personal protective equipment to continue in-office appointments, vaccinations, and medical care if a resident or other members of the team are exposed to an infectious disease.7 If in-person appointments are limited or impossible, telemedicine capabilities may still allow residents to meet program requirements.7,10,15 However, reduced patient volume due to decreased elective visits or procedures may complicate the fulfillment of clinical requirements, which may need to be adjusted in the wake of a disaster.7
Use of Immunosuppressive Therapies—Residency programs should address the risks of prescribing immunosuppressive therapies (eg, biologics) during an infectious threat with their residents and encourage trainees to counsel patients on the importance of preventative measures to reduce risks for severe infection.17
Final Thoughts
- Davis W. Hurricane Katrina: the challenge to graduate medical education. Ochsner J. 2006;6:39.
- Cefalu CA, Schwartz RS. Salvaging a geriatric medicine academic program in disaster mode—the LSU training program post-Katrina.J Natl Med Assoc. 2007;99:590-596.
- Ayyala R. Lessons from Katrina: a program director’s perspective. Ophthalmology. 2007;114:1425-1426.
- Wiese JG. Leadership in graduate medical education: eleven steps instrumental in recovering residency programs after a disaster. Am J Med Sci. 2008;336:168-173.
- Griffies WS. Post-Katrina stabilization of the LSU/Ochsner Psychiatry Residency Program: caveats for disaster preparedness. Acad Psychiatry. 2009;33:418-422.
- Kearns DG, Chat VS, Uppal S, et al. Applying to dermatology residency during the COVID-19 pandemic. J Am Acad Dermatol. 2020;83:1214-1215.
- Matthews JB, Blair PG, Ellison EC, et al. Checklist framework for surgical education disaster plans. J Am Coll Surg. 2021;233:557-563.
- Litchman GH, Marson JW, Rigel DS. The continuing impact of COVID-19 on dermatology practice: office workflow, economics, and future implications. J Am Acad Dermatol. 2021;84:576-579.
- Accreditation Council for Graduate Medical Education. Sponsoring institution emergency categorization. Accessed October 20, 2022. https://www.acgme.org/covid-19/sponsoring-institution-emergency-categorization/
- Li YM, Galimberti F, Abrouk M, et al. US dermatology resident responses about the COVID-19 pandemic: results from a nationwide survey. South Med J. 2020;113:462-465.
- Newman B, Gallion C. Hurricane Harvey: firsthand perspectives for disaster preparedness in graduate medical education. Acad Med. 2019;94:1267-1269.
- Pero CD, Pou AM, Arriaga MA, et al. Post-Katrina: study in crisis-related program adaptability. Otolaryngol Head Neck Surg. 2008;138:394-397.
- Hattaway R, Singh N, Rais-Bahrami S, et al. Adaptations of dermatology residency programs to changes in medical education amid the COVID-19 pandemic: virtual opportunities and social media. SKIN. 2021;5:94-100.
- Hillier K, Paskaradevan J, Wilkes JK, et al. Disaster plans: resident involvement and well-being during Hurricane Harvey. J Grad Med Educ. 2019;11:129-131.
- Samimi S, Choi J, Rosman IS, et al. Impact of COVID-19 on dermatology residency. Dermatol Clin. 2021;39:609-618.
- Bastola M, Locatis C, Fontelo P. Diagnostic reliability of in-person versus remote dermatology: a meta-analysis. Telemed J E Health. 2021;27:247-250.
- Bashyam AM, Feldman SR. Should patients stop their biologic treatment during the COVID-19 pandemic? J Dermatolog Treat. 2020;31:317-318.
- Davis W. Hurricane Katrina: the challenge to graduate medical education. Ochsner J. 2006;6:39.
- Cefalu CA, Schwartz RS. Salvaging a geriatric medicine academic program in disaster mode—the LSU training program post-Katrina.J Natl Med Assoc. 2007;99:590-596.
- Ayyala R. Lessons from Katrina: a program director’s perspective. Ophthalmology. 2007;114:1425-1426.
- Wiese JG. Leadership in graduate medical education: eleven steps instrumental in recovering residency programs after a disaster. Am J Med Sci. 2008;336:168-173.
- Griffies WS. Post-Katrina stabilization of the LSU/Ochsner Psychiatry Residency Program: caveats for disaster preparedness. Acad Psychiatry. 2009;33:418-422.
- Kearns DG, Chat VS, Uppal S, et al. Applying to dermatology residency during the COVID-19 pandemic. J Am Acad Dermatol. 2020;83:1214-1215.
- Matthews JB, Blair PG, Ellison EC, et al. Checklist framework for surgical education disaster plans. J Am Coll Surg. 2021;233:557-563.
- Litchman GH, Marson JW, Rigel DS. The continuing impact of COVID-19 on dermatology practice: office workflow, economics, and future implications. J Am Acad Dermatol. 2021;84:576-579.
- Accreditation Council for Graduate Medical Education. Sponsoring institution emergency categorization. Accessed October 20, 2022. https://www.acgme.org/covid-19/sponsoring-institution-emergency-categorization/
- Li YM, Galimberti F, Abrouk M, et al. US dermatology resident responses about the COVID-19 pandemic: results from a nationwide survey. South Med J. 2020;113:462-465.
- Newman B, Gallion C. Hurricane Harvey: firsthand perspectives for disaster preparedness in graduate medical education. Acad Med. 2019;94:1267-1269.
- Pero CD, Pou AM, Arriaga MA, et al. Post-Katrina: study in crisis-related program adaptability. Otolaryngol Head Neck Surg. 2008;138:394-397.
- Hattaway R, Singh N, Rais-Bahrami S, et al. Adaptations of dermatology residency programs to changes in medical education amid the COVID-19 pandemic: virtual opportunities and social media. SKIN. 2021;5:94-100.
- Hillier K, Paskaradevan J, Wilkes JK, et al. Disaster plans: resident involvement and well-being during Hurricane Harvey. J Grad Med Educ. 2019;11:129-131.
- Samimi S, Choi J, Rosman IS, et al. Impact of COVID-19 on dermatology residency. Dermatol Clin. 2021;39:609-618.
- Bastola M, Locatis C, Fontelo P. Diagnostic reliability of in-person versus remote dermatology: a meta-analysis. Telemed J E Health. 2021;27:247-250.
- Bashyam AM, Feldman SR. Should patients stop their biologic treatment during the COVID-19 pandemic? J Dermatolog Treat. 2020;31:317-318.
Practice Points
- Dermatology residency programs should prioritize the development of disaster preparedness plans prior to the onset of disasters.
- Comprehensive disaster preparedness addresses many possible disruptions to dermatology resident training and clinic operations, including natural and manmade disasters and threats of widespread infectious disease.
- Safety being paramount, dermatology residency programs may be tasked with maintaining resident wellness, continuing resident education—potentially in unconventional ways—and adapting clinical operations to continue patient care.
Simplify Postoperative Self-removal of Bandages for Isolated Patients With Limited Range of Motion Using Pull Tabs
Practice Gap
A male patient presented with 2 concerning lesions, which histopathology revealed were invasive squamous cell carcinoma (SCC) on the right medial chest and SCC in situ on the right upper scapular region. Both were treated with wide local excision; margins were clear in our office the same day.
This case highlighted a practice gap in postoperative care. Two factors posed a challenge to proper postoperative wound care for our patient:
• Because of the high risk of transmission of SARS-CoV-2, the patient hoped to limit exposure by avoiding an office visit to remove the bandage.
• The patient did not have someone at home to serve as an immediate support system, which made it impossible for him to rely on others for postoperative wound care.
Previously, the patient had to ask a friend to remove a bandage for melanoma in situ on the inner aspect of the left upper arm. Therefore, after this procedure, the patient asked if the bandage could be fashioned in a manner that would allow him to remove it without assistance (Figure 1).
Technique
In constructing a bandage that is easier to remove, some necessary pressure that is provided by the bandage often is sacrificed by making it looser. Considering that our patient had moderate bleeding during the procedure—in part because he took low-dose aspirin (81 mg/d)—it was important to maintain firm pressure under the bandage postoperatively to help prevent untoward bleeding. Furthermore, because of the location of the treated site and the patient’s limited range of motion, it was not feasible for him to reach the area on the scapula and remove the bandage.1
For easy self-removal, we designed a bandage with a pull tab that was within the patient’s reach. Suitable materials for the pull tab bandage included surgical tape, bandaging tape with adequate stretch, sterile nonadhesive gauze, fenestrated surgical gauze, and a topical emollient such as petroleum jelly or antibacterial ointment.
To clean the site and decrease the amount of oil that would reduce the effectiveness of the adhesive, the wound was prepared with 70% alcohol. The site was then treated with petroleum jelly.
Next, we designed 2 pull tab bandage prototypes that allowed easy self-removal. For both prototypes, sterile nonadhesive gauze was applied to the wound along with folded and fenestrated gauze, which provided pressure. We used prototype #1 in our patient, and prototype #2 was demonstrated as an option.
Prototype #1—We created 2 tabs—each 2-feet long—using bandaging tape that was folded on itself once horizontally (Figure 2). The tabs were aligned on either side of the wound, the tops of which sat approximately 2 inches above the top of the first layer of adhesive bandage. An initial layer of adhesive surgical dressing was applied to cover the wound; 1 inch of the dressing was left exposed on the top of each tab. In addition, there were 2 “feet” running on the bottom.
The tops of the tabs were folded back over the adhesive tape, creating a type of “hook.” An additional final layer of adhesive tape was applied to ensure adequate pressure on the surgical site.
The patient was instructed to remove the bandage 2 days after the procedure. The outcome was qualified through a 3-day postoperative telephone call. The patient was asked about postoperative pain and his level of satisfaction with treatment. He was asked if he had any changes such as bleeding, swelling, signs of infection, or increased pain in the days after surgery or perceived postoperative complications, such as irritation. We asked the patient about the relative ease of removing the bandage and if removal was painful. He reported that the bandage was easy to remove, and that doing so was not painful; furthermore, he did not have problems with the bandage or healing and did not experience any medical changes. He found the bandage to be comfortable. The patient stated that the hanging feet of the prototype #1 bandage were not bothersome and were sturdy for the time that the bandage was on.
Prototype #2—We prepared a bandage using surgical packing as the tab (Figure 3). The packing was slowly placed around the site, which was already covered with nonadhesive gauze and fenestrated surgical gauze, with adequate spacing between each loop (for a total of 3 loops), 1 of which crossed over the third loop so that the adhesive bandaging tape could be removed easily. This allowed for a single tab that could be removed by a single pull. A final layer of adhesive tape was applied to ensure adequate pressure, similar to prototype #1. The same postoperative protocol was employed to provide a consistent standard of care. We recommend use of this prototype when surgical tape is not available, and surgical packing can be used as a substitute.
Practice Implications
Patients have a better appreciation for avoiding excess visits to medical offices due to the COVID-19 pandemic. The risk for exposure to SARS-CoV-2 infection is greater when patients who lack a support system must return to the office for aftercare or to have a bandage removed. Although protection offered by the COVID-19 vaccine alleviates concern, many patients have realized the benefits of only visiting medical offices in person when necessary.
The concept of pull tab bandages that can be removed by the patient at home has other applications. For example, patients who travel a long distance to see their physician will benefit from easier aftercare and avoid additional follow-up visits when provided with a self-removable bandage.
- Stathokostas, L, McDonald MW, Little RMD, et al. Flexibility of older adults aged 55-86 years and the influence of physical activity. J Aging Res. 2013;2013:1-8. doi:10.1155/2013/743843
Practice Gap
A male patient presented with 2 concerning lesions, which histopathology revealed were invasive squamous cell carcinoma (SCC) on the right medial chest and SCC in situ on the right upper scapular region. Both were treated with wide local excision; margins were clear in our office the same day.
This case highlighted a practice gap in postoperative care. Two factors posed a challenge to proper postoperative wound care for our patient:
• Because of the high risk of transmission of SARS-CoV-2, the patient hoped to limit exposure by avoiding an office visit to remove the bandage.
• The patient did not have someone at home to serve as an immediate support system, which made it impossible for him to rely on others for postoperative wound care.
Previously, the patient had to ask a friend to remove a bandage for melanoma in situ on the inner aspect of the left upper arm. Therefore, after this procedure, the patient asked if the bandage could be fashioned in a manner that would allow him to remove it without assistance (Figure 1).
Technique
In constructing a bandage that is easier to remove, some necessary pressure that is provided by the bandage often is sacrificed by making it looser. Considering that our patient had moderate bleeding during the procedure—in part because he took low-dose aspirin (81 mg/d)—it was important to maintain firm pressure under the bandage postoperatively to help prevent untoward bleeding. Furthermore, because of the location of the treated site and the patient’s limited range of motion, it was not feasible for him to reach the area on the scapula and remove the bandage.1
For easy self-removal, we designed a bandage with a pull tab that was within the patient’s reach. Suitable materials for the pull tab bandage included surgical tape, bandaging tape with adequate stretch, sterile nonadhesive gauze, fenestrated surgical gauze, and a topical emollient such as petroleum jelly or antibacterial ointment.
To clean the site and decrease the amount of oil that would reduce the effectiveness of the adhesive, the wound was prepared with 70% alcohol. The site was then treated with petroleum jelly.
Next, we designed 2 pull tab bandage prototypes that allowed easy self-removal. For both prototypes, sterile nonadhesive gauze was applied to the wound along with folded and fenestrated gauze, which provided pressure. We used prototype #1 in our patient, and prototype #2 was demonstrated as an option.
Prototype #1—We created 2 tabs—each 2-feet long—using bandaging tape that was folded on itself once horizontally (Figure 2). The tabs were aligned on either side of the wound, the tops of which sat approximately 2 inches above the top of the first layer of adhesive bandage. An initial layer of adhesive surgical dressing was applied to cover the wound; 1 inch of the dressing was left exposed on the top of each tab. In addition, there were 2 “feet” running on the bottom.
The tops of the tabs were folded back over the adhesive tape, creating a type of “hook.” An additional final layer of adhesive tape was applied to ensure adequate pressure on the surgical site.
The patient was instructed to remove the bandage 2 days after the procedure. The outcome was qualified through a 3-day postoperative telephone call. The patient was asked about postoperative pain and his level of satisfaction with treatment. He was asked if he had any changes such as bleeding, swelling, signs of infection, or increased pain in the days after surgery or perceived postoperative complications, such as irritation. We asked the patient about the relative ease of removing the bandage and if removal was painful. He reported that the bandage was easy to remove, and that doing so was not painful; furthermore, he did not have problems with the bandage or healing and did not experience any medical changes. He found the bandage to be comfortable. The patient stated that the hanging feet of the prototype #1 bandage were not bothersome and were sturdy for the time that the bandage was on.
Prototype #2—We prepared a bandage using surgical packing as the tab (Figure 3). The packing was slowly placed around the site, which was already covered with nonadhesive gauze and fenestrated surgical gauze, with adequate spacing between each loop (for a total of 3 loops), 1 of which crossed over the third loop so that the adhesive bandaging tape could be removed easily. This allowed for a single tab that could be removed by a single pull. A final layer of adhesive tape was applied to ensure adequate pressure, similar to prototype #1. The same postoperative protocol was employed to provide a consistent standard of care. We recommend use of this prototype when surgical tape is not available, and surgical packing can be used as a substitute.
Practice Implications
Patients have a better appreciation for avoiding excess visits to medical offices due to the COVID-19 pandemic. The risk for exposure to SARS-CoV-2 infection is greater when patients who lack a support system must return to the office for aftercare or to have a bandage removed. Although protection offered by the COVID-19 vaccine alleviates concern, many patients have realized the benefits of only visiting medical offices in person when necessary.
The concept of pull tab bandages that can be removed by the patient at home has other applications. For example, patients who travel a long distance to see their physician will benefit from easier aftercare and avoid additional follow-up visits when provided with a self-removable bandage.
Practice Gap
A male patient presented with 2 concerning lesions, which histopathology revealed were invasive squamous cell carcinoma (SCC) on the right medial chest and SCC in situ on the right upper scapular region. Both were treated with wide local excision; margins were clear in our office the same day.
This case highlighted a practice gap in postoperative care. Two factors posed a challenge to proper postoperative wound care for our patient:
• Because of the high risk of transmission of SARS-CoV-2, the patient hoped to limit exposure by avoiding an office visit to remove the bandage.
• The patient did not have someone at home to serve as an immediate support system, which made it impossible for him to rely on others for postoperative wound care.
Previously, the patient had to ask a friend to remove a bandage for melanoma in situ on the inner aspect of the left upper arm. Therefore, after this procedure, the patient asked if the bandage could be fashioned in a manner that would allow him to remove it without assistance (Figure 1).
Technique
In constructing a bandage that is easier to remove, some necessary pressure that is provided by the bandage often is sacrificed by making it looser. Considering that our patient had moderate bleeding during the procedure—in part because he took low-dose aspirin (81 mg/d)—it was important to maintain firm pressure under the bandage postoperatively to help prevent untoward bleeding. Furthermore, because of the location of the treated site and the patient’s limited range of motion, it was not feasible for him to reach the area on the scapula and remove the bandage.1
For easy self-removal, we designed a bandage with a pull tab that was within the patient’s reach. Suitable materials for the pull tab bandage included surgical tape, bandaging tape with adequate stretch, sterile nonadhesive gauze, fenestrated surgical gauze, and a topical emollient such as petroleum jelly or antibacterial ointment.
To clean the site and decrease the amount of oil that would reduce the effectiveness of the adhesive, the wound was prepared with 70% alcohol. The site was then treated with petroleum jelly.
Next, we designed 2 pull tab bandage prototypes that allowed easy self-removal. For both prototypes, sterile nonadhesive gauze was applied to the wound along with folded and fenestrated gauze, which provided pressure. We used prototype #1 in our patient, and prototype #2 was demonstrated as an option.
Prototype #1—We created 2 tabs—each 2-feet long—using bandaging tape that was folded on itself once horizontally (Figure 2). The tabs were aligned on either side of the wound, the tops of which sat approximately 2 inches above the top of the first layer of adhesive bandage. An initial layer of adhesive surgical dressing was applied to cover the wound; 1 inch of the dressing was left exposed on the top of each tab. In addition, there were 2 “feet” running on the bottom.
The tops of the tabs were folded back over the adhesive tape, creating a type of “hook.” An additional final layer of adhesive tape was applied to ensure adequate pressure on the surgical site.
The patient was instructed to remove the bandage 2 days after the procedure. The outcome was qualified through a 3-day postoperative telephone call. The patient was asked about postoperative pain and his level of satisfaction with treatment. He was asked if he had any changes such as bleeding, swelling, signs of infection, or increased pain in the days after surgery or perceived postoperative complications, such as irritation. We asked the patient about the relative ease of removing the bandage and if removal was painful. He reported that the bandage was easy to remove, and that doing so was not painful; furthermore, he did not have problems with the bandage or healing and did not experience any medical changes. He found the bandage to be comfortable. The patient stated that the hanging feet of the prototype #1 bandage were not bothersome and were sturdy for the time that the bandage was on.
Prototype #2—We prepared a bandage using surgical packing as the tab (Figure 3). The packing was slowly placed around the site, which was already covered with nonadhesive gauze and fenestrated surgical gauze, with adequate spacing between each loop (for a total of 3 loops), 1 of which crossed over the third loop so that the adhesive bandaging tape could be removed easily. This allowed for a single tab that could be removed by a single pull. A final layer of adhesive tape was applied to ensure adequate pressure, similar to prototype #1. The same postoperative protocol was employed to provide a consistent standard of care. We recommend use of this prototype when surgical tape is not available, and surgical packing can be used as a substitute.
Practice Implications
Patients have a better appreciation for avoiding excess visits to medical offices due to the COVID-19 pandemic. The risk for exposure to SARS-CoV-2 infection is greater when patients who lack a support system must return to the office for aftercare or to have a bandage removed. Although protection offered by the COVID-19 vaccine alleviates concern, many patients have realized the benefits of only visiting medical offices in person when necessary.
The concept of pull tab bandages that can be removed by the patient at home has other applications. For example, patients who travel a long distance to see their physician will benefit from easier aftercare and avoid additional follow-up visits when provided with a self-removable bandage.
- Stathokostas, L, McDonald MW, Little RMD, et al. Flexibility of older adults aged 55-86 years and the influence of physical activity. J Aging Res. 2013;2013:1-8. doi:10.1155/2013/743843
- Stathokostas, L, McDonald MW, Little RMD, et al. Flexibility of older adults aged 55-86 years and the influence of physical activity. J Aging Res. 2013;2013:1-8. doi:10.1155/2013/743843
What does it take for men to embrace cosmetic treatments?
with the same gusto as women.
However, this could be changing as millennials – who tend to be more proactive about efforts to prevent skin aging – are getting older.
At a virtual course on laser and aesthetic skin therapy, Dr. Carruthers referred to the results of an online survey of 600 men aged 30-65 years conducted by Jared Jagdeo, MD, and colleagues in 2016, to gauge attitudes toward age-related changes of their facial features and their preferences for prioritizing treatment. The top five barriers to treatment cited by the respondents were: “I don’t think I need it yet” (47%); “concerned about safety/side effects” (46%); “concerned about injecting a foreign substance into my body” (45%); “cost” (42%), and “concerned my face won’t look natural” (41%).
“Since then, millennials took over as the largest portion of our workforce in North America,” said Dr. Carruthers who, with her husband, Alastair Carruthers, MD, pioneered the cosmetic use of onabotulinumtoxinA (Botox). “Millennials are interested in how they look and how to keep their aesthetic the best it can possibly be,” she said, so there may be “a generational aspect to this.”
Another factor that may affect the uptake of cosmetic procedures among men is the number of hours they spend gazing at their own image on a computer screen. Since the beginning of the COVID-19 pandemic, men have spent an increasing number of hours on video-conferencing calls via Zoom and other platforms, causing them to rethink how they view their appearance, Dr. Carruthers added. “Zoom dysmorphia” is the term that describes the phenomenon that developed during the pandemic where more patients expressed a desire to make changes to their appearance, including nose jobs and smoothing out forehead wrinkles.
“When we’re on a Zoom call, we’re spending 40% of our time looking at ourselves,” said Dr. Carruthers, clinical professor of ophthalmology and visual sciences at the University of British Columbia in Vancouver. “This would hint that the looking glass is not as powerful as the computer screen to motivate men” to pursue aesthetic treatments.
According to data from the American Society of Plastic Surgeons, the top 5 cosmetic surgical procedures performed in men in 2020 were nose shaping, eyelid surgery, cheek implants, liposuction, and ear surgery. The top 5 minimally-invasive procedures in men were botulinum toxin type A, followed by laser skin resurfacing, laser hair removal, soft tissue fillers, and microdermabrasion.
Why might men consider an injectable instead of surgery? Dr. Carruthers asked. “According to the 2016 survey by Dr. Jagdeo and colleagues, it’s to appear more youthful and to appear good for their age.”
From a clinical standpoint, success comes from understanding the subtle differences between treating men and women, she added.
In a 2022 article about optimizing skin tightening in aesthetics in men, Christian A. Albornoz, MD, and colleagues noted that in contrast to women, men “tend to have higher levels of collagen density and greater skin thickness, but these begin to decrease earlier on. They can also more frequently have severe photodamage”.
In another article published in 2018, Terrence Keaney, MD, and colleagues reviewed the objective data available on male aging and aesthetics. They stated that a “communication gap exists for men, as evidenced by the lack of information available online or by word of mouth about injectable treatments” and concluded that “educating men about available aesthetic treatments and about the safety and side effects associated with each treatment, as well as addressing concerns about their treatment results looking natural, are key considerations.”
That sentiment resonates with Dr. Carruthers. Part of the reason why men have not sought cosmetic treatments along with their female partners and friends seeking cosmetic treatments “is that they haven’t had anything in their cup,” she said. “Maybe this is something we need to think about, to try and help men come in and enjoy the positive benefits of aesthetic, noninvasive cosmetic treatments.”
The course was sponsored by Harvard Medical School, Massachusetts General Hospital, and Wellman Center for Photomedicine.
Dr. Carruthers disclosed that she is a consultant and researcher for Alastin, Appiell, Allergan Aesthetics, Avari Medical, Bonti, Evolus, Fount Bio, Jeune Aesthetics, Merz, and Revance Biopharma.
with the same gusto as women.
However, this could be changing as millennials – who tend to be more proactive about efforts to prevent skin aging – are getting older.
At a virtual course on laser and aesthetic skin therapy, Dr. Carruthers referred to the results of an online survey of 600 men aged 30-65 years conducted by Jared Jagdeo, MD, and colleagues in 2016, to gauge attitudes toward age-related changes of their facial features and their preferences for prioritizing treatment. The top five barriers to treatment cited by the respondents were: “I don’t think I need it yet” (47%); “concerned about safety/side effects” (46%); “concerned about injecting a foreign substance into my body” (45%); “cost” (42%), and “concerned my face won’t look natural” (41%).
“Since then, millennials took over as the largest portion of our workforce in North America,” said Dr. Carruthers who, with her husband, Alastair Carruthers, MD, pioneered the cosmetic use of onabotulinumtoxinA (Botox). “Millennials are interested in how they look and how to keep their aesthetic the best it can possibly be,” she said, so there may be “a generational aspect to this.”
Another factor that may affect the uptake of cosmetic procedures among men is the number of hours they spend gazing at their own image on a computer screen. Since the beginning of the COVID-19 pandemic, men have spent an increasing number of hours on video-conferencing calls via Zoom and other platforms, causing them to rethink how they view their appearance, Dr. Carruthers added. “Zoom dysmorphia” is the term that describes the phenomenon that developed during the pandemic where more patients expressed a desire to make changes to their appearance, including nose jobs and smoothing out forehead wrinkles.
“When we’re on a Zoom call, we’re spending 40% of our time looking at ourselves,” said Dr. Carruthers, clinical professor of ophthalmology and visual sciences at the University of British Columbia in Vancouver. “This would hint that the looking glass is not as powerful as the computer screen to motivate men” to pursue aesthetic treatments.
According to data from the American Society of Plastic Surgeons, the top 5 cosmetic surgical procedures performed in men in 2020 were nose shaping, eyelid surgery, cheek implants, liposuction, and ear surgery. The top 5 minimally-invasive procedures in men were botulinum toxin type A, followed by laser skin resurfacing, laser hair removal, soft tissue fillers, and microdermabrasion.
Why might men consider an injectable instead of surgery? Dr. Carruthers asked. “According to the 2016 survey by Dr. Jagdeo and colleagues, it’s to appear more youthful and to appear good for their age.”
From a clinical standpoint, success comes from understanding the subtle differences between treating men and women, she added.
In a 2022 article about optimizing skin tightening in aesthetics in men, Christian A. Albornoz, MD, and colleagues noted that in contrast to women, men “tend to have higher levels of collagen density and greater skin thickness, but these begin to decrease earlier on. They can also more frequently have severe photodamage”.
In another article published in 2018, Terrence Keaney, MD, and colleagues reviewed the objective data available on male aging and aesthetics. They stated that a “communication gap exists for men, as evidenced by the lack of information available online or by word of mouth about injectable treatments” and concluded that “educating men about available aesthetic treatments and about the safety and side effects associated with each treatment, as well as addressing concerns about their treatment results looking natural, are key considerations.”
That sentiment resonates with Dr. Carruthers. Part of the reason why men have not sought cosmetic treatments along with their female partners and friends seeking cosmetic treatments “is that they haven’t had anything in their cup,” she said. “Maybe this is something we need to think about, to try and help men come in and enjoy the positive benefits of aesthetic, noninvasive cosmetic treatments.”
The course was sponsored by Harvard Medical School, Massachusetts General Hospital, and Wellman Center for Photomedicine.
Dr. Carruthers disclosed that she is a consultant and researcher for Alastin, Appiell, Allergan Aesthetics, Avari Medical, Bonti, Evolus, Fount Bio, Jeune Aesthetics, Merz, and Revance Biopharma.
with the same gusto as women.
However, this could be changing as millennials – who tend to be more proactive about efforts to prevent skin aging – are getting older.
At a virtual course on laser and aesthetic skin therapy, Dr. Carruthers referred to the results of an online survey of 600 men aged 30-65 years conducted by Jared Jagdeo, MD, and colleagues in 2016, to gauge attitudes toward age-related changes of their facial features and their preferences for prioritizing treatment. The top five barriers to treatment cited by the respondents were: “I don’t think I need it yet” (47%); “concerned about safety/side effects” (46%); “concerned about injecting a foreign substance into my body” (45%); “cost” (42%), and “concerned my face won’t look natural” (41%).
“Since then, millennials took over as the largest portion of our workforce in North America,” said Dr. Carruthers who, with her husband, Alastair Carruthers, MD, pioneered the cosmetic use of onabotulinumtoxinA (Botox). “Millennials are interested in how they look and how to keep their aesthetic the best it can possibly be,” she said, so there may be “a generational aspect to this.”
Another factor that may affect the uptake of cosmetic procedures among men is the number of hours they spend gazing at their own image on a computer screen. Since the beginning of the COVID-19 pandemic, men have spent an increasing number of hours on video-conferencing calls via Zoom and other platforms, causing them to rethink how they view their appearance, Dr. Carruthers added. “Zoom dysmorphia” is the term that describes the phenomenon that developed during the pandemic where more patients expressed a desire to make changes to their appearance, including nose jobs and smoothing out forehead wrinkles.
“When we’re on a Zoom call, we’re spending 40% of our time looking at ourselves,” said Dr. Carruthers, clinical professor of ophthalmology and visual sciences at the University of British Columbia in Vancouver. “This would hint that the looking glass is not as powerful as the computer screen to motivate men” to pursue aesthetic treatments.
According to data from the American Society of Plastic Surgeons, the top 5 cosmetic surgical procedures performed in men in 2020 were nose shaping, eyelid surgery, cheek implants, liposuction, and ear surgery. The top 5 minimally-invasive procedures in men were botulinum toxin type A, followed by laser skin resurfacing, laser hair removal, soft tissue fillers, and microdermabrasion.
Why might men consider an injectable instead of surgery? Dr. Carruthers asked. “According to the 2016 survey by Dr. Jagdeo and colleagues, it’s to appear more youthful and to appear good for their age.”
From a clinical standpoint, success comes from understanding the subtle differences between treating men and women, she added.
In a 2022 article about optimizing skin tightening in aesthetics in men, Christian A. Albornoz, MD, and colleagues noted that in contrast to women, men “tend to have higher levels of collagen density and greater skin thickness, but these begin to decrease earlier on. They can also more frequently have severe photodamage”.
In another article published in 2018, Terrence Keaney, MD, and colleagues reviewed the objective data available on male aging and aesthetics. They stated that a “communication gap exists for men, as evidenced by the lack of information available online or by word of mouth about injectable treatments” and concluded that “educating men about available aesthetic treatments and about the safety and side effects associated with each treatment, as well as addressing concerns about their treatment results looking natural, are key considerations.”
That sentiment resonates with Dr. Carruthers. Part of the reason why men have not sought cosmetic treatments along with their female partners and friends seeking cosmetic treatments “is that they haven’t had anything in their cup,” she said. “Maybe this is something we need to think about, to try and help men come in and enjoy the positive benefits of aesthetic, noninvasive cosmetic treatments.”
The course was sponsored by Harvard Medical School, Massachusetts General Hospital, and Wellman Center for Photomedicine.
Dr. Carruthers disclosed that she is a consultant and researcher for Alastin, Appiell, Allergan Aesthetics, Avari Medical, Bonti, Evolus, Fount Bio, Jeune Aesthetics, Merz, and Revance Biopharma.
FROM A LASER & AESTHETIC SKIN THERAPY COURSE
Painful and Pruritic Eruptions on the Entire Body
The Diagnosis: IgA Pemphigus
Histopathology revealed a neutrophilic pustule and vesicle formation underlying the corneal layer (Figure). Direct immunofluorescence (DIF) showed weak positive staining for IgA within the intercellular keratinocyte in the epithelial compartment and a negative pattern with IgG, IgM, C3, and fibrinogen. The patient received a 40-mg intralesional triamcinolone injection and was placed on an oral prednisone 50-mg taper within 5 days. The plaques, bullae, and pustules began to resolve, but the lesions returned 1 day later. Oral prednisone 10 mg daily was initiated for 1 month, which resulted in full resolution of the lesions.
IgA pemphigus is a rare autoimmune disorder characterized by the occurrence of painful pruritic blisters caused by circulating IgA antibodies, which react against keratinocyte cellular components responsible for mediating cell-to-cell adherence.1 The etiology of IgA pemphigus presently remains elusive, though it has been reported to occur concomitantly with several chronic malignancies and inflammatory conditions. Although its etiology is unknown, IgA pemphigus most commonly is treated with oral dapsone and corticosteroids.2
IgA pemphigus can be divided into 2 primary subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis.1,3 The former is characterized by intercellular deposition of IgA that reacts to the glycoprotein desmocollin-1 in the upper layer of the epidermis. Intraepidermal neutrophilic dermatosis is distinguished by the presence of autoantibodies against the desmoglein members of the cadherin superfamily of proteins. Additionally, unlike subcorneal pustular dermatosis, intraepidermal neutrophilic dermatosis autoantibody reactivity occurs in the lower epidermis.4
The differential includes dermatitis herpetiformis, which is commonly seen on the elbows, knees, and buttocks, with DIF showing IgA deposition at the dermal papillae. Pemphigus foliaceus is distributed on the scalp, face, and trunk, with DIF showing IgG intercellular deposition. Pustular psoriasis presents as erythematous sterile pustules in a more localized annular pattern. Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) has similar clinical and histological findings to IgA pemphigus; however, DIF is negative.
- Kridin K, Patel PM, Jones VA, et al. IgA pemphigus: a systematic review. J Am Acad Dermatol. 2020;82:1386-1392.
- Moreno ACL, Santi CG, Gabbi TVB, et al. IgA pemphigus: case series with emphasis on therapeutic response. J Am Acad Dermatol. 2014;70:200-201.
- Niimi Y, Kawana S, Kusunoki T. IgA pemphigus: a case report and its characteristic clinical features compared with subcorneal pustular dermatosis. J Am Acad Dermatol. 2000;43:546-549.
- Aslanova M, Yarrarapu SNS, Zito PM. IgA pemphigus. StatPearls. StatPearls Publishing; 2021.
The Diagnosis: IgA Pemphigus
Histopathology revealed a neutrophilic pustule and vesicle formation underlying the corneal layer (Figure). Direct immunofluorescence (DIF) showed weak positive staining for IgA within the intercellular keratinocyte in the epithelial compartment and a negative pattern with IgG, IgM, C3, and fibrinogen. The patient received a 40-mg intralesional triamcinolone injection and was placed on an oral prednisone 50-mg taper within 5 days. The plaques, bullae, and pustules began to resolve, but the lesions returned 1 day later. Oral prednisone 10 mg daily was initiated for 1 month, which resulted in full resolution of the lesions.
IgA pemphigus is a rare autoimmune disorder characterized by the occurrence of painful pruritic blisters caused by circulating IgA antibodies, which react against keratinocyte cellular components responsible for mediating cell-to-cell adherence.1 The etiology of IgA pemphigus presently remains elusive, though it has been reported to occur concomitantly with several chronic malignancies and inflammatory conditions. Although its etiology is unknown, IgA pemphigus most commonly is treated with oral dapsone and corticosteroids.2
IgA pemphigus can be divided into 2 primary subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis.1,3 The former is characterized by intercellular deposition of IgA that reacts to the glycoprotein desmocollin-1 in the upper layer of the epidermis. Intraepidermal neutrophilic dermatosis is distinguished by the presence of autoantibodies against the desmoglein members of the cadherin superfamily of proteins. Additionally, unlike subcorneal pustular dermatosis, intraepidermal neutrophilic dermatosis autoantibody reactivity occurs in the lower epidermis.4
The differential includes dermatitis herpetiformis, which is commonly seen on the elbows, knees, and buttocks, with DIF showing IgA deposition at the dermal papillae. Pemphigus foliaceus is distributed on the scalp, face, and trunk, with DIF showing IgG intercellular deposition. Pustular psoriasis presents as erythematous sterile pustules in a more localized annular pattern. Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) has similar clinical and histological findings to IgA pemphigus; however, DIF is negative.
The Diagnosis: IgA Pemphigus
Histopathology revealed a neutrophilic pustule and vesicle formation underlying the corneal layer (Figure). Direct immunofluorescence (DIF) showed weak positive staining for IgA within the intercellular keratinocyte in the epithelial compartment and a negative pattern with IgG, IgM, C3, and fibrinogen. The patient received a 40-mg intralesional triamcinolone injection and was placed on an oral prednisone 50-mg taper within 5 days. The plaques, bullae, and pustules began to resolve, but the lesions returned 1 day later. Oral prednisone 10 mg daily was initiated for 1 month, which resulted in full resolution of the lesions.
IgA pemphigus is a rare autoimmune disorder characterized by the occurrence of painful pruritic blisters caused by circulating IgA antibodies, which react against keratinocyte cellular components responsible for mediating cell-to-cell adherence.1 The etiology of IgA pemphigus presently remains elusive, though it has been reported to occur concomitantly with several chronic malignancies and inflammatory conditions. Although its etiology is unknown, IgA pemphigus most commonly is treated with oral dapsone and corticosteroids.2
IgA pemphigus can be divided into 2 primary subtypes: subcorneal pustular dermatosis and intraepidermal neutrophilic dermatosis.1,3 The former is characterized by intercellular deposition of IgA that reacts to the glycoprotein desmocollin-1 in the upper layer of the epidermis. Intraepidermal neutrophilic dermatosis is distinguished by the presence of autoantibodies against the desmoglein members of the cadherin superfamily of proteins. Additionally, unlike subcorneal pustular dermatosis, intraepidermal neutrophilic dermatosis autoantibody reactivity occurs in the lower epidermis.4
The differential includes dermatitis herpetiformis, which is commonly seen on the elbows, knees, and buttocks, with DIF showing IgA deposition at the dermal papillae. Pemphigus foliaceus is distributed on the scalp, face, and trunk, with DIF showing IgG intercellular deposition. Pustular psoriasis presents as erythematous sterile pustules in a more localized annular pattern. Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) has similar clinical and histological findings to IgA pemphigus; however, DIF is negative.
- Kridin K, Patel PM, Jones VA, et al. IgA pemphigus: a systematic review. J Am Acad Dermatol. 2020;82:1386-1392.
- Moreno ACL, Santi CG, Gabbi TVB, et al. IgA pemphigus: case series with emphasis on therapeutic response. J Am Acad Dermatol. 2014;70:200-201.
- Niimi Y, Kawana S, Kusunoki T. IgA pemphigus: a case report and its characteristic clinical features compared with subcorneal pustular dermatosis. J Am Acad Dermatol. 2000;43:546-549.
- Aslanova M, Yarrarapu SNS, Zito PM. IgA pemphigus. StatPearls. StatPearls Publishing; 2021.
- Kridin K, Patel PM, Jones VA, et al. IgA pemphigus: a systematic review. J Am Acad Dermatol. 2020;82:1386-1392.
- Moreno ACL, Santi CG, Gabbi TVB, et al. IgA pemphigus: case series with emphasis on therapeutic response. J Am Acad Dermatol. 2014;70:200-201.
- Niimi Y, Kawana S, Kusunoki T. IgA pemphigus: a case report and its characteristic clinical features compared with subcorneal pustular dermatosis. J Am Acad Dermatol. 2000;43:546-549.
- Aslanova M, Yarrarapu SNS, Zito PM. IgA pemphigus. StatPearls. StatPearls Publishing; 2021.
A 36-year-old man presented with painful tender blisters and rashes on the entire body, including the ears and tongue. The rash began as a few pinpointed red dots on the abdomen, which subsequently increased in size and spread over the last week. He initially felt red and flushed and noticed new lesions appearing throughout the day. He did not attempt any specific treatment for these lesions. The patient tested positive for COVID-19 four months prior to the skin eruption. He denied systemic symptoms, smoking, or recent travel. He had no history of skin cancer, skin disorders, HIV, or hepatitis. He had no known medication allergies. Physical examination revealed multiple disseminated pustules on the ears, superficial ulcerations on the tongue, and blisters on the right lip. Few lesions were tender to the touch and drained clear fluid. Bacterial, viral, HIV, herpes, and rapid plasma reagin culture and laboratory screenings were negative. He was started on valaciclovir and cephalexin; however, no improvement was noticed. Punch biopsies were taken from the blisters on the chest and perilesional area.