Lessons from an ethnic skin center: Awareness and respect for diversity

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With the strong likelihood that dermatologists in the United States will have to resolve dermatologic issues created by cultural cosmetic practices originating elsewhere, strategies for an open nonjudgmental approach are instrumental, according to a dermatologist with expertise in these types of cases who spoke at the Skin of Color Update 2021.

Dr. Neelam Ajit Vashi

“Instead of avoiding the discussion of cultural practices, we should discuss them and be open about them. It fosters a comfortable environment, trust, and better compliance,” reported Neelam Ajit Vashi, MD, founding director of the Boston University Center for Ethnic Skin.

Out of fear of causing offense, a desire to be discreet, or of personal discomfort with foreign cultural practices, some clinicians might elect to limit themselves to the information that the patient volunteers, which is a mistake, according to Dr. Vashi.

“The avoidance of topics around culture actually limits the ability to have a successful relationship,” she maintained.

Successful encounters are not just based on a willingness to listen, Dr. Vashi said. Clinicians should be seeking a base of knowledge. With growing globalization and widespread immigration, “it is increasingly important for dermatologists in the U.S. to understand the role of cultural practices [in creating skin problems] and recognize the sequelae,” Dr. Vashi said.

Taking some common examples of dermatologic complaints created by cosmetic practices originating elsewhere, Dr. Vashi described key clinical points in addressing complications related to henna, hair removal through threading, and placement of decorative adornments on the forehead, called bindi. In addition, she pointed out common issues with facial and body marking created with kumkum powder, hair oils, and skin lightening agents.
 

Black henna

For cosmetic enhancement, henna is relatively benign. It is also no longer confined to the south Asian communities where it originated. However, Dr. Vashi pointed out that patients of south Asian origin or descent might be more likely to use black henna, a variety with more risks.

Black henna contains additives, such as diaminobenzenes and p-phenylenediamine (PPD), to darken the tone of the product as well as provide other desired characteristics, such as an accelerated drying time. While some patients do develop reactions to conventional henna, the risks of black henna are greater.



“The acute contact dermatitis reactions can include dyspigmentation, leukoderma, and keloids,” Dr. Vashi said. Other complications include erythema multiforme, temporary hypertrichosis, and systemic allergic reactions, such as angioedema.

While those who have had a reaction to henna should avoid further contact, Dr. Vashi warned that sequelae can include cross reactions with latex and rubber as well as some pharmaceutical agents, such as sulfonamides. When taking a patient history, she noted, be aware that risks of henna extend to the hairdressers and cosmeticians who sometimes apply these products on others.

Hair threading, bindi, and kumkum

Hair threading, another practice popularized in south Asia and now growing in popularity globally, involves capturing hairs between cotton threads for removal of both the hair and its follicle. It is a relatively rapid and efficient method of permanent depilation. In addition to pain and erythema, Dr. Vashi reported that the complications associated with hair threading include pigmentary changes, infections such as bullous impetigo, and lesions of koebnerization – such as vitiligo and lichen planus.

Bindi, a Hindi tradition that involves placing adornments between the eyebrows, and kumkum, a powder typically made from turmeric to be employed for decorative markings, have also spread to use outside of their cultural context, according to Dr. Vashi. She said that the complications of these two cosmetic practices are shared, and stem largely from contact dermatitis.

Veena Nair/Moment/Getty Images
Sindooram, also called kumkum, is a traditional vermilion red or orange-red colored cosmetic powder from the Indian subcontinent, usually worn by married women along the part of their hair.


In the case of bindi, para-tertiary-butylphenol in adhesives is one source of reactions, whereas kumkum itself can be an irritant. As these are typically local to the site of application, the diagnosis is not difficult, but treatment can be more challenging for patients unwilling to abandon the practice.
 

Hair oils, skin-lightening agents

Culturally-linked hair oils among patients from south Asia or Africa – or descendants from these areas – can damage hair in a variety of ways as well as cause contact dermatitis. The oils can also exacerbate existing skin diseases.

“Oils with high oleic acid, such as coconut or olive oils or shea butter, can worsen seborrheic dermatitis,” Dr. Vashi cautioned.

Of this list of dermatologic issues induced by culturally linked cosmetic practices, skin lightening agents might pose the most risk for permanent and irreversible complications. Dr. Vashi said that up to 70% of patients using lighteners develop complications, and there is a relationship between the severity of side effects as duration of use increases.

“The problem is that ingredients of many of these products, which are imported illegally and sold on the black market, are often not disclosed,” Dr. Vashi said. Some contain a high content of metals such as lead, copper, and iron, whether they are added intentionally or end up in the product because of poor quality control. For those developing adverse events associated with the products, the obvious treatment is discontinuation.

When patients are unwilling to discontinue any of the products that have led to dermatologic issues, Dr. Vashi encouraged physicians “to take a middle ground.” Simple avoidance can be challenging for practices that are culturally meaningful. In respecting cultural differences, she encouraged tolerance and compromise.

“Often these patients will be doing an alternative medication or intervention, but this does not mean that they are not accepting what we have to offer,” she said. She indicated that mutual respect will lead to better solutions.

The awareness of common cultural practices that can have a harmful impact on the skin is an area of practice that deserves more attention, Andrew F. Alexis, MD, vice-chair for diversity and inclusion in the department of dermatology at Weill Cornell Medical Center, New York, said in an interview.

Dr. Andrew F. Alexis


He said that he agreed with Dr. Vashi that understanding the role of cultural practices leading to dermatoses is not enough.

“Advising patients to alter or discontinue a specific cultural practice due to a dermatologic complication should be done with respect, humility, and understanding that may be challenging,” said Dr. Alexis.

While being aware of the specific cultural practices that might be causing or exacerbating dermatoses is important for accurate diagnosis, he said he believes that “partnering with the patient to modify the cultural practices in question” is important for a clinical outcome acceptable to the patient.

“Educational resources to inform clinicians of dermatoses associated with cultural practices are available and can be helpful for dermatologists in any practice setting,” he said.

Dr. Vashi reports that she has no relevant financial relationships to disclose. Dr. Alexis reports financial relationships with Abbvie, Allergan, Almirall, Amgen, Arcutis, AstraZeneca, Bristol-Myers Squibb, Cara, Galderma, Genzyme, Janssen, Leo, Menlo, Novartis, Regeneron, Sanofi, and Valeant.
 

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With the strong likelihood that dermatologists in the United States will have to resolve dermatologic issues created by cultural cosmetic practices originating elsewhere, strategies for an open nonjudgmental approach are instrumental, according to a dermatologist with expertise in these types of cases who spoke at the Skin of Color Update 2021.

Dr. Neelam Ajit Vashi

“Instead of avoiding the discussion of cultural practices, we should discuss them and be open about them. It fosters a comfortable environment, trust, and better compliance,” reported Neelam Ajit Vashi, MD, founding director of the Boston University Center for Ethnic Skin.

Out of fear of causing offense, a desire to be discreet, or of personal discomfort with foreign cultural practices, some clinicians might elect to limit themselves to the information that the patient volunteers, which is a mistake, according to Dr. Vashi.

“The avoidance of topics around culture actually limits the ability to have a successful relationship,” she maintained.

Successful encounters are not just based on a willingness to listen, Dr. Vashi said. Clinicians should be seeking a base of knowledge. With growing globalization and widespread immigration, “it is increasingly important for dermatologists in the U.S. to understand the role of cultural practices [in creating skin problems] and recognize the sequelae,” Dr. Vashi said.

Taking some common examples of dermatologic complaints created by cosmetic practices originating elsewhere, Dr. Vashi described key clinical points in addressing complications related to henna, hair removal through threading, and placement of decorative adornments on the forehead, called bindi. In addition, she pointed out common issues with facial and body marking created with kumkum powder, hair oils, and skin lightening agents.
 

Black henna

For cosmetic enhancement, henna is relatively benign. It is also no longer confined to the south Asian communities where it originated. However, Dr. Vashi pointed out that patients of south Asian origin or descent might be more likely to use black henna, a variety with more risks.

Black henna contains additives, such as diaminobenzenes and p-phenylenediamine (PPD), to darken the tone of the product as well as provide other desired characteristics, such as an accelerated drying time. While some patients do develop reactions to conventional henna, the risks of black henna are greater.



“The acute contact dermatitis reactions can include dyspigmentation, leukoderma, and keloids,” Dr. Vashi said. Other complications include erythema multiforme, temporary hypertrichosis, and systemic allergic reactions, such as angioedema.

While those who have had a reaction to henna should avoid further contact, Dr. Vashi warned that sequelae can include cross reactions with latex and rubber as well as some pharmaceutical agents, such as sulfonamides. When taking a patient history, she noted, be aware that risks of henna extend to the hairdressers and cosmeticians who sometimes apply these products on others.

Hair threading, bindi, and kumkum

Hair threading, another practice popularized in south Asia and now growing in popularity globally, involves capturing hairs between cotton threads for removal of both the hair and its follicle. It is a relatively rapid and efficient method of permanent depilation. In addition to pain and erythema, Dr. Vashi reported that the complications associated with hair threading include pigmentary changes, infections such as bullous impetigo, and lesions of koebnerization – such as vitiligo and lichen planus.

Bindi, a Hindi tradition that involves placing adornments between the eyebrows, and kumkum, a powder typically made from turmeric to be employed for decorative markings, have also spread to use outside of their cultural context, according to Dr. Vashi. She said that the complications of these two cosmetic practices are shared, and stem largely from contact dermatitis.

Veena Nair/Moment/Getty Images
Sindooram, also called kumkum, is a traditional vermilion red or orange-red colored cosmetic powder from the Indian subcontinent, usually worn by married women along the part of their hair.


In the case of bindi, para-tertiary-butylphenol in adhesives is one source of reactions, whereas kumkum itself can be an irritant. As these are typically local to the site of application, the diagnosis is not difficult, but treatment can be more challenging for patients unwilling to abandon the practice.
 

Hair oils, skin-lightening agents

Culturally-linked hair oils among patients from south Asia or Africa – or descendants from these areas – can damage hair in a variety of ways as well as cause contact dermatitis. The oils can also exacerbate existing skin diseases.

“Oils with high oleic acid, such as coconut or olive oils or shea butter, can worsen seborrheic dermatitis,” Dr. Vashi cautioned.

Of this list of dermatologic issues induced by culturally linked cosmetic practices, skin lightening agents might pose the most risk for permanent and irreversible complications. Dr. Vashi said that up to 70% of patients using lighteners develop complications, and there is a relationship between the severity of side effects as duration of use increases.

“The problem is that ingredients of many of these products, which are imported illegally and sold on the black market, are often not disclosed,” Dr. Vashi said. Some contain a high content of metals such as lead, copper, and iron, whether they are added intentionally or end up in the product because of poor quality control. For those developing adverse events associated with the products, the obvious treatment is discontinuation.

When patients are unwilling to discontinue any of the products that have led to dermatologic issues, Dr. Vashi encouraged physicians “to take a middle ground.” Simple avoidance can be challenging for practices that are culturally meaningful. In respecting cultural differences, she encouraged tolerance and compromise.

“Often these patients will be doing an alternative medication or intervention, but this does not mean that they are not accepting what we have to offer,” she said. She indicated that mutual respect will lead to better solutions.

The awareness of common cultural practices that can have a harmful impact on the skin is an area of practice that deserves more attention, Andrew F. Alexis, MD, vice-chair for diversity and inclusion in the department of dermatology at Weill Cornell Medical Center, New York, said in an interview.

Dr. Andrew F. Alexis


He said that he agreed with Dr. Vashi that understanding the role of cultural practices leading to dermatoses is not enough.

“Advising patients to alter or discontinue a specific cultural practice due to a dermatologic complication should be done with respect, humility, and understanding that may be challenging,” said Dr. Alexis.

While being aware of the specific cultural practices that might be causing or exacerbating dermatoses is important for accurate diagnosis, he said he believes that “partnering with the patient to modify the cultural practices in question” is important for a clinical outcome acceptable to the patient.

“Educational resources to inform clinicians of dermatoses associated with cultural practices are available and can be helpful for dermatologists in any practice setting,” he said.

Dr. Vashi reports that she has no relevant financial relationships to disclose. Dr. Alexis reports financial relationships with Abbvie, Allergan, Almirall, Amgen, Arcutis, AstraZeneca, Bristol-Myers Squibb, Cara, Galderma, Genzyme, Janssen, Leo, Menlo, Novartis, Regeneron, Sanofi, and Valeant.
 

With the strong likelihood that dermatologists in the United States will have to resolve dermatologic issues created by cultural cosmetic practices originating elsewhere, strategies for an open nonjudgmental approach are instrumental, according to a dermatologist with expertise in these types of cases who spoke at the Skin of Color Update 2021.

Dr. Neelam Ajit Vashi

“Instead of avoiding the discussion of cultural practices, we should discuss them and be open about them. It fosters a comfortable environment, trust, and better compliance,” reported Neelam Ajit Vashi, MD, founding director of the Boston University Center for Ethnic Skin.

Out of fear of causing offense, a desire to be discreet, or of personal discomfort with foreign cultural practices, some clinicians might elect to limit themselves to the information that the patient volunteers, which is a mistake, according to Dr. Vashi.

“The avoidance of topics around culture actually limits the ability to have a successful relationship,” she maintained.

Successful encounters are not just based on a willingness to listen, Dr. Vashi said. Clinicians should be seeking a base of knowledge. With growing globalization and widespread immigration, “it is increasingly important for dermatologists in the U.S. to understand the role of cultural practices [in creating skin problems] and recognize the sequelae,” Dr. Vashi said.

Taking some common examples of dermatologic complaints created by cosmetic practices originating elsewhere, Dr. Vashi described key clinical points in addressing complications related to henna, hair removal through threading, and placement of decorative adornments on the forehead, called bindi. In addition, she pointed out common issues with facial and body marking created with kumkum powder, hair oils, and skin lightening agents.
 

Black henna

For cosmetic enhancement, henna is relatively benign. It is also no longer confined to the south Asian communities where it originated. However, Dr. Vashi pointed out that patients of south Asian origin or descent might be more likely to use black henna, a variety with more risks.

Black henna contains additives, such as diaminobenzenes and p-phenylenediamine (PPD), to darken the tone of the product as well as provide other desired characteristics, such as an accelerated drying time. While some patients do develop reactions to conventional henna, the risks of black henna are greater.



“The acute contact dermatitis reactions can include dyspigmentation, leukoderma, and keloids,” Dr. Vashi said. Other complications include erythema multiforme, temporary hypertrichosis, and systemic allergic reactions, such as angioedema.

While those who have had a reaction to henna should avoid further contact, Dr. Vashi warned that sequelae can include cross reactions with latex and rubber as well as some pharmaceutical agents, such as sulfonamides. When taking a patient history, she noted, be aware that risks of henna extend to the hairdressers and cosmeticians who sometimes apply these products on others.

Hair threading, bindi, and kumkum

Hair threading, another practice popularized in south Asia and now growing in popularity globally, involves capturing hairs between cotton threads for removal of both the hair and its follicle. It is a relatively rapid and efficient method of permanent depilation. In addition to pain and erythema, Dr. Vashi reported that the complications associated with hair threading include pigmentary changes, infections such as bullous impetigo, and lesions of koebnerization – such as vitiligo and lichen planus.

Bindi, a Hindi tradition that involves placing adornments between the eyebrows, and kumkum, a powder typically made from turmeric to be employed for decorative markings, have also spread to use outside of their cultural context, according to Dr. Vashi. She said that the complications of these two cosmetic practices are shared, and stem largely from contact dermatitis.

Veena Nair/Moment/Getty Images
Sindooram, also called kumkum, is a traditional vermilion red or orange-red colored cosmetic powder from the Indian subcontinent, usually worn by married women along the part of their hair.


In the case of bindi, para-tertiary-butylphenol in adhesives is one source of reactions, whereas kumkum itself can be an irritant. As these are typically local to the site of application, the diagnosis is not difficult, but treatment can be more challenging for patients unwilling to abandon the practice.
 

Hair oils, skin-lightening agents

Culturally-linked hair oils among patients from south Asia or Africa – or descendants from these areas – can damage hair in a variety of ways as well as cause contact dermatitis. The oils can also exacerbate existing skin diseases.

“Oils with high oleic acid, such as coconut or olive oils or shea butter, can worsen seborrheic dermatitis,” Dr. Vashi cautioned.

Of this list of dermatologic issues induced by culturally linked cosmetic practices, skin lightening agents might pose the most risk for permanent and irreversible complications. Dr. Vashi said that up to 70% of patients using lighteners develop complications, and there is a relationship between the severity of side effects as duration of use increases.

“The problem is that ingredients of many of these products, which are imported illegally and sold on the black market, are often not disclosed,” Dr. Vashi said. Some contain a high content of metals such as lead, copper, and iron, whether they are added intentionally or end up in the product because of poor quality control. For those developing adverse events associated with the products, the obvious treatment is discontinuation.

When patients are unwilling to discontinue any of the products that have led to dermatologic issues, Dr. Vashi encouraged physicians “to take a middle ground.” Simple avoidance can be challenging for practices that are culturally meaningful. In respecting cultural differences, she encouraged tolerance and compromise.

“Often these patients will be doing an alternative medication or intervention, but this does not mean that they are not accepting what we have to offer,” she said. She indicated that mutual respect will lead to better solutions.

The awareness of common cultural practices that can have a harmful impact on the skin is an area of practice that deserves more attention, Andrew F. Alexis, MD, vice-chair for diversity and inclusion in the department of dermatology at Weill Cornell Medical Center, New York, said in an interview.

Dr. Andrew F. Alexis


He said that he agreed with Dr. Vashi that understanding the role of cultural practices leading to dermatoses is not enough.

“Advising patients to alter or discontinue a specific cultural practice due to a dermatologic complication should be done with respect, humility, and understanding that may be challenging,” said Dr. Alexis.

While being aware of the specific cultural practices that might be causing or exacerbating dermatoses is important for accurate diagnosis, he said he believes that “partnering with the patient to modify the cultural practices in question” is important for a clinical outcome acceptable to the patient.

“Educational resources to inform clinicians of dermatoses associated with cultural practices are available and can be helpful for dermatologists in any practice setting,” he said.

Dr. Vashi reports that she has no relevant financial relationships to disclose. Dr. Alexis reports financial relationships with Abbvie, Allergan, Almirall, Amgen, Arcutis, AstraZeneca, Bristol-Myers Squibb, Cara, Galderma, Genzyme, Janssen, Leo, Menlo, Novartis, Regeneron, Sanofi, and Valeant.
 

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Infant with edematous, erythematous toe

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Infant with edematous, erythematous toe

History, presentation, and clinical suspicion led to the diagnosis of hair tourniquet syndrome.

Hair tourniquet syndrome was first described in 1612 by French surgeon Jacques Guillemeau.1 It typically occurs in infants when a long hair gets tightly wrapped around tissue. It most commonly affects the digits, but the penis, labia, or clitoris may also be involved. If left untreated, this condition may lead to serious complications including ischemia and necrosis of the site, and more rarely, bone erosion.

Clinicians who work with children should be aware of this condition, as early diagnosis and treatment can prevent adverse outcomes. Diagnosis requires a high-level of clinical suspicion. Use of ultrasound guidance to confirm the presence of a foreign body may aid in prompt diagnosis.2

Treatment involves release of the constricting hair(s). Hair removal cream may be used if the skin barrier is not compromised. If the hair is visible, clinicians may also attempt to remove it with tweezers. If the hair is deeply embedded within the skin, as in this case, surgical dissection may be necessary.

For this patient, the physician used local anesthesia and surgical loupes to remove 3 strands of hair from beneath newly epithelialized tissue. The digit immediately turned warm and pink. Two minutes later, capillary-refill time was normal. The mother was counseled that women often lose more hair than usual during the postpartum period, and that as a result, it’s important to watch for strands of hair that may get wrapped around the baby’s fingers or toes. Follow-up, 1 month later, showed a healed lesion on a well-perfused and nontender toe.

Image courtesy of Omar Osmani, MD, Spine and Orthopedic Center of New Mexico, Roswell. Text courtesy of Sabah Osmani, BA, University of New Mexico School of Medicine, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

References

1. Zimmerman LN, Wagner AJ. Clitoral hair tourniquet: a case report and review of the literature. Int J Pediatr Res. 2015;1:1-2. doi: 10.23937/2469-5769/1510007

2. Sebaratnam DF, Hernández‐Martín Á. Utility of ultrasonography in hair-thread tourniquet syndrome. Pediatr Dermatolo. 2018;35:e138–e139. doi: 10.1111/pde.13400

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History, presentation, and clinical suspicion led to the diagnosis of hair tourniquet syndrome.

Hair tourniquet syndrome was first described in 1612 by French surgeon Jacques Guillemeau.1 It typically occurs in infants when a long hair gets tightly wrapped around tissue. It most commonly affects the digits, but the penis, labia, or clitoris may also be involved. If left untreated, this condition may lead to serious complications including ischemia and necrosis of the site, and more rarely, bone erosion.

Clinicians who work with children should be aware of this condition, as early diagnosis and treatment can prevent adverse outcomes. Diagnosis requires a high-level of clinical suspicion. Use of ultrasound guidance to confirm the presence of a foreign body may aid in prompt diagnosis.2

Treatment involves release of the constricting hair(s). Hair removal cream may be used if the skin barrier is not compromised. If the hair is visible, clinicians may also attempt to remove it with tweezers. If the hair is deeply embedded within the skin, as in this case, surgical dissection may be necessary.

For this patient, the physician used local anesthesia and surgical loupes to remove 3 strands of hair from beneath newly epithelialized tissue. The digit immediately turned warm and pink. Two minutes later, capillary-refill time was normal. The mother was counseled that women often lose more hair than usual during the postpartum period, and that as a result, it’s important to watch for strands of hair that may get wrapped around the baby’s fingers or toes. Follow-up, 1 month later, showed a healed lesion on a well-perfused and nontender toe.

Image courtesy of Omar Osmani, MD, Spine and Orthopedic Center of New Mexico, Roswell. Text courtesy of Sabah Osmani, BA, University of New Mexico School of Medicine, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

History, presentation, and clinical suspicion led to the diagnosis of hair tourniquet syndrome.

Hair tourniquet syndrome was first described in 1612 by French surgeon Jacques Guillemeau.1 It typically occurs in infants when a long hair gets tightly wrapped around tissue. It most commonly affects the digits, but the penis, labia, or clitoris may also be involved. If left untreated, this condition may lead to serious complications including ischemia and necrosis of the site, and more rarely, bone erosion.

Clinicians who work with children should be aware of this condition, as early diagnosis and treatment can prevent adverse outcomes. Diagnosis requires a high-level of clinical suspicion. Use of ultrasound guidance to confirm the presence of a foreign body may aid in prompt diagnosis.2

Treatment involves release of the constricting hair(s). Hair removal cream may be used if the skin barrier is not compromised. If the hair is visible, clinicians may also attempt to remove it with tweezers. If the hair is deeply embedded within the skin, as in this case, surgical dissection may be necessary.

For this patient, the physician used local anesthesia and surgical loupes to remove 3 strands of hair from beneath newly epithelialized tissue. The digit immediately turned warm and pink. Two minutes later, capillary-refill time was normal. The mother was counseled that women often lose more hair than usual during the postpartum period, and that as a result, it’s important to watch for strands of hair that may get wrapped around the baby’s fingers or toes. Follow-up, 1 month later, showed a healed lesion on a well-perfused and nontender toe.

Image courtesy of Omar Osmani, MD, Spine and Orthopedic Center of New Mexico, Roswell. Text courtesy of Sabah Osmani, BA, University of New Mexico School of Medicine, and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

References

1. Zimmerman LN, Wagner AJ. Clitoral hair tourniquet: a case report and review of the literature. Int J Pediatr Res. 2015;1:1-2. doi: 10.23937/2469-5769/1510007

2. Sebaratnam DF, Hernández‐Martín Á. Utility of ultrasonography in hair-thread tourniquet syndrome. Pediatr Dermatolo. 2018;35:e138–e139. doi: 10.1111/pde.13400

References

1. Zimmerman LN, Wagner AJ. Clitoral hair tourniquet: a case report and review of the literature. Int J Pediatr Res. 2015;1:1-2. doi: 10.23937/2469-5769/1510007

2. Sebaratnam DF, Hernández‐Martín Á. Utility of ultrasonography in hair-thread tourniquet syndrome. Pediatr Dermatolo. 2018;35:e138–e139. doi: 10.1111/pde.13400

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Mentoring is key to growing women’s leadership in medicine

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Men may think they are supportive of women in the workplace, but if you ask women, they say there is a discrepancy, according to W. Brad Johnson, PhD, a clinical psychologist and professor at the United States Naval Academy in Annapolis, Md.

Dr. W. Brad Johnson

“We may think we are acting as allies to women because we believe in it, but it may not be showing up in the execution,” he said in a presentation at the virtual Advance PHM Gender Equity Conference.

Although women currently account for the majority of medical school students, they make up only 16% of the population of medical school deans, 18% of department chairs, and 25% of full professors, according to 2019 data from the Association of American Medical Colleges, Dr. Johnson said.

The “missing ingredient” in increasing the number of women in medical faculty positions is that women are less mentored. Some barriers to mentorship include men’s concerns that women will take offers of mentorship the wrong way, but “it is incredibly rare for women to make a false accusation” of harassment in a mentorship situation, said Dr. Johnson.

Dr. Johnson offered some guidance for how men can become better allies for women in the workplace through interpersonal allyship, public allyship, and systemic allyship.

Interpersonal allyship and opportunities for mentoring women in medicine start by building trust, friendship, and collegiality between men and women colleagues, Dr. Johnson explained.

He provided some guidance for men to “sharpen their gender intelligence,” which starts with listening. Surveys of women show that they would like male colleagues to be a sounding board, rather than simply offering to jump in with a fix for a problem. “Show humility,” he said, don’t be afraid to ask questions, and don’t assume that a colleague wants something in particular because she is a woman.

“A lot of men get stuck on breaking the ice and getting started with a mentoring conversation,” Dr. Johnson said. One way to is by telling a female colleague who gave an outstanding presentation, or has conducted outstanding research, that you want to keep her in your organization and that she is welcome to talk about her goals. Women appreciate mentoring as “a constellation” and a way to build support, and have one person introduce them to others who can build a network and promote opportunities for leadership. Also, he encouraged men to be open to feedback from female colleagues on how they can be more supportive in the workplace. Sincerity and genuine effort go a long way towards improving gender equity.

Public allyship can take many forms, including putting women center stage to share their own ideas, Dr. Johnson said. Surveys of women show that they often feel dismissed or slighted and not given credit for an idea that was ultimately presented by a male colleague, he noted. Instead, be a female colleague’s biggest fan, and put her in the spotlight if she is truly the expert on the topic at hand.

Women also may be hamstrung in acceding to leadership positions by the use of subjective evaluations, said Dr. Johnson. He cited a 2018 analysis of 81,000 performance evaluations by the Harvard Business Review in which the top positive term used to describe men was analytical, while the top positive term used to describe women was compassionate. “All these things go with pay and promotions, and they tend to disadvantage women,” he said.

Dr. Johnson provided two avenues for how men can effectively show up as allies for women in the workplace.

First, start at the top. CEOs and senior men in an organization have a unique opportunity to set an example and talk publicly about supporting and promoting women, said Dr. Johnson.

Second, work at the grassroots level. He encouraged men to educate themselves with gender equity workshops, and act as collaborators. “Don’t tell women how to do gender equity,” he said, but show up, be present, be mindful, and be patient if someone seems not to respond immediately to opportunities for mentoring or sponsorship.

“Claiming ally or mentor status with someone from a nondominant group may invoke power, privilege, or even ownership” without intention, he said. Instead, “Always let others label you and the nature of the relationship [such as ally or mentor].”

For more information about allyship, visit Dr. Johnson’s website, workplaceallies.com.

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Men may think they are supportive of women in the workplace, but if you ask women, they say there is a discrepancy, according to W. Brad Johnson, PhD, a clinical psychologist and professor at the United States Naval Academy in Annapolis, Md.

Dr. W. Brad Johnson

“We may think we are acting as allies to women because we believe in it, but it may not be showing up in the execution,” he said in a presentation at the virtual Advance PHM Gender Equity Conference.

Although women currently account for the majority of medical school students, they make up only 16% of the population of medical school deans, 18% of department chairs, and 25% of full professors, according to 2019 data from the Association of American Medical Colleges, Dr. Johnson said.

The “missing ingredient” in increasing the number of women in medical faculty positions is that women are less mentored. Some barriers to mentorship include men’s concerns that women will take offers of mentorship the wrong way, but “it is incredibly rare for women to make a false accusation” of harassment in a mentorship situation, said Dr. Johnson.

Dr. Johnson offered some guidance for how men can become better allies for women in the workplace through interpersonal allyship, public allyship, and systemic allyship.

Interpersonal allyship and opportunities for mentoring women in medicine start by building trust, friendship, and collegiality between men and women colleagues, Dr. Johnson explained.

He provided some guidance for men to “sharpen their gender intelligence,” which starts with listening. Surveys of women show that they would like male colleagues to be a sounding board, rather than simply offering to jump in with a fix for a problem. “Show humility,” he said, don’t be afraid to ask questions, and don’t assume that a colleague wants something in particular because she is a woman.

“A lot of men get stuck on breaking the ice and getting started with a mentoring conversation,” Dr. Johnson said. One way to is by telling a female colleague who gave an outstanding presentation, or has conducted outstanding research, that you want to keep her in your organization and that she is welcome to talk about her goals. Women appreciate mentoring as “a constellation” and a way to build support, and have one person introduce them to others who can build a network and promote opportunities for leadership. Also, he encouraged men to be open to feedback from female colleagues on how they can be more supportive in the workplace. Sincerity and genuine effort go a long way towards improving gender equity.

Public allyship can take many forms, including putting women center stage to share their own ideas, Dr. Johnson said. Surveys of women show that they often feel dismissed or slighted and not given credit for an idea that was ultimately presented by a male colleague, he noted. Instead, be a female colleague’s biggest fan, and put her in the spotlight if she is truly the expert on the topic at hand.

Women also may be hamstrung in acceding to leadership positions by the use of subjective evaluations, said Dr. Johnson. He cited a 2018 analysis of 81,000 performance evaluations by the Harvard Business Review in which the top positive term used to describe men was analytical, while the top positive term used to describe women was compassionate. “All these things go with pay and promotions, and they tend to disadvantage women,” he said.

Dr. Johnson provided two avenues for how men can effectively show up as allies for women in the workplace.

First, start at the top. CEOs and senior men in an organization have a unique opportunity to set an example and talk publicly about supporting and promoting women, said Dr. Johnson.

Second, work at the grassroots level. He encouraged men to educate themselves with gender equity workshops, and act as collaborators. “Don’t tell women how to do gender equity,” he said, but show up, be present, be mindful, and be patient if someone seems not to respond immediately to opportunities for mentoring or sponsorship.

“Claiming ally or mentor status with someone from a nondominant group may invoke power, privilege, or even ownership” without intention, he said. Instead, “Always let others label you and the nature of the relationship [such as ally or mentor].”

For more information about allyship, visit Dr. Johnson’s website, workplaceallies.com.

Men may think they are supportive of women in the workplace, but if you ask women, they say there is a discrepancy, according to W. Brad Johnson, PhD, a clinical psychologist and professor at the United States Naval Academy in Annapolis, Md.

Dr. W. Brad Johnson

“We may think we are acting as allies to women because we believe in it, but it may not be showing up in the execution,” he said in a presentation at the virtual Advance PHM Gender Equity Conference.

Although women currently account for the majority of medical school students, they make up only 16% of the population of medical school deans, 18% of department chairs, and 25% of full professors, according to 2019 data from the Association of American Medical Colleges, Dr. Johnson said.

The “missing ingredient” in increasing the number of women in medical faculty positions is that women are less mentored. Some barriers to mentorship include men’s concerns that women will take offers of mentorship the wrong way, but “it is incredibly rare for women to make a false accusation” of harassment in a mentorship situation, said Dr. Johnson.

Dr. Johnson offered some guidance for how men can become better allies for women in the workplace through interpersonal allyship, public allyship, and systemic allyship.

Interpersonal allyship and opportunities for mentoring women in medicine start by building trust, friendship, and collegiality between men and women colleagues, Dr. Johnson explained.

He provided some guidance for men to “sharpen their gender intelligence,” which starts with listening. Surveys of women show that they would like male colleagues to be a sounding board, rather than simply offering to jump in with a fix for a problem. “Show humility,” he said, don’t be afraid to ask questions, and don’t assume that a colleague wants something in particular because she is a woman.

“A lot of men get stuck on breaking the ice and getting started with a mentoring conversation,” Dr. Johnson said. One way to is by telling a female colleague who gave an outstanding presentation, or has conducted outstanding research, that you want to keep her in your organization and that she is welcome to talk about her goals. Women appreciate mentoring as “a constellation” and a way to build support, and have one person introduce them to others who can build a network and promote opportunities for leadership. Also, he encouraged men to be open to feedback from female colleagues on how they can be more supportive in the workplace. Sincerity and genuine effort go a long way towards improving gender equity.

Public allyship can take many forms, including putting women center stage to share their own ideas, Dr. Johnson said. Surveys of women show that they often feel dismissed or slighted and not given credit for an idea that was ultimately presented by a male colleague, he noted. Instead, be a female colleague’s biggest fan, and put her in the spotlight if she is truly the expert on the topic at hand.

Women also may be hamstrung in acceding to leadership positions by the use of subjective evaluations, said Dr. Johnson. He cited a 2018 analysis of 81,000 performance evaluations by the Harvard Business Review in which the top positive term used to describe men was analytical, while the top positive term used to describe women was compassionate. “All these things go with pay and promotions, and they tend to disadvantage women,” he said.

Dr. Johnson provided two avenues for how men can effectively show up as allies for women in the workplace.

First, start at the top. CEOs and senior men in an organization have a unique opportunity to set an example and talk publicly about supporting and promoting women, said Dr. Johnson.

Second, work at the grassroots level. He encouraged men to educate themselves with gender equity workshops, and act as collaborators. “Don’t tell women how to do gender equity,” he said, but show up, be present, be mindful, and be patient if someone seems not to respond immediately to opportunities for mentoring or sponsorship.

“Claiming ally or mentor status with someone from a nondominant group may invoke power, privilege, or even ownership” without intention, he said. Instead, “Always let others label you and the nature of the relationship [such as ally or mentor].”

For more information about allyship, visit Dr. Johnson’s website, workplaceallies.com.

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Painful Psoriasiform Plaques

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The Diagnosis: Acquired Acrodermatitis Enteropathica

A punch biopsy of an elevated scaly border of the rash on the thigh revealed parakeratosis, absence of the granular layer, and epidermal pallor with psoriasiform and spongiotic dermatitis (Figure). Serum zinc levels were 60.1 μg/dL (reference range, 75.0–120.0 μg/dL), suggestive of a nutritional deficiency dermatitis. Laboratory and histopathologic findings were most consistent with a diagnosis of acquired acrodermatitis enteropathica (AE).

Acquired acrodermatitis enteropathica. Histopathology showed parakeratosis, absence of the granular layer, and epidermal pallor with psoriasiform and spongiotic dermatitis (H&E, original magnification ×20).

Acrodermatitis enteropathica has been associated with Roux-en-Y gastric bypass and alcohol use disorder working synergistically to cause malabsorption and malnutrition, respectively.1 Zinc functions in the structural integrity, wound healing, and anti-inflammatory properties of the skin. There is a 17.3% risk for hypozincemia worldwide; in developed nations there is an estimated 3% to 10% occurrence rate.2 Acrodermatitis enteropathica can be classified as either acquired or hereditary. Both classically present as a triad of acral dermatitis, diarrhea, and alopecia, though the complete triad is seen in 20% of cases.3,4

Hereditary AE is an autosomal-recessive disorder presenting in infancy that results in the loss of a zinc transporter. In contrast, acquired AE occurs later in life and usually is seen in patients who have decreased intake, malabsorption, or excessive loss of zinc.4 Acrodermatitis enteropathica is observed in individuals with conditions such as anorexia nervosa, pancreatic insufficiency, celiac disease, Crohn disease, or gastric bypass surgery (as in our case) and alcohol recidivism. In early disease, AE often presents with angular cheilitis and paronychia, but if left untreated, it can progress to mental status changes, hypogonadism, and depression.4 Acrodermatitis enteropathica presents as erythematous, erosive, scaly plaques or a papulosquamous psoriasiform rash with well-demarcated borders typically involving the orificial, acral, and intertriginous areas of the body.1,4

Acrodermatitis enteropathica belongs to a family of deficiency dermatoses that includes pellagra, necrolytic acral erythema (NAE), and necrolytic migratory erythema (NME).5 It is important to distinguish AE from NAE, as they can present similarly with well-defined and tender psoriasiform lesions peripherally. Histologically, NAE mimics AE with psoriasiform hyperplasia with parakeratosis.6 Necrolytic acral erythema characteristically is associated with active hepatitis C infection, which was absent in our patient.7

Similar to AE, NME affects the perineal and intertriginous surfaces.8 However, necrolytic migratory erythema has cutaneous manifestations in up to 70% of patients with glucagonoma syndrome, which classically presents as a triad of NME, weight loss, and diabetes mellitus.5 Laboratory studies show marked hyperglucagonemia, and imaging reveals enteropancreatic neoplasia. Necrolytic migratory erythema will rapidly resolve once the glucagonoma has been surgically removed.5 Bazex syndrome, or acrokeratosis paraneoplastica, is a paraneoplastic skin disease that is linked to underlying aerodigestive tract malignancies.

Bazex syndrome clinically is characterized by hyperkeratotic and psoriasiform lesions favoring the ears, nails, and nose.9

Psoriasis vulgaris is a common chronic inflammatory skin condition that usually presents as well-demarcated plaques with silvery scale and observed pinpoint bleeding when layers of scale are removed (Auspitz sign). Lesions typically are found on the extensor surfaces of the body in addition to the neck, feet, hands, and trunk. Treatment of psoriasis vulgaris ranges from topical steroids for mild cases to systemic biologics for moderate to severe circumstances.10 In our patient, topical triamcinolone offered little relief.

Acrodermatitis enteropathica displays clinical and histologic characteristics analogous to many deficiency dermatoses and may represent a spectrum of disease. Because the clinicopathologic findings are nonspecific, it is critical to obtain a comprehensive history and maintain a high index of suspicion in patients with risk factors for malnutrition. The treatment for AE is supplemental oral zinc usually initiated at 0.5 to 1 mg/kg daily in children and 30 to 45 mg daily in adults.3 Our patient initially was prescribed oral zinc supplementation; however, at 1-month follow-up, the rash had not improved. Failure of zinc monotherapy supports a multifactorial nutritional deficiency, which necessitated comprehensive nutritional appraisal and supplementation in our patient. Due to the steatorrhea, fecal pancreatic elastase levels were evaluated and were less than 15 μg/g (reference range, ≥201 μg/g), confirming pancreatic exocrine insufficiency, a known complication of Roux-en-Y gastric bypass.11 Pancrelipase 500 U/kg per meal was added in addition to zinc oxide 40% paste to apply to the rash twice daily, with more frequent applications to the anogenital regions after bowel movements. The patient had substantial clinical improvement after 2 months.

References
  1. Shahsavari D, Ahmed Z, Karikkineth A, et al. Zinc-deficiency acrodermatitis in a patient with chronic alcoholism and gastric bypass: a case report. J Community Hosp Intern Med Perspect. 2014. doi:10.3402/jchimp.v4.24707
  2. Kelly S, Stelzer JW, Esplin N, et al. Acquired acrodermatitis enteropathica: a case study. Cureus. 2017;9:E1667.
  3. Guliani A, Bishnoi A. Acquired acrodermatitis enteropathica. JAMA Dermatol. 2019;155:1305.
  4. Baruch D, Naga L, Driscoll M, et al. Acrodermatitis enteropathica from zinc-deficient total parenteral nutrition. Cutis. 2018;101:450-453.
  5. van Beek AP, de Haas ER, van Vloten WA, et al. The glucagonoma syndrome and necrolytic migratory erythema: a clinical review. Eur J Endocrinol. 2004;151:531-537.
  6. Botelho LF, Enokihara MM, Enokihara MY. Necrolytic acral erythema: a rare skin disease associated with hepatitis C virus infection. An Bras Dermatol. 2016;91:649-651.
  7. Abdallah MA, Ghozzi MY, Monib HA, et al. Necrolytic acral erythema: a cutaneous sign of hepatitis C virus infection. J Am Acad Dermatol. 2005;53:247-251.
  8. Tolliver S, Graham J, Kaffenberger BH. A review of cutaneous manifestations within glucagonoma syndrome: necrolytic migratory erythema. Int J Dermatol. 2018;57:642-645.
  9. Poligone B, Christensen SR, Lazova R, et al. Bazex syndrome (acrokeratosis paraneoplastica). Lancet. 2007;369:530. 10. Kupetsky EA, Keller M. Psoriasis vulgaris: an evidencebased guide for primary care. J Am Board Fam Med. 2013; 26:787-801.
  10. Borbély Y, Plebani A, Kröll D, et al. Exocrine pancreatic insufficiency after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2016;12:790-794.
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Dr. Gozo is from the USS Anchorage, Naval Base San Diego, California. Drs. Manalo and Cheeley are from the Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia. Dr. Cheeley also is from the Department of Medicine.

The authors report no conflict of interest.

The views expressed are those of the authors and do not reflect the opinions of the USS Anchorage (LPD-23), the US Navy, or the US Government.

Correspondence: Maria Amoreth R. Gozo, MD, Health Services Department, USS Anchorage (LPD 23) FPO AP 96660 ([email protected]).

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Dr. Gozo is from the USS Anchorage, Naval Base San Diego, California. Drs. Manalo and Cheeley are from the Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia. Dr. Cheeley also is from the Department of Medicine.

The authors report no conflict of interest.

The views expressed are those of the authors and do not reflect the opinions of the USS Anchorage (LPD-23), the US Navy, or the US Government.

Correspondence: Maria Amoreth R. Gozo, MD, Health Services Department, USS Anchorage (LPD 23) FPO AP 96660 ([email protected]).

Author and Disclosure Information

Dr. Gozo is from the USS Anchorage, Naval Base San Diego, California. Drs. Manalo and Cheeley are from the Department of Dermatology, Emory University School of Medicine, Atlanta, Georgia. Dr. Cheeley also is from the Department of Medicine.

The authors report no conflict of interest.

The views expressed are those of the authors and do not reflect the opinions of the USS Anchorage (LPD-23), the US Navy, or the US Government.

Correspondence: Maria Amoreth R. Gozo, MD, Health Services Department, USS Anchorage (LPD 23) FPO AP 96660 ([email protected]).

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The Diagnosis: Acquired Acrodermatitis Enteropathica

A punch biopsy of an elevated scaly border of the rash on the thigh revealed parakeratosis, absence of the granular layer, and epidermal pallor with psoriasiform and spongiotic dermatitis (Figure). Serum zinc levels were 60.1 μg/dL (reference range, 75.0–120.0 μg/dL), suggestive of a nutritional deficiency dermatitis. Laboratory and histopathologic findings were most consistent with a diagnosis of acquired acrodermatitis enteropathica (AE).

Acquired acrodermatitis enteropathica. Histopathology showed parakeratosis, absence of the granular layer, and epidermal pallor with psoriasiform and spongiotic dermatitis (H&E, original magnification ×20).

Acrodermatitis enteropathica has been associated with Roux-en-Y gastric bypass and alcohol use disorder working synergistically to cause malabsorption and malnutrition, respectively.1 Zinc functions in the structural integrity, wound healing, and anti-inflammatory properties of the skin. There is a 17.3% risk for hypozincemia worldwide; in developed nations there is an estimated 3% to 10% occurrence rate.2 Acrodermatitis enteropathica can be classified as either acquired or hereditary. Both classically present as a triad of acral dermatitis, diarrhea, and alopecia, though the complete triad is seen in 20% of cases.3,4

Hereditary AE is an autosomal-recessive disorder presenting in infancy that results in the loss of a zinc transporter. In contrast, acquired AE occurs later in life and usually is seen in patients who have decreased intake, malabsorption, or excessive loss of zinc.4 Acrodermatitis enteropathica is observed in individuals with conditions such as anorexia nervosa, pancreatic insufficiency, celiac disease, Crohn disease, or gastric bypass surgery (as in our case) and alcohol recidivism. In early disease, AE often presents with angular cheilitis and paronychia, but if left untreated, it can progress to mental status changes, hypogonadism, and depression.4 Acrodermatitis enteropathica presents as erythematous, erosive, scaly plaques or a papulosquamous psoriasiform rash with well-demarcated borders typically involving the orificial, acral, and intertriginous areas of the body.1,4

Acrodermatitis enteropathica belongs to a family of deficiency dermatoses that includes pellagra, necrolytic acral erythema (NAE), and necrolytic migratory erythema (NME).5 It is important to distinguish AE from NAE, as they can present similarly with well-defined and tender psoriasiform lesions peripherally. Histologically, NAE mimics AE with psoriasiform hyperplasia with parakeratosis.6 Necrolytic acral erythema characteristically is associated with active hepatitis C infection, which was absent in our patient.7

Similar to AE, NME affects the perineal and intertriginous surfaces.8 However, necrolytic migratory erythema has cutaneous manifestations in up to 70% of patients with glucagonoma syndrome, which classically presents as a triad of NME, weight loss, and diabetes mellitus.5 Laboratory studies show marked hyperglucagonemia, and imaging reveals enteropancreatic neoplasia. Necrolytic migratory erythema will rapidly resolve once the glucagonoma has been surgically removed.5 Bazex syndrome, or acrokeratosis paraneoplastica, is a paraneoplastic skin disease that is linked to underlying aerodigestive tract malignancies.

Bazex syndrome clinically is characterized by hyperkeratotic and psoriasiform lesions favoring the ears, nails, and nose.9

Psoriasis vulgaris is a common chronic inflammatory skin condition that usually presents as well-demarcated plaques with silvery scale and observed pinpoint bleeding when layers of scale are removed (Auspitz sign). Lesions typically are found on the extensor surfaces of the body in addition to the neck, feet, hands, and trunk. Treatment of psoriasis vulgaris ranges from topical steroids for mild cases to systemic biologics for moderate to severe circumstances.10 In our patient, topical triamcinolone offered little relief.

Acrodermatitis enteropathica displays clinical and histologic characteristics analogous to many deficiency dermatoses and may represent a spectrum of disease. Because the clinicopathologic findings are nonspecific, it is critical to obtain a comprehensive history and maintain a high index of suspicion in patients with risk factors for malnutrition. The treatment for AE is supplemental oral zinc usually initiated at 0.5 to 1 mg/kg daily in children and 30 to 45 mg daily in adults.3 Our patient initially was prescribed oral zinc supplementation; however, at 1-month follow-up, the rash had not improved. Failure of zinc monotherapy supports a multifactorial nutritional deficiency, which necessitated comprehensive nutritional appraisal and supplementation in our patient. Due to the steatorrhea, fecal pancreatic elastase levels were evaluated and were less than 15 μg/g (reference range, ≥201 μg/g), confirming pancreatic exocrine insufficiency, a known complication of Roux-en-Y gastric bypass.11 Pancrelipase 500 U/kg per meal was added in addition to zinc oxide 40% paste to apply to the rash twice daily, with more frequent applications to the anogenital regions after bowel movements. The patient had substantial clinical improvement after 2 months.

The Diagnosis: Acquired Acrodermatitis Enteropathica

A punch biopsy of an elevated scaly border of the rash on the thigh revealed parakeratosis, absence of the granular layer, and epidermal pallor with psoriasiform and spongiotic dermatitis (Figure). Serum zinc levels were 60.1 μg/dL (reference range, 75.0–120.0 μg/dL), suggestive of a nutritional deficiency dermatitis. Laboratory and histopathologic findings were most consistent with a diagnosis of acquired acrodermatitis enteropathica (AE).

Acquired acrodermatitis enteropathica. Histopathology showed parakeratosis, absence of the granular layer, and epidermal pallor with psoriasiform and spongiotic dermatitis (H&E, original magnification ×20).

Acrodermatitis enteropathica has been associated with Roux-en-Y gastric bypass and alcohol use disorder working synergistically to cause malabsorption and malnutrition, respectively.1 Zinc functions in the structural integrity, wound healing, and anti-inflammatory properties of the skin. There is a 17.3% risk for hypozincemia worldwide; in developed nations there is an estimated 3% to 10% occurrence rate.2 Acrodermatitis enteropathica can be classified as either acquired or hereditary. Both classically present as a triad of acral dermatitis, diarrhea, and alopecia, though the complete triad is seen in 20% of cases.3,4

Hereditary AE is an autosomal-recessive disorder presenting in infancy that results in the loss of a zinc transporter. In contrast, acquired AE occurs later in life and usually is seen in patients who have decreased intake, malabsorption, or excessive loss of zinc.4 Acrodermatitis enteropathica is observed in individuals with conditions such as anorexia nervosa, pancreatic insufficiency, celiac disease, Crohn disease, or gastric bypass surgery (as in our case) and alcohol recidivism. In early disease, AE often presents with angular cheilitis and paronychia, but if left untreated, it can progress to mental status changes, hypogonadism, and depression.4 Acrodermatitis enteropathica presents as erythematous, erosive, scaly plaques or a papulosquamous psoriasiform rash with well-demarcated borders typically involving the orificial, acral, and intertriginous areas of the body.1,4

Acrodermatitis enteropathica belongs to a family of deficiency dermatoses that includes pellagra, necrolytic acral erythema (NAE), and necrolytic migratory erythema (NME).5 It is important to distinguish AE from NAE, as they can present similarly with well-defined and tender psoriasiform lesions peripherally. Histologically, NAE mimics AE with psoriasiform hyperplasia with parakeratosis.6 Necrolytic acral erythema characteristically is associated with active hepatitis C infection, which was absent in our patient.7

Similar to AE, NME affects the perineal and intertriginous surfaces.8 However, necrolytic migratory erythema has cutaneous manifestations in up to 70% of patients with glucagonoma syndrome, which classically presents as a triad of NME, weight loss, and diabetes mellitus.5 Laboratory studies show marked hyperglucagonemia, and imaging reveals enteropancreatic neoplasia. Necrolytic migratory erythema will rapidly resolve once the glucagonoma has been surgically removed.5 Bazex syndrome, or acrokeratosis paraneoplastica, is a paraneoplastic skin disease that is linked to underlying aerodigestive tract malignancies.

Bazex syndrome clinically is characterized by hyperkeratotic and psoriasiform lesions favoring the ears, nails, and nose.9

Psoriasis vulgaris is a common chronic inflammatory skin condition that usually presents as well-demarcated plaques with silvery scale and observed pinpoint bleeding when layers of scale are removed (Auspitz sign). Lesions typically are found on the extensor surfaces of the body in addition to the neck, feet, hands, and trunk. Treatment of psoriasis vulgaris ranges from topical steroids for mild cases to systemic biologics for moderate to severe circumstances.10 In our patient, topical triamcinolone offered little relief.

Acrodermatitis enteropathica displays clinical and histologic characteristics analogous to many deficiency dermatoses and may represent a spectrum of disease. Because the clinicopathologic findings are nonspecific, it is critical to obtain a comprehensive history and maintain a high index of suspicion in patients with risk factors for malnutrition. The treatment for AE is supplemental oral zinc usually initiated at 0.5 to 1 mg/kg daily in children and 30 to 45 mg daily in adults.3 Our patient initially was prescribed oral zinc supplementation; however, at 1-month follow-up, the rash had not improved. Failure of zinc monotherapy supports a multifactorial nutritional deficiency, which necessitated comprehensive nutritional appraisal and supplementation in our patient. Due to the steatorrhea, fecal pancreatic elastase levels were evaluated and were less than 15 μg/g (reference range, ≥201 μg/g), confirming pancreatic exocrine insufficiency, a known complication of Roux-en-Y gastric bypass.11 Pancrelipase 500 U/kg per meal was added in addition to zinc oxide 40% paste to apply to the rash twice daily, with more frequent applications to the anogenital regions after bowel movements. The patient had substantial clinical improvement after 2 months.

References
  1. Shahsavari D, Ahmed Z, Karikkineth A, et al. Zinc-deficiency acrodermatitis in a patient with chronic alcoholism and gastric bypass: a case report. J Community Hosp Intern Med Perspect. 2014. doi:10.3402/jchimp.v4.24707
  2. Kelly S, Stelzer JW, Esplin N, et al. Acquired acrodermatitis enteropathica: a case study. Cureus. 2017;9:E1667.
  3. Guliani A, Bishnoi A. Acquired acrodermatitis enteropathica. JAMA Dermatol. 2019;155:1305.
  4. Baruch D, Naga L, Driscoll M, et al. Acrodermatitis enteropathica from zinc-deficient total parenteral nutrition. Cutis. 2018;101:450-453.
  5. van Beek AP, de Haas ER, van Vloten WA, et al. The glucagonoma syndrome and necrolytic migratory erythema: a clinical review. Eur J Endocrinol. 2004;151:531-537.
  6. Botelho LF, Enokihara MM, Enokihara MY. Necrolytic acral erythema: a rare skin disease associated with hepatitis C virus infection. An Bras Dermatol. 2016;91:649-651.
  7. Abdallah MA, Ghozzi MY, Monib HA, et al. Necrolytic acral erythema: a cutaneous sign of hepatitis C virus infection. J Am Acad Dermatol. 2005;53:247-251.
  8. Tolliver S, Graham J, Kaffenberger BH. A review of cutaneous manifestations within glucagonoma syndrome: necrolytic migratory erythema. Int J Dermatol. 2018;57:642-645.
  9. Poligone B, Christensen SR, Lazova R, et al. Bazex syndrome (acrokeratosis paraneoplastica). Lancet. 2007;369:530. 10. Kupetsky EA, Keller M. Psoriasis vulgaris: an evidencebased guide for primary care. J Am Board Fam Med. 2013; 26:787-801.
  10. Borbély Y, Plebani A, Kröll D, et al. Exocrine pancreatic insufficiency after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2016;12:790-794.
References
  1. Shahsavari D, Ahmed Z, Karikkineth A, et al. Zinc-deficiency acrodermatitis in a patient with chronic alcoholism and gastric bypass: a case report. J Community Hosp Intern Med Perspect. 2014. doi:10.3402/jchimp.v4.24707
  2. Kelly S, Stelzer JW, Esplin N, et al. Acquired acrodermatitis enteropathica: a case study. Cureus. 2017;9:E1667.
  3. Guliani A, Bishnoi A. Acquired acrodermatitis enteropathica. JAMA Dermatol. 2019;155:1305.
  4. Baruch D, Naga L, Driscoll M, et al. Acrodermatitis enteropathica from zinc-deficient total parenteral nutrition. Cutis. 2018;101:450-453.
  5. van Beek AP, de Haas ER, van Vloten WA, et al. The glucagonoma syndrome and necrolytic migratory erythema: a clinical review. Eur J Endocrinol. 2004;151:531-537.
  6. Botelho LF, Enokihara MM, Enokihara MY. Necrolytic acral erythema: a rare skin disease associated with hepatitis C virus infection. An Bras Dermatol. 2016;91:649-651.
  7. Abdallah MA, Ghozzi MY, Monib HA, et al. Necrolytic acral erythema: a cutaneous sign of hepatitis C virus infection. J Am Acad Dermatol. 2005;53:247-251.
  8. Tolliver S, Graham J, Kaffenberger BH. A review of cutaneous manifestations within glucagonoma syndrome: necrolytic migratory erythema. Int J Dermatol. 2018;57:642-645.
  9. Poligone B, Christensen SR, Lazova R, et al. Bazex syndrome (acrokeratosis paraneoplastica). Lancet. 2007;369:530. 10. Kupetsky EA, Keller M. Psoriasis vulgaris: an evidencebased guide for primary care. J Am Board Fam Med. 2013; 26:787-801.
  10. Borbély Y, Plebani A, Kröll D, et al. Exocrine pancreatic insufficiency after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2016;12:790-794.
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A 45-year-old woman presented to the emergency department with a painful skin eruption and malaise of 5 weeks’ duration. She had an orthotopic liver transplant 5 years prior for end-stage liver disease due to mixed nonalcoholic and alcoholic steatohepatitis and was on mycophenolate mofetil and tacrolimus for graft rejection prophylaxis. Her medical history also included Roux-en-Y gastric bypass 15 years prior, alcohol use disorder, hypothyroidism, and depression.

The exanthem began on the legs as pruritic, red, raised, exudative lesions that gradually crusted. Over the 2 weeks prior to the current presentation, the rash became tender as it spread to the feet, thighs, perianal skin, buttocks, and elbows. Triamcinolone ointment prescribed for a presumed nummular dermatitis effected marginal benefit. A review of systems was notable for a 15-pound weight loss over several weeks; lowgrade fever of 3 days’ duration; epigastric abdominal pain; and long-standing, frequent defecation of oily, foul-smelling feces.

Physical examination revealed a combination of flat-topped, violaceous papules and serpiginous, polycyclic, annular plaques coalescing to form larger psoriasiform plaques with hyperkeratotic rims and dusky borders on the dorsal aspect of the feet (top), lateral ankles, legs (bottom), lateral thighs, buttocks, perianal skin, and elbows. Bilateral angular cheilitis, a smooth and fissured tongue, and pitting of all fingernails were noted.

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Web of antimicrobials doesn’t hold water

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Changed
Thu, 10/07/2021 - 09:19

 

Music plus mushrooms equals therapy

Magic mushrooms have been used recreationally and medicinally for thousands of years, but researchers have found adding music could be a game changer in antidepressant treatment.

chrissmith12/Pixabay

The ingredient that makes these mushrooms so magical is psilocybin. It works well for the clinical treatment of mental health conditions and some forms of depression because the “trip” can be contained to one work day, making it easy to administer under supervision. With the accompaniment of music, scientists have found that psilocybin evokes emotion.

This recent study, presented at the European College of Neuropsychopharmacology Congress in Lisbon, tested participants’ emotional response to music before and after the psilocybin. Ketanserin, an antihypertensive drug, was used to test against the effects of psilocybin. The scientist played Mozart and Elgar and found that participants on psilocybin had an emotional response increase of 60%. That response was even greater, compared with ketanserin, which actually lessened the emotional response to music.

“This shows that combination of psilocybin and music has a strong emotional effect, and we believe that this will be important for the therapeutic application of psychedelics if they are approved for clinical use,” said lead researcher Dea Siggaard Stenbæk of the University of Copenhagen.

Professor David J. Nutt of Imperial College in London, who was not involved in the study, said that it supports the use of music for treatment efficacy with psychedelics and suggested that the next step is to “optimise this approach probably through individualising and personalising music tracks in therapy.”

Cue the 1960s LSD music montage.
 

Chicken ‘white striping is not a disease’

Have you ever sliced open a new pack of chicken breasts to start dinner and noticed white fatty lines running through the chicken? Maybe you thought it was just some extra fat to trim off, but the Humane League calls it “white striping disease.”

rawpixel

Chicken is the No. 1 meat consumed by Americans, so it’s not surprising that chickens are factory farmed and raised to be ready for slaughter quickly, according to CBSNews.com, which reported that the Humane League claims white striping is found in 70% of the chicken in popular grocery stores. The league expressed concern for the chickens’ welfare as they are bred to grow bigger quickly, which is causing the white striping and increasing the fat content of the meat by as much as 224%.

The National Chicken Council told CBS that the league’s findings were unscientific. A spokesperson said, “White striping is not a disease. It is a quality factor in chicken breast meat caused by deposits of fat in the muscle during the bird’s growth and development.” He went on to say that severe white striping happens in 3%-6% of birds, which are mostly used in further processed products, not in chicken breast packages.

Somehow, that’s not making us feel any better.
 

The itsy bitsy spider lets us all down

Most people do not like spiders. That’s too bad, because spiders are generally nothing but helpful little creatures that prey upon annoying flies and other pests. Then there’s the silk they produce. The ancient Romans used it to treat conditions such as warts and skin lesions. Spiders wrap their eggs in silk to protect them from harmful bacteria.

Simon Fruergaard

Of course, we can hardly trust the medical opinions of people from 2,000 years ago, but modern-day studies have not definitively proved whether or not spider silk has any antimicrobial properties.

To settle the matter once and for all, researchers from Denmark built a silk-harvesting machine using the most famous of Danish inventions: Legos. The contraption, sort of a paddle wheel, pulled the silk from several different species of spider pinned down by the researchers. The silk was then tested against three different bacteria species, including good old Escherichia coli.

Unfortunately for our spider friends, their silk has no antimicrobial activity. The researchers suspected that any such activity seen in previous studies was actually caused by improper control for the solvents used to extract the silk; those solvents can have antimicrobial properties on their own. As for protecting their eggs, rather than killing bacteria, the silk likely provides a physical barrier alone.

It is bad news for spiders on the benefit-to-humanity front, but look at the bright side: If their silk had antimicrobial activity, we’d have to start farming them to acquire more silk. And that’s no good. Spiders deserve to roam free, hunt as they please, and drop down on your head from the ceiling.
 

Anxiety and allergies: Cause, effect, confusion

We’re big fans of science, but as longtime, totally impartial (Science rules!) observers of science’s medical realm, we can see that the day-to-day process of practicing the scientific method occasionally gets a bit messy. And no, we’re not talking about COVID-19.

pxfuel

We’re talking allergies. We’re talking mental health. We’re talking allergic disease and mental health.

We’re talking about a pair of press releases we came across during our never-ending search for material to educate, entertain, and astound our fabulously wonderful and loyal readers. (We say that, of course, in the most impartial way possible.)

The first release was titled, “Allergies including asthma and hay fever not linked to mental health traits” and covered research from the University of Bristol (England). The investigators were trying to determine if “allergic diseases actually causes mental health traits including anxiety, depression, bipolar disorder, and schizophrenia, or vice versa,” according to the release.

What they found, however, was “little evidence of a causal relationship between the onset of allergic disease and mental health.” Again, this is the press release talking.

The second release seemed to suggest the exact opposite: “Study uncovers link between allergies and mental health conditions.” That got our attention. A little more reading revealed that “people with asthma, atopic dermatitis, and hay fever also had a higher likelihood of having depression, anxiety, bipolar disorder, or neuroticism.”

One of the investigators was quoted as saying, “Establishing whether allergic disease causes mental health problems, or vice versa, is important to ensure that resources and treatment strategies are targeted appropriately.”

Did you notice the “vice versa”? Did you notice that it appeared in quotes from both releases? We did, so we took a closer look at the source. The second release covered a group of investigators from the University of Bristol – the same group, and the same study, in fact, as the first one.

So there you have it. One study, two press releases, and one confused journalist. Thank you, science.

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Topics
Sections

 

Music plus mushrooms equals therapy

Magic mushrooms have been used recreationally and medicinally for thousands of years, but researchers have found adding music could be a game changer in antidepressant treatment.

chrissmith12/Pixabay

The ingredient that makes these mushrooms so magical is psilocybin. It works well for the clinical treatment of mental health conditions and some forms of depression because the “trip” can be contained to one work day, making it easy to administer under supervision. With the accompaniment of music, scientists have found that psilocybin evokes emotion.

This recent study, presented at the European College of Neuropsychopharmacology Congress in Lisbon, tested participants’ emotional response to music before and after the psilocybin. Ketanserin, an antihypertensive drug, was used to test against the effects of psilocybin. The scientist played Mozart and Elgar and found that participants on psilocybin had an emotional response increase of 60%. That response was even greater, compared with ketanserin, which actually lessened the emotional response to music.

“This shows that combination of psilocybin and music has a strong emotional effect, and we believe that this will be important for the therapeutic application of psychedelics if they are approved for clinical use,” said lead researcher Dea Siggaard Stenbæk of the University of Copenhagen.

Professor David J. Nutt of Imperial College in London, who was not involved in the study, said that it supports the use of music for treatment efficacy with psychedelics and suggested that the next step is to “optimise this approach probably through individualising and personalising music tracks in therapy.”

Cue the 1960s LSD music montage.
 

Chicken ‘white striping is not a disease’

Have you ever sliced open a new pack of chicken breasts to start dinner and noticed white fatty lines running through the chicken? Maybe you thought it was just some extra fat to trim off, but the Humane League calls it “white striping disease.”

rawpixel

Chicken is the No. 1 meat consumed by Americans, so it’s not surprising that chickens are factory farmed and raised to be ready for slaughter quickly, according to CBSNews.com, which reported that the Humane League claims white striping is found in 70% of the chicken in popular grocery stores. The league expressed concern for the chickens’ welfare as they are bred to grow bigger quickly, which is causing the white striping and increasing the fat content of the meat by as much as 224%.

The National Chicken Council told CBS that the league’s findings were unscientific. A spokesperson said, “White striping is not a disease. It is a quality factor in chicken breast meat caused by deposits of fat in the muscle during the bird’s growth and development.” He went on to say that severe white striping happens in 3%-6% of birds, which are mostly used in further processed products, not in chicken breast packages.

Somehow, that’s not making us feel any better.
 

The itsy bitsy spider lets us all down

Most people do not like spiders. That’s too bad, because spiders are generally nothing but helpful little creatures that prey upon annoying flies and other pests. Then there’s the silk they produce. The ancient Romans used it to treat conditions such as warts and skin lesions. Spiders wrap their eggs in silk to protect them from harmful bacteria.

Simon Fruergaard

Of course, we can hardly trust the medical opinions of people from 2,000 years ago, but modern-day studies have not definitively proved whether or not spider silk has any antimicrobial properties.

To settle the matter once and for all, researchers from Denmark built a silk-harvesting machine using the most famous of Danish inventions: Legos. The contraption, sort of a paddle wheel, pulled the silk from several different species of spider pinned down by the researchers. The silk was then tested against three different bacteria species, including good old Escherichia coli.

Unfortunately for our spider friends, their silk has no antimicrobial activity. The researchers suspected that any such activity seen in previous studies was actually caused by improper control for the solvents used to extract the silk; those solvents can have antimicrobial properties on their own. As for protecting their eggs, rather than killing bacteria, the silk likely provides a physical barrier alone.

It is bad news for spiders on the benefit-to-humanity front, but look at the bright side: If their silk had antimicrobial activity, we’d have to start farming them to acquire more silk. And that’s no good. Spiders deserve to roam free, hunt as they please, and drop down on your head from the ceiling.
 

Anxiety and allergies: Cause, effect, confusion

We’re big fans of science, but as longtime, totally impartial (Science rules!) observers of science’s medical realm, we can see that the day-to-day process of practicing the scientific method occasionally gets a bit messy. And no, we’re not talking about COVID-19.

pxfuel

We’re talking allergies. We’re talking mental health. We’re talking allergic disease and mental health.

We’re talking about a pair of press releases we came across during our never-ending search for material to educate, entertain, and astound our fabulously wonderful and loyal readers. (We say that, of course, in the most impartial way possible.)

The first release was titled, “Allergies including asthma and hay fever not linked to mental health traits” and covered research from the University of Bristol (England). The investigators were trying to determine if “allergic diseases actually causes mental health traits including anxiety, depression, bipolar disorder, and schizophrenia, or vice versa,” according to the release.

What they found, however, was “little evidence of a causal relationship between the onset of allergic disease and mental health.” Again, this is the press release talking.

The second release seemed to suggest the exact opposite: “Study uncovers link between allergies and mental health conditions.” That got our attention. A little more reading revealed that “people with asthma, atopic dermatitis, and hay fever also had a higher likelihood of having depression, anxiety, bipolar disorder, or neuroticism.”

One of the investigators was quoted as saying, “Establishing whether allergic disease causes mental health problems, or vice versa, is important to ensure that resources and treatment strategies are targeted appropriately.”

Did you notice the “vice versa”? Did you notice that it appeared in quotes from both releases? We did, so we took a closer look at the source. The second release covered a group of investigators from the University of Bristol – the same group, and the same study, in fact, as the first one.

So there you have it. One study, two press releases, and one confused journalist. Thank you, science.

 

Music plus mushrooms equals therapy

Magic mushrooms have been used recreationally and medicinally for thousands of years, but researchers have found adding music could be a game changer in antidepressant treatment.

chrissmith12/Pixabay

The ingredient that makes these mushrooms so magical is psilocybin. It works well for the clinical treatment of mental health conditions and some forms of depression because the “trip” can be contained to one work day, making it easy to administer under supervision. With the accompaniment of music, scientists have found that psilocybin evokes emotion.

This recent study, presented at the European College of Neuropsychopharmacology Congress in Lisbon, tested participants’ emotional response to music before and after the psilocybin. Ketanserin, an antihypertensive drug, was used to test against the effects of psilocybin. The scientist played Mozart and Elgar and found that participants on psilocybin had an emotional response increase of 60%. That response was even greater, compared with ketanserin, which actually lessened the emotional response to music.

“This shows that combination of psilocybin and music has a strong emotional effect, and we believe that this will be important for the therapeutic application of psychedelics if they are approved for clinical use,” said lead researcher Dea Siggaard Stenbæk of the University of Copenhagen.

Professor David J. Nutt of Imperial College in London, who was not involved in the study, said that it supports the use of music for treatment efficacy with psychedelics and suggested that the next step is to “optimise this approach probably through individualising and personalising music tracks in therapy.”

Cue the 1960s LSD music montage.
 

Chicken ‘white striping is not a disease’

Have you ever sliced open a new pack of chicken breasts to start dinner and noticed white fatty lines running through the chicken? Maybe you thought it was just some extra fat to trim off, but the Humane League calls it “white striping disease.”

rawpixel

Chicken is the No. 1 meat consumed by Americans, so it’s not surprising that chickens are factory farmed and raised to be ready for slaughter quickly, according to CBSNews.com, which reported that the Humane League claims white striping is found in 70% of the chicken in popular grocery stores. The league expressed concern for the chickens’ welfare as they are bred to grow bigger quickly, which is causing the white striping and increasing the fat content of the meat by as much as 224%.

The National Chicken Council told CBS that the league’s findings were unscientific. A spokesperson said, “White striping is not a disease. It is a quality factor in chicken breast meat caused by deposits of fat in the muscle during the bird’s growth and development.” He went on to say that severe white striping happens in 3%-6% of birds, which are mostly used in further processed products, not in chicken breast packages.

Somehow, that’s not making us feel any better.
 

The itsy bitsy spider lets us all down

Most people do not like spiders. That’s too bad, because spiders are generally nothing but helpful little creatures that prey upon annoying flies and other pests. Then there’s the silk they produce. The ancient Romans used it to treat conditions such as warts and skin lesions. Spiders wrap their eggs in silk to protect them from harmful bacteria.

Simon Fruergaard

Of course, we can hardly trust the medical opinions of people from 2,000 years ago, but modern-day studies have not definitively proved whether or not spider silk has any antimicrobial properties.

To settle the matter once and for all, researchers from Denmark built a silk-harvesting machine using the most famous of Danish inventions: Legos. The contraption, sort of a paddle wheel, pulled the silk from several different species of spider pinned down by the researchers. The silk was then tested against three different bacteria species, including good old Escherichia coli.

Unfortunately for our spider friends, their silk has no antimicrobial activity. The researchers suspected that any such activity seen in previous studies was actually caused by improper control for the solvents used to extract the silk; those solvents can have antimicrobial properties on their own. As for protecting their eggs, rather than killing bacteria, the silk likely provides a physical barrier alone.

It is bad news for spiders on the benefit-to-humanity front, but look at the bright side: If their silk had antimicrobial activity, we’d have to start farming them to acquire more silk. And that’s no good. Spiders deserve to roam free, hunt as they please, and drop down on your head from the ceiling.
 

Anxiety and allergies: Cause, effect, confusion

We’re big fans of science, but as longtime, totally impartial (Science rules!) observers of science’s medical realm, we can see that the day-to-day process of practicing the scientific method occasionally gets a bit messy. And no, we’re not talking about COVID-19.

pxfuel

We’re talking allergies. We’re talking mental health. We’re talking allergic disease and mental health.

We’re talking about a pair of press releases we came across during our never-ending search for material to educate, entertain, and astound our fabulously wonderful and loyal readers. (We say that, of course, in the most impartial way possible.)

The first release was titled, “Allergies including asthma and hay fever not linked to mental health traits” and covered research from the University of Bristol (England). The investigators were trying to determine if “allergic diseases actually causes mental health traits including anxiety, depression, bipolar disorder, and schizophrenia, or vice versa,” according to the release.

What they found, however, was “little evidence of a causal relationship between the onset of allergic disease and mental health.” Again, this is the press release talking.

The second release seemed to suggest the exact opposite: “Study uncovers link between allergies and mental health conditions.” That got our attention. A little more reading revealed that “people with asthma, atopic dermatitis, and hay fever also had a higher likelihood of having depression, anxiety, bipolar disorder, or neuroticism.”

One of the investigators was quoted as saying, “Establishing whether allergic disease causes mental health problems, or vice versa, is important to ensure that resources and treatment strategies are targeted appropriately.”

Did you notice the “vice versa”? Did you notice that it appeared in quotes from both releases? We did, so we took a closer look at the source. The second release covered a group of investigators from the University of Bristol – the same group, and the same study, in fact, as the first one.

So there you have it. One study, two press releases, and one confused journalist. Thank you, science.

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Cut risedronate drug holiday to under 2 years in older patients

Article Type
Changed
Wed, 10/06/2021 - 17:53

 

Any pause in taking the osteoporosis drug risedronate (Actonel) should last no longer than 2 years rather than the 2-3 years currently recommended for bisphosphonates, new research suggests.

BananaStock/thinkstockphotos.com

In a cohort of patients aged 66 and older in Ontario, Canada, those who had been taking risedronate had a 34% greater risk of a hip fracture during year 2 to year 3 of a pause in taking the drug – a drug holiday – compared with those who had been taking alendronate (Fosamax). 

The study showed that “risedronate, which has a shorter half-life, confers relatively less hip fracture protection than alendronate during drug holidays longer than 2 years and careful monitoring and follow-up after 2 years is likely warranted,” Kaley (Kaleen) N. Hayes, Pharm D, PhD, summarized in an oral presentation at the annual meeting of the American Society for Bone and Mineral Research. Dr. Hayes is an assistant professor in the department of health services, policy, and practice at Brown University School of Public Health, Providence, R.I.

“Although alendronate and risedronate have similar effectiveness for preventing fractures on treatment, our findings suggest that older patients on a risedronate drug holiday may benefit from assessment to consider resuming therapy after 2 years to prevent hip fractures,” she elaborated in an email.

Juliet Compston, MD, identified this study as one of the meeting’s clinical science highlights.

“This is the first study to directly compare fracture incidence during a drug holiday after treatment with the two most commonly prescribed oral bisphosphonates, alendronate and risedronate,” she told this news organization in an email.

The difference in fracture incidence during the 3-year drug holiday is “consistent with the known difference in pharmacokinetic properties of the two drugs,” noted Dr. Compston, professor of bone medicine and honorary consultant physician at the University of Cambridge (England) School of Clinical Medicine.

Since the increased risk of fracture after stopping risedronate vs. alendronate was seen by 2 years, “reevaluation of risk in risedronate-treated patients should therefore be considered earlier than the recommended period of 2-3 years after discontinuation,” she said.

“The study does not provide information about the optimal duration of drug holiday for either risedronate or alendronate, but it supports a shorter duration for the former of up to 2 years,” according to Dr. Compston.

Study rationale and findings

“The question of whether people treated for osteoporosis with oral bisphosphonates should have drug holidays is controversial,” Dr. Compston noted, “but many guidelines recommend that in lower-risk individuals who have received bisphosphonates for 5 years, a break from treatment of 2-3 years should be considered.”

Five or more years of bisphosphonate treatment for osteoporosis has been associated with rare adverse effects such as atypical femoral fractures, and these drugs appear to have fracture protection effects that linger for a while, so a drug holiday is recommended for most patients, Dr. Hayes added.

Guidelines such as the 2016 ASBMR task force report on long-term bisphosphonates for osteoporosis, she continued, “acknowledge that evidence for this recommendation comes primarily from the extension trial for alendronate, and patients undergoing a risedronate drug holiday may need to be reassessed earlier because of risedronate’s shorter half-life.”

Compared with alendronate, risedronate accumulates less in the bone and is eliminated more quickly from the body, so its fracture protection during drug holidays may be shorter.



The researchers aimed to estimate the 3-year fracture risk after discontinuing long-term (3 or more years) risedronate vs. alendronate therapy among older adults in Ontario.

From health care administrative data, they identified 120,368 patients aged 66 years and older who had started taking risedronate or alendronate as initial therapy for osteoporosis during the period 2000-2016. They had taken the therapy for 3 or more years (with at least 80% adherence) before stopping it for 120 days or longer.

The researchers found that 45% of patients were taking risedronate and 55% were taking alendronate, which are the main bisphosphonates used in Ontario, Dr. Hayes noted. Etidronate (Didronel) is recommended as second-line therapy and accounts for less than 2% of patients starting oral bisphosphonate therapy. 

In an earlier study, the researchers identified a shift toward greater use of risedronate than alendronate since 2008, likely related to newer formulations (for example, monthly and weekly delayed-release formulations of risedronate vs. only weekly alendronate formulations).

The researchers matched 25,077 patients taking alendronate with 25,077 patients taking risedronate, based on fracture risk–related characteristics, including demographics, diagnoses, medication use, and health care use.

The patients had a mean age of 74 when they started taking an oral bisphosphonate; 82% were women and most were White.  

Most patients (78%) had received a prescription from a general practitioner and, on average, they took the bisphosphonate therapy for 5.9 years before the drug holiday.  

The primary outcome of incident hip fracture during a 3-year drug holiday occurred in 915 patients. There were 12.4 events per 1,000 patients in the risedronate group vs. 10.6 events per 1,000 patients in the alendronate group (hazard ratio, 1.18; 95% confidence interval, 1.04-1.34).

The risks were not significantly higher during year 1 or year 2 of the drug holiday, but the curves began to diverge after 2 years, coauthor Suzanne Cadarette, PhD, of the Leslie Dan Faculty of Pharmacy at the University of Toronto, explained when replying to a question after the presentation. Dr. Cadarette supervised this PhD dissertation research by Dr. Hayes.

The researchers acknowledged that the limitations of their study include a lack of information about race or bone mineral density, and the findings may not apply to a younger, more racially diverse population.

The research was supported by the University of Toronto Dalla Lana School of Public Health and the Leslie Dan Faculty of Pharmacy, a Canadian Institutes of Health Research grant, and a doctoral research award. The authors have disclosed no relevant financial relationships.

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

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Any pause in taking the osteoporosis drug risedronate (Actonel) should last no longer than 2 years rather than the 2-3 years currently recommended for bisphosphonates, new research suggests.

BananaStock/thinkstockphotos.com

In a cohort of patients aged 66 and older in Ontario, Canada, those who had been taking risedronate had a 34% greater risk of a hip fracture during year 2 to year 3 of a pause in taking the drug – a drug holiday – compared with those who had been taking alendronate (Fosamax). 

The study showed that “risedronate, which has a shorter half-life, confers relatively less hip fracture protection than alendronate during drug holidays longer than 2 years and careful monitoring and follow-up after 2 years is likely warranted,” Kaley (Kaleen) N. Hayes, Pharm D, PhD, summarized in an oral presentation at the annual meeting of the American Society for Bone and Mineral Research. Dr. Hayes is an assistant professor in the department of health services, policy, and practice at Brown University School of Public Health, Providence, R.I.

“Although alendronate and risedronate have similar effectiveness for preventing fractures on treatment, our findings suggest that older patients on a risedronate drug holiday may benefit from assessment to consider resuming therapy after 2 years to prevent hip fractures,” she elaborated in an email.

Juliet Compston, MD, identified this study as one of the meeting’s clinical science highlights.

“This is the first study to directly compare fracture incidence during a drug holiday after treatment with the two most commonly prescribed oral bisphosphonates, alendronate and risedronate,” she told this news organization in an email.

The difference in fracture incidence during the 3-year drug holiday is “consistent with the known difference in pharmacokinetic properties of the two drugs,” noted Dr. Compston, professor of bone medicine and honorary consultant physician at the University of Cambridge (England) School of Clinical Medicine.

Since the increased risk of fracture after stopping risedronate vs. alendronate was seen by 2 years, “reevaluation of risk in risedronate-treated patients should therefore be considered earlier than the recommended period of 2-3 years after discontinuation,” she said.

“The study does not provide information about the optimal duration of drug holiday for either risedronate or alendronate, but it supports a shorter duration for the former of up to 2 years,” according to Dr. Compston.

Study rationale and findings

“The question of whether people treated for osteoporosis with oral bisphosphonates should have drug holidays is controversial,” Dr. Compston noted, “but many guidelines recommend that in lower-risk individuals who have received bisphosphonates for 5 years, a break from treatment of 2-3 years should be considered.”

Five or more years of bisphosphonate treatment for osteoporosis has been associated with rare adverse effects such as atypical femoral fractures, and these drugs appear to have fracture protection effects that linger for a while, so a drug holiday is recommended for most patients, Dr. Hayes added.

Guidelines such as the 2016 ASBMR task force report on long-term bisphosphonates for osteoporosis, she continued, “acknowledge that evidence for this recommendation comes primarily from the extension trial for alendronate, and patients undergoing a risedronate drug holiday may need to be reassessed earlier because of risedronate’s shorter half-life.”

Compared with alendronate, risedronate accumulates less in the bone and is eliminated more quickly from the body, so its fracture protection during drug holidays may be shorter.



The researchers aimed to estimate the 3-year fracture risk after discontinuing long-term (3 or more years) risedronate vs. alendronate therapy among older adults in Ontario.

From health care administrative data, they identified 120,368 patients aged 66 years and older who had started taking risedronate or alendronate as initial therapy for osteoporosis during the period 2000-2016. They had taken the therapy for 3 or more years (with at least 80% adherence) before stopping it for 120 days or longer.

The researchers found that 45% of patients were taking risedronate and 55% were taking alendronate, which are the main bisphosphonates used in Ontario, Dr. Hayes noted. Etidronate (Didronel) is recommended as second-line therapy and accounts for less than 2% of patients starting oral bisphosphonate therapy. 

In an earlier study, the researchers identified a shift toward greater use of risedronate than alendronate since 2008, likely related to newer formulations (for example, monthly and weekly delayed-release formulations of risedronate vs. only weekly alendronate formulations).

The researchers matched 25,077 patients taking alendronate with 25,077 patients taking risedronate, based on fracture risk–related characteristics, including demographics, diagnoses, medication use, and health care use.

The patients had a mean age of 74 when they started taking an oral bisphosphonate; 82% were women and most were White.  

Most patients (78%) had received a prescription from a general practitioner and, on average, they took the bisphosphonate therapy for 5.9 years before the drug holiday.  

The primary outcome of incident hip fracture during a 3-year drug holiday occurred in 915 patients. There were 12.4 events per 1,000 patients in the risedronate group vs. 10.6 events per 1,000 patients in the alendronate group (hazard ratio, 1.18; 95% confidence interval, 1.04-1.34).

The risks were not significantly higher during year 1 or year 2 of the drug holiday, but the curves began to diverge after 2 years, coauthor Suzanne Cadarette, PhD, of the Leslie Dan Faculty of Pharmacy at the University of Toronto, explained when replying to a question after the presentation. Dr. Cadarette supervised this PhD dissertation research by Dr. Hayes.

The researchers acknowledged that the limitations of their study include a lack of information about race or bone mineral density, and the findings may not apply to a younger, more racially diverse population.

The research was supported by the University of Toronto Dalla Lana School of Public Health and the Leslie Dan Faculty of Pharmacy, a Canadian Institutes of Health Research grant, and a doctoral research award. The authors have disclosed no relevant financial relationships.

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

 

Any pause in taking the osteoporosis drug risedronate (Actonel) should last no longer than 2 years rather than the 2-3 years currently recommended for bisphosphonates, new research suggests.

BananaStock/thinkstockphotos.com

In a cohort of patients aged 66 and older in Ontario, Canada, those who had been taking risedronate had a 34% greater risk of a hip fracture during year 2 to year 3 of a pause in taking the drug – a drug holiday – compared with those who had been taking alendronate (Fosamax). 

The study showed that “risedronate, which has a shorter half-life, confers relatively less hip fracture protection than alendronate during drug holidays longer than 2 years and careful monitoring and follow-up after 2 years is likely warranted,” Kaley (Kaleen) N. Hayes, Pharm D, PhD, summarized in an oral presentation at the annual meeting of the American Society for Bone and Mineral Research. Dr. Hayes is an assistant professor in the department of health services, policy, and practice at Brown University School of Public Health, Providence, R.I.

“Although alendronate and risedronate have similar effectiveness for preventing fractures on treatment, our findings suggest that older patients on a risedronate drug holiday may benefit from assessment to consider resuming therapy after 2 years to prevent hip fractures,” she elaborated in an email.

Juliet Compston, MD, identified this study as one of the meeting’s clinical science highlights.

“This is the first study to directly compare fracture incidence during a drug holiday after treatment with the two most commonly prescribed oral bisphosphonates, alendronate and risedronate,” she told this news organization in an email.

The difference in fracture incidence during the 3-year drug holiday is “consistent with the known difference in pharmacokinetic properties of the two drugs,” noted Dr. Compston, professor of bone medicine and honorary consultant physician at the University of Cambridge (England) School of Clinical Medicine.

Since the increased risk of fracture after stopping risedronate vs. alendronate was seen by 2 years, “reevaluation of risk in risedronate-treated patients should therefore be considered earlier than the recommended period of 2-3 years after discontinuation,” she said.

“The study does not provide information about the optimal duration of drug holiday for either risedronate or alendronate, but it supports a shorter duration for the former of up to 2 years,” according to Dr. Compston.

Study rationale and findings

“The question of whether people treated for osteoporosis with oral bisphosphonates should have drug holidays is controversial,” Dr. Compston noted, “but many guidelines recommend that in lower-risk individuals who have received bisphosphonates for 5 years, a break from treatment of 2-3 years should be considered.”

Five or more years of bisphosphonate treatment for osteoporosis has been associated with rare adverse effects such as atypical femoral fractures, and these drugs appear to have fracture protection effects that linger for a while, so a drug holiday is recommended for most patients, Dr. Hayes added.

Guidelines such as the 2016 ASBMR task force report on long-term bisphosphonates for osteoporosis, she continued, “acknowledge that evidence for this recommendation comes primarily from the extension trial for alendronate, and patients undergoing a risedronate drug holiday may need to be reassessed earlier because of risedronate’s shorter half-life.”

Compared with alendronate, risedronate accumulates less in the bone and is eliminated more quickly from the body, so its fracture protection during drug holidays may be shorter.



The researchers aimed to estimate the 3-year fracture risk after discontinuing long-term (3 or more years) risedronate vs. alendronate therapy among older adults in Ontario.

From health care administrative data, they identified 120,368 patients aged 66 years and older who had started taking risedronate or alendronate as initial therapy for osteoporosis during the period 2000-2016. They had taken the therapy for 3 or more years (with at least 80% adherence) before stopping it for 120 days or longer.

The researchers found that 45% of patients were taking risedronate and 55% were taking alendronate, which are the main bisphosphonates used in Ontario, Dr. Hayes noted. Etidronate (Didronel) is recommended as second-line therapy and accounts for less than 2% of patients starting oral bisphosphonate therapy. 

In an earlier study, the researchers identified a shift toward greater use of risedronate than alendronate since 2008, likely related to newer formulations (for example, monthly and weekly delayed-release formulations of risedronate vs. only weekly alendronate formulations).

The researchers matched 25,077 patients taking alendronate with 25,077 patients taking risedronate, based on fracture risk–related characteristics, including demographics, diagnoses, medication use, and health care use.

The patients had a mean age of 74 when they started taking an oral bisphosphonate; 82% were women and most were White.  

Most patients (78%) had received a prescription from a general practitioner and, on average, they took the bisphosphonate therapy for 5.9 years before the drug holiday.  

The primary outcome of incident hip fracture during a 3-year drug holiday occurred in 915 patients. There were 12.4 events per 1,000 patients in the risedronate group vs. 10.6 events per 1,000 patients in the alendronate group (hazard ratio, 1.18; 95% confidence interval, 1.04-1.34).

The risks were not significantly higher during year 1 or year 2 of the drug holiday, but the curves began to diverge after 2 years, coauthor Suzanne Cadarette, PhD, of the Leslie Dan Faculty of Pharmacy at the University of Toronto, explained when replying to a question after the presentation. Dr. Cadarette supervised this PhD dissertation research by Dr. Hayes.

The researchers acknowledged that the limitations of their study include a lack of information about race or bone mineral density, and the findings may not apply to a younger, more racially diverse population.

The research was supported by the University of Toronto Dalla Lana School of Public Health and the Leslie Dan Faculty of Pharmacy, a Canadian Institutes of Health Research grant, and a doctoral research award. The authors have disclosed no relevant financial relationships.

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

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Customized brain stimulation: New hope for severe depression

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Personalized deep brain stimulation (DBS) appears to rapidly and effectively improve symptoms of treatment-resistant depression, new research suggests.

KatarzynaBialasiewicz/Getty Images

In a proof-of-concept study, investigators identified specific brain activity patterns responsible for a single patient’s severe depression and customized a DBS protocol to modulate the patterns. Results showed rapid and sustained improvement in depression scores.

“This study points the way to a new paradigm that is desperately needed in psychiatry,” Andrew Krystal, PhD, Weill Institute for Neurosciences, University of California, San Francisco, said in a news release.

We’ve developed a precision-medicine approach that has successfully managed our patient’s treatment-resistant depression by identifying and modulating the circuit in her brain that’s uniquely associated with her symptoms,” Dr. Krystal added.

The findings were published online Oct. 4 in Nature Medicine.
 

Closed-loop, on-demand stimulation

The patient was a 36-year-old woman with longstanding, severe, and treatment-resistant major depressive disorder. She was unresponsive to multiple antidepressant combinations and electroconvulsive therapy.

The researchers used intracranial electrophysiology and focal electrical stimulation to identify the specific pattern of electrical brain activity that correlated with her depressed mood.

They identified the right ventral striatum – which is involved in emotion, motivation, and reward – as the stimulation site that led to consistent, sustained, and dose-dependent improvement of symptoms and served as the neural biomarker.

In addition, the investigators identified a neural activity pattern in the amygdala that predicted both the mood symptoms, symptom severity, and stimulation efficacy.

The patient was implanted with the Food and Drug Administration–approved NeuroPace RNS System. The device was placed in the right hemisphere. A single sensing lead was positioned in the amygdala and the second stimulation lead was placed in the ventral striatum.

When the sensing lead detected the activity pattern associated with depression, the other lead delivered a tiny dose (1 milliampere/1 mA) of electricity for 6 seconds, which altered the neural activity and relieved mood symptoms.
 

Remission achieved

Once this personalized, closed-loop therapy was fully operational, the patient’s depression score on the Montgomery-Åsberg Depression Rating Scale (MADRS) dropped from 33 before turning treatment ON to 14 at the first ON-treatment assessment carried out after 12 days of stimulation. The score dropped below 10, representing remission, several months later.

The treatment also rapidly improved symptom severity, as measured daily with Hamilton Depression Rating Scale (HAMD-6) and visual analog scales.

“Success was predicated on a clinical mapping stage before chronic device placement, a strategy that has been utilized in epilepsy to map seizure foci in a personalized manner but has not previously been performed in other neuropsychiatric conditions,” the investigators wrote.

This patient represents “one of the first examples of precision psychiatry – a treatment tailored to an individual,” the study’s lead author, Katherine Scangos, MD, also with UCSF Weill Institute, said in an interview.

She added that the treatment “was personally tailored both spatially,” meaning at the brain location, and temporally – the time it was delivered.

“This is the first time a neural biomarker has been used to automatically trigger therapeutic stimulation in depression as a successful long-term treatment,” said Dr. Scangos. However, “we have a lot of work left to do,” she added.

“This study provides proof-of-principle that we can utilize a multimodal brain mapping approach to identify a personalized depression circuit and target that circuit with successful treatment. We will need to test the approach in more patients before we can determine its efficacy,” Dr. Scangos said.
 

 

 

First reliable biomarker in psychiatry

In a statement from the UK nonprofit Science Media Centre, Vladimir Litvak, PhD, with the Wellcome Centre for Human Neuroimaging, University College London, said that the study is interesting, noting that it is from “one of the leading groups in the field.”

The fact that depression symptoms can be treated in some patients by electrical stimulation of the ventral striatum is not new, Dr. Litvak said. However, what is “exciting” is that the authors identified a particular neural activity pattern in the amygdala as a reliable predictor of both symptom severity and stimulation effectiveness, he noted.

“Patterns of brain activity correlated with disease symptoms when testing over a large group of patients are commonly discovered. But there are just a handful of examples of patterns that are reliable enough to be predictive on a short time scale in a single patient,” said Dr. Litvak, who was not associated with the research.

“Furthermore, to my knowledge, this is the first example of such a reliable biomarker for psychiatric symptoms. The other examples were all for neurological disorders such as Parkinson’s disease, dystonia, and epilepsy,” he added.

He cautioned that this is a single case, but “if reproduced in additional patients, it will bring at least some psychiatric conditions into the domain of brain diseases that can be characterized and diagnosed objectively rather than based on symptoms alone.”

Dr. Litvak pointed out two other critical aspects of the study: the use of exploratory recordings and stimulation to determine the most effective treatment strategy, and the use of a closed-loop device that stimulates only when detecting the amygdala biomarker.

“It is hard to say based on this single case how important these will be in the future. There is no comparison to constant stimulation that might have worked as well because the implanted device used in the study is not suitable for that,” Dr. Litvak said.

It should also be noted that implanting multiple depth electrodes at different brain sites is a “traumatic invasive procedure only reserved to date for severe cases of drug-resistant epilepsy,” he said. “Furthermore, it only allows [researchers] to test a small number of candidate sites, so it relies heavily on prior knowledge.

“Once clinicians know better what to look for, it might be possible to avoid this procedure altogether by using noninvasive methods,” such as functional MRI or EEG, to match the right treatment option to a patient, Dr. Litvak concluded.

The research was funded by the National Institutes of Health, the Brain & Behavior Research Foundation, and the Ray and Dagmar Dolby Family Fund through the department of psychiatry at UCSF. Dr. Scangos has reported no relevant financial relationships. A complete list of author disclosures is available in the original article. Dr. Litvak is participating in a research funding application to search for electrophysiological biomarkers of depression symptoms using invasive recordings.

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

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Personalized deep brain stimulation (DBS) appears to rapidly and effectively improve symptoms of treatment-resistant depression, new research suggests.

KatarzynaBialasiewicz/Getty Images

In a proof-of-concept study, investigators identified specific brain activity patterns responsible for a single patient’s severe depression and customized a DBS protocol to modulate the patterns. Results showed rapid and sustained improvement in depression scores.

“This study points the way to a new paradigm that is desperately needed in psychiatry,” Andrew Krystal, PhD, Weill Institute for Neurosciences, University of California, San Francisco, said in a news release.

We’ve developed a precision-medicine approach that has successfully managed our patient’s treatment-resistant depression by identifying and modulating the circuit in her brain that’s uniquely associated with her symptoms,” Dr. Krystal added.

The findings were published online Oct. 4 in Nature Medicine.
 

Closed-loop, on-demand stimulation

The patient was a 36-year-old woman with longstanding, severe, and treatment-resistant major depressive disorder. She was unresponsive to multiple antidepressant combinations and electroconvulsive therapy.

The researchers used intracranial electrophysiology and focal electrical stimulation to identify the specific pattern of electrical brain activity that correlated with her depressed mood.

They identified the right ventral striatum – which is involved in emotion, motivation, and reward – as the stimulation site that led to consistent, sustained, and dose-dependent improvement of symptoms and served as the neural biomarker.

In addition, the investigators identified a neural activity pattern in the amygdala that predicted both the mood symptoms, symptom severity, and stimulation efficacy.

The patient was implanted with the Food and Drug Administration–approved NeuroPace RNS System. The device was placed in the right hemisphere. A single sensing lead was positioned in the amygdala and the second stimulation lead was placed in the ventral striatum.

When the sensing lead detected the activity pattern associated with depression, the other lead delivered a tiny dose (1 milliampere/1 mA) of electricity for 6 seconds, which altered the neural activity and relieved mood symptoms.
 

Remission achieved

Once this personalized, closed-loop therapy was fully operational, the patient’s depression score on the Montgomery-Åsberg Depression Rating Scale (MADRS) dropped from 33 before turning treatment ON to 14 at the first ON-treatment assessment carried out after 12 days of stimulation. The score dropped below 10, representing remission, several months later.

The treatment also rapidly improved symptom severity, as measured daily with Hamilton Depression Rating Scale (HAMD-6) and visual analog scales.

“Success was predicated on a clinical mapping stage before chronic device placement, a strategy that has been utilized in epilepsy to map seizure foci in a personalized manner but has not previously been performed in other neuropsychiatric conditions,” the investigators wrote.

This patient represents “one of the first examples of precision psychiatry – a treatment tailored to an individual,” the study’s lead author, Katherine Scangos, MD, also with UCSF Weill Institute, said in an interview.

She added that the treatment “was personally tailored both spatially,” meaning at the brain location, and temporally – the time it was delivered.

“This is the first time a neural biomarker has been used to automatically trigger therapeutic stimulation in depression as a successful long-term treatment,” said Dr. Scangos. However, “we have a lot of work left to do,” she added.

“This study provides proof-of-principle that we can utilize a multimodal brain mapping approach to identify a personalized depression circuit and target that circuit with successful treatment. We will need to test the approach in more patients before we can determine its efficacy,” Dr. Scangos said.
 

 

 

First reliable biomarker in psychiatry

In a statement from the UK nonprofit Science Media Centre, Vladimir Litvak, PhD, with the Wellcome Centre for Human Neuroimaging, University College London, said that the study is interesting, noting that it is from “one of the leading groups in the field.”

The fact that depression symptoms can be treated in some patients by electrical stimulation of the ventral striatum is not new, Dr. Litvak said. However, what is “exciting” is that the authors identified a particular neural activity pattern in the amygdala as a reliable predictor of both symptom severity and stimulation effectiveness, he noted.

“Patterns of brain activity correlated with disease symptoms when testing over a large group of patients are commonly discovered. But there are just a handful of examples of patterns that are reliable enough to be predictive on a short time scale in a single patient,” said Dr. Litvak, who was not associated with the research.

“Furthermore, to my knowledge, this is the first example of such a reliable biomarker for psychiatric symptoms. The other examples were all for neurological disorders such as Parkinson’s disease, dystonia, and epilepsy,” he added.

He cautioned that this is a single case, but “if reproduced in additional patients, it will bring at least some psychiatric conditions into the domain of brain diseases that can be characterized and diagnosed objectively rather than based on symptoms alone.”

Dr. Litvak pointed out two other critical aspects of the study: the use of exploratory recordings and stimulation to determine the most effective treatment strategy, and the use of a closed-loop device that stimulates only when detecting the amygdala biomarker.

“It is hard to say based on this single case how important these will be in the future. There is no comparison to constant stimulation that might have worked as well because the implanted device used in the study is not suitable for that,” Dr. Litvak said.

It should also be noted that implanting multiple depth electrodes at different brain sites is a “traumatic invasive procedure only reserved to date for severe cases of drug-resistant epilepsy,” he said. “Furthermore, it only allows [researchers] to test a small number of candidate sites, so it relies heavily on prior knowledge.

“Once clinicians know better what to look for, it might be possible to avoid this procedure altogether by using noninvasive methods,” such as functional MRI or EEG, to match the right treatment option to a patient, Dr. Litvak concluded.

The research was funded by the National Institutes of Health, the Brain & Behavior Research Foundation, and the Ray and Dagmar Dolby Family Fund through the department of psychiatry at UCSF. Dr. Scangos has reported no relevant financial relationships. A complete list of author disclosures is available in the original article. Dr. Litvak is participating in a research funding application to search for electrophysiological biomarkers of depression symptoms using invasive recordings.

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

Personalized deep brain stimulation (DBS) appears to rapidly and effectively improve symptoms of treatment-resistant depression, new research suggests.

KatarzynaBialasiewicz/Getty Images

In a proof-of-concept study, investigators identified specific brain activity patterns responsible for a single patient’s severe depression and customized a DBS protocol to modulate the patterns. Results showed rapid and sustained improvement in depression scores.

“This study points the way to a new paradigm that is desperately needed in psychiatry,” Andrew Krystal, PhD, Weill Institute for Neurosciences, University of California, San Francisco, said in a news release.

We’ve developed a precision-medicine approach that has successfully managed our patient’s treatment-resistant depression by identifying and modulating the circuit in her brain that’s uniquely associated with her symptoms,” Dr. Krystal added.

The findings were published online Oct. 4 in Nature Medicine.
 

Closed-loop, on-demand stimulation

The patient was a 36-year-old woman with longstanding, severe, and treatment-resistant major depressive disorder. She was unresponsive to multiple antidepressant combinations and electroconvulsive therapy.

The researchers used intracranial electrophysiology and focal electrical stimulation to identify the specific pattern of electrical brain activity that correlated with her depressed mood.

They identified the right ventral striatum – which is involved in emotion, motivation, and reward – as the stimulation site that led to consistent, sustained, and dose-dependent improvement of symptoms and served as the neural biomarker.

In addition, the investigators identified a neural activity pattern in the amygdala that predicted both the mood symptoms, symptom severity, and stimulation efficacy.

The patient was implanted with the Food and Drug Administration–approved NeuroPace RNS System. The device was placed in the right hemisphere. A single sensing lead was positioned in the amygdala and the second stimulation lead was placed in the ventral striatum.

When the sensing lead detected the activity pattern associated with depression, the other lead delivered a tiny dose (1 milliampere/1 mA) of electricity for 6 seconds, which altered the neural activity and relieved mood symptoms.
 

Remission achieved

Once this personalized, closed-loop therapy was fully operational, the patient’s depression score on the Montgomery-Åsberg Depression Rating Scale (MADRS) dropped from 33 before turning treatment ON to 14 at the first ON-treatment assessment carried out after 12 days of stimulation. The score dropped below 10, representing remission, several months later.

The treatment also rapidly improved symptom severity, as measured daily with Hamilton Depression Rating Scale (HAMD-6) and visual analog scales.

“Success was predicated on a clinical mapping stage before chronic device placement, a strategy that has been utilized in epilepsy to map seizure foci in a personalized manner but has not previously been performed in other neuropsychiatric conditions,” the investigators wrote.

This patient represents “one of the first examples of precision psychiatry – a treatment tailored to an individual,” the study’s lead author, Katherine Scangos, MD, also with UCSF Weill Institute, said in an interview.

She added that the treatment “was personally tailored both spatially,” meaning at the brain location, and temporally – the time it was delivered.

“This is the first time a neural biomarker has been used to automatically trigger therapeutic stimulation in depression as a successful long-term treatment,” said Dr. Scangos. However, “we have a lot of work left to do,” she added.

“This study provides proof-of-principle that we can utilize a multimodal brain mapping approach to identify a personalized depression circuit and target that circuit with successful treatment. We will need to test the approach in more patients before we can determine its efficacy,” Dr. Scangos said.
 

 

 

First reliable biomarker in psychiatry

In a statement from the UK nonprofit Science Media Centre, Vladimir Litvak, PhD, with the Wellcome Centre for Human Neuroimaging, University College London, said that the study is interesting, noting that it is from “one of the leading groups in the field.”

The fact that depression symptoms can be treated in some patients by electrical stimulation of the ventral striatum is not new, Dr. Litvak said. However, what is “exciting” is that the authors identified a particular neural activity pattern in the amygdala as a reliable predictor of both symptom severity and stimulation effectiveness, he noted.

“Patterns of brain activity correlated with disease symptoms when testing over a large group of patients are commonly discovered. But there are just a handful of examples of patterns that are reliable enough to be predictive on a short time scale in a single patient,” said Dr. Litvak, who was not associated with the research.

“Furthermore, to my knowledge, this is the first example of such a reliable biomarker for psychiatric symptoms. The other examples were all for neurological disorders such as Parkinson’s disease, dystonia, and epilepsy,” he added.

He cautioned that this is a single case, but “if reproduced in additional patients, it will bring at least some psychiatric conditions into the domain of brain diseases that can be characterized and diagnosed objectively rather than based on symptoms alone.”

Dr. Litvak pointed out two other critical aspects of the study: the use of exploratory recordings and stimulation to determine the most effective treatment strategy, and the use of a closed-loop device that stimulates only when detecting the amygdala biomarker.

“It is hard to say based on this single case how important these will be in the future. There is no comparison to constant stimulation that might have worked as well because the implanted device used in the study is not suitable for that,” Dr. Litvak said.

It should also be noted that implanting multiple depth electrodes at different brain sites is a “traumatic invasive procedure only reserved to date for severe cases of drug-resistant epilepsy,” he said. “Furthermore, it only allows [researchers] to test a small number of candidate sites, so it relies heavily on prior knowledge.

“Once clinicians know better what to look for, it might be possible to avoid this procedure altogether by using noninvasive methods,” such as functional MRI or EEG, to match the right treatment option to a patient, Dr. Litvak concluded.

The research was funded by the National Institutes of Health, the Brain & Behavior Research Foundation, and the Ray and Dagmar Dolby Family Fund through the department of psychiatry at UCSF. Dr. Scangos has reported no relevant financial relationships. A complete list of author disclosures is available in the original article. Dr. Litvak is participating in a research funding application to search for electrophysiological biomarkers of depression symptoms using invasive recordings.

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

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Men die more often than women after bariatric surgery

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Tue, 05/03/2022 - 15:03

Men had a much higher rate of death following bariatric surgery performed in Austria during 2010-2018, compared with women in a retrospective analysis of nearly 20,000 patients based on health insurance records.

The reason may be that men undergoing bariatric surgery have “worse overall health at the time of surgery” than women, Hannes Beiglböck, MD, suggested at the annual meeting of the European Association for the Study of Diabetes.

The results also showed that “men tend to be older [at time of surgery] and that might have the biggest impact on outcomes after bariatric surgery,” said Dr. Beiglböck, a researcher in the division of endocrinology and metabolism at the Medical University of Vienna.

The findings confirm those of prior studies in various worldwide locations, he noted; that is, men undergoing bariatric surgery tend to be older than women and have more comorbidities and perioperative mortality. 

Dr. Beiglböck also highlighted earlier reports that indicate “profound” sex-specific differences in why patients undergo bariatric surgery, with men often driven by a medical condition and women motivated by appearance.

Hence, for men, it may be important to focus on preoperative counseling to try to get them to think about bariatric surgery earlier, “which may improve their postsurgical mortality rate,” he observed.
 

Nearly threefold higher mortality among men

Dr. Beiglböck and associates used medical claims data filed with the Austrian health system, which includes nearly all residents. In 2010-2018, 19,901 Austrian patients underwent bariatric surgery, and researchers tracked their outcomes for a median of 5.4 years, through April 2020.

During the 9-year period, 74% of patients who underwent bariatric surgery were women, again, a finding consistent with prior reports from other countries.

The 5,220 men were an average of 41.8 years old, with 65% undergoing gastric bypass and 30% gastric banding. The 14,681 women were an average of 40.1 years old, with 70% undergoing gastric bypass and 22% gastric banding.

During follow-up, 367 patients (1.8%) died. Among men, the overall mortality rate was 2.6-fold higher, compared with women (1.3% vs. 3.4%) and average mortality per year was 2.8-fold higher (0.64% vs. 0.24%).

The rate of death on the day of surgery among men also substantially exceeded that of women (0.29% vs. 0.05%), as did death within 30 days of surgery (0.48% vs. 0.08%). All of these between-sex differences were significant.

Baseline prevalence of four categories of comorbidities and how these differed by sex among patients who died during follow-up was also examined. Underlying cardiovascular disease was prevalent in 299 patients (81% of the deceased group), 200 (54%) had a psychiatric disorder, 138 (38%) had diabetes, and 132 (36%) had a malignancy.

The prevalence of cardiovascular disease and psychiatric disorders was roughly the same in men and women. Men had a significantly higher prevalence of diabetes, and a higher proportion of women had a malignancy.
 

Consistent with U.S. studies

U.S. report in 2015 documented a higher prevalence of comorbidities and more severe illness among men undergoing bariatric surgery, compared with women, noted session chair Zhila Semnani-Azad, PhD, a researcher in the department of nutrition at Harvard School of Public Health in Boston.

“I think the [Austrian] data presented have relevance to the U.S. population,” Dr. Semnani-Azad said in an interview.

“The main limitation of these univariate analyses is they don’t account for potential confounding variables that could affect the association, such as lifestyle variables, age, and family history. There is always potential for other variables” to influence apparent sex-specific associations, she commented. Another limitation is the small total number of deaths analyzed, at 367.

“These results are a good starting point for future studies. More work is needed to better understand the impact of comorbidities and sex on postsurgical mortality,” Dr. Semnani-Azad concluded.

Dr. Beiglböck and Dr. Semnani-Azad have reported no relevant financial relationships.

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

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Men had a much higher rate of death following bariatric surgery performed in Austria during 2010-2018, compared with women in a retrospective analysis of nearly 20,000 patients based on health insurance records.

The reason may be that men undergoing bariatric surgery have “worse overall health at the time of surgery” than women, Hannes Beiglböck, MD, suggested at the annual meeting of the European Association for the Study of Diabetes.

The results also showed that “men tend to be older [at time of surgery] and that might have the biggest impact on outcomes after bariatric surgery,” said Dr. Beiglböck, a researcher in the division of endocrinology and metabolism at the Medical University of Vienna.

The findings confirm those of prior studies in various worldwide locations, he noted; that is, men undergoing bariatric surgery tend to be older than women and have more comorbidities and perioperative mortality. 

Dr. Beiglböck also highlighted earlier reports that indicate “profound” sex-specific differences in why patients undergo bariatric surgery, with men often driven by a medical condition and women motivated by appearance.

Hence, for men, it may be important to focus on preoperative counseling to try to get them to think about bariatric surgery earlier, “which may improve their postsurgical mortality rate,” he observed.
 

Nearly threefold higher mortality among men

Dr. Beiglböck and associates used medical claims data filed with the Austrian health system, which includes nearly all residents. In 2010-2018, 19,901 Austrian patients underwent bariatric surgery, and researchers tracked their outcomes for a median of 5.4 years, through April 2020.

During the 9-year period, 74% of patients who underwent bariatric surgery were women, again, a finding consistent with prior reports from other countries.

The 5,220 men were an average of 41.8 years old, with 65% undergoing gastric bypass and 30% gastric banding. The 14,681 women were an average of 40.1 years old, with 70% undergoing gastric bypass and 22% gastric banding.

During follow-up, 367 patients (1.8%) died. Among men, the overall mortality rate was 2.6-fold higher, compared with women (1.3% vs. 3.4%) and average mortality per year was 2.8-fold higher (0.64% vs. 0.24%).

The rate of death on the day of surgery among men also substantially exceeded that of women (0.29% vs. 0.05%), as did death within 30 days of surgery (0.48% vs. 0.08%). All of these between-sex differences were significant.

Baseline prevalence of four categories of comorbidities and how these differed by sex among patients who died during follow-up was also examined. Underlying cardiovascular disease was prevalent in 299 patients (81% of the deceased group), 200 (54%) had a psychiatric disorder, 138 (38%) had diabetes, and 132 (36%) had a malignancy.

The prevalence of cardiovascular disease and psychiatric disorders was roughly the same in men and women. Men had a significantly higher prevalence of diabetes, and a higher proportion of women had a malignancy.
 

Consistent with U.S. studies

U.S. report in 2015 documented a higher prevalence of comorbidities and more severe illness among men undergoing bariatric surgery, compared with women, noted session chair Zhila Semnani-Azad, PhD, a researcher in the department of nutrition at Harvard School of Public Health in Boston.

“I think the [Austrian] data presented have relevance to the U.S. population,” Dr. Semnani-Azad said in an interview.

“The main limitation of these univariate analyses is they don’t account for potential confounding variables that could affect the association, such as lifestyle variables, age, and family history. There is always potential for other variables” to influence apparent sex-specific associations, she commented. Another limitation is the small total number of deaths analyzed, at 367.

“These results are a good starting point for future studies. More work is needed to better understand the impact of comorbidities and sex on postsurgical mortality,” Dr. Semnani-Azad concluded.

Dr. Beiglböck and Dr. Semnani-Azad have reported no relevant financial relationships.

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

Men had a much higher rate of death following bariatric surgery performed in Austria during 2010-2018, compared with women in a retrospective analysis of nearly 20,000 patients based on health insurance records.

The reason may be that men undergoing bariatric surgery have “worse overall health at the time of surgery” than women, Hannes Beiglböck, MD, suggested at the annual meeting of the European Association for the Study of Diabetes.

The results also showed that “men tend to be older [at time of surgery] and that might have the biggest impact on outcomes after bariatric surgery,” said Dr. Beiglböck, a researcher in the division of endocrinology and metabolism at the Medical University of Vienna.

The findings confirm those of prior studies in various worldwide locations, he noted; that is, men undergoing bariatric surgery tend to be older than women and have more comorbidities and perioperative mortality. 

Dr. Beiglböck also highlighted earlier reports that indicate “profound” sex-specific differences in why patients undergo bariatric surgery, with men often driven by a medical condition and women motivated by appearance.

Hence, for men, it may be important to focus on preoperative counseling to try to get them to think about bariatric surgery earlier, “which may improve their postsurgical mortality rate,” he observed.
 

Nearly threefold higher mortality among men

Dr. Beiglböck and associates used medical claims data filed with the Austrian health system, which includes nearly all residents. In 2010-2018, 19,901 Austrian patients underwent bariatric surgery, and researchers tracked their outcomes for a median of 5.4 years, through April 2020.

During the 9-year period, 74% of patients who underwent bariatric surgery were women, again, a finding consistent with prior reports from other countries.

The 5,220 men were an average of 41.8 years old, with 65% undergoing gastric bypass and 30% gastric banding. The 14,681 women were an average of 40.1 years old, with 70% undergoing gastric bypass and 22% gastric banding.

During follow-up, 367 patients (1.8%) died. Among men, the overall mortality rate was 2.6-fold higher, compared with women (1.3% vs. 3.4%) and average mortality per year was 2.8-fold higher (0.64% vs. 0.24%).

The rate of death on the day of surgery among men also substantially exceeded that of women (0.29% vs. 0.05%), as did death within 30 days of surgery (0.48% vs. 0.08%). All of these between-sex differences were significant.

Baseline prevalence of four categories of comorbidities and how these differed by sex among patients who died during follow-up was also examined. Underlying cardiovascular disease was prevalent in 299 patients (81% of the deceased group), 200 (54%) had a psychiatric disorder, 138 (38%) had diabetes, and 132 (36%) had a malignancy.

The prevalence of cardiovascular disease and psychiatric disorders was roughly the same in men and women. Men had a significantly higher prevalence of diabetes, and a higher proportion of women had a malignancy.
 

Consistent with U.S. studies

U.S. report in 2015 documented a higher prevalence of comorbidities and more severe illness among men undergoing bariatric surgery, compared with women, noted session chair Zhila Semnani-Azad, PhD, a researcher in the department of nutrition at Harvard School of Public Health in Boston.

“I think the [Austrian] data presented have relevance to the U.S. population,” Dr. Semnani-Azad said in an interview.

“The main limitation of these univariate analyses is they don’t account for potential confounding variables that could affect the association, such as lifestyle variables, age, and family history. There is always potential for other variables” to influence apparent sex-specific associations, she commented. Another limitation is the small total number of deaths analyzed, at 367.

“These results are a good starting point for future studies. More work is needed to better understand the impact of comorbidities and sex on postsurgical mortality,” Dr. Semnani-Azad concluded.

Dr. Beiglböck and Dr. Semnani-Azad have reported no relevant financial relationships.

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

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Botanical Briefs: Bloodroot (Sanguinaria canadensis)

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Botanical Briefs: Bloodroot (Sanguinaria canadensis)

Bloodroot (Sanguinaria canadensis) is a member of the family Papaveraceae.1 This North American plant commonly is found in widespread distribution from Nova Scotia, Canada, to Florida and from the Great Lakes to Mississippi.2 Historically, Native Americans used bloodroot as a skin dye and as a medicine for many ailments.3

Bloodroot blooms for only a few days, starting in March, and fruits in June. The flowers comprise 8 to 10 white petals, surrounding a bed of yellow stamens (Figure). The plant thrives in wooded areas and grows to 12 inches tall. In its off-season, the plant remains dormant and can survive below-freezing temperatures.4

Flowered bloodroot (Sanguinaria canadensis).

Chemical Constituents

Bloodroot gets its colloquial name from its red sap, which is released when the plant’s rhizome is cut. This sap contains a high concentration of alkaloids that are used for protection against predators. The rhizome itself has a rusty, red-brown color; the roots are a brighter red-orange.4

The rhizome of S canadensis contains the highest concentration of active alkaloids; the roots also contain these chemicals, though to a lesser degree; and the leaves, flowers, and fruits harvest approximately 1% of the alkaloids found in the roots.4 The concentration of alkaloids can vary from one plant to the next, depending on environmental conditions.5,6

The major alkaloids in S canadensis include both quaternary benzophenanthridine alkaloids (eg, sanguinarine, chelerythrine, sanguilutine, chelilutine, sanguirubine, chelirubine) and protopin alkaloids (eg, protopine, allocryptopine).3,7 Of these, sanguinarine and chelerythrine typically are the most potent.1 Oral ingestion or topical application of these molecules can have therapeutic and toxic effects.8

Biophysiological Effects

Bloodroot has been shown to have remarkable antimicrobial effects.9 The plant produces hydrogen peroxide and superoxide anion.10 These mediators cause oxidative stress, thus inducing destruction of cellular DNA and the cell membrane.11 Although these effects can be helpful when fighting infection, they are not necessarily selective against healthy cells.12

Alkaloids of bloodroot also have cardiovascular therapeutic effects. Sanguinarine blocks angiotensin II and causes vasodilation, thus helping treat hypertension.13 It also acts as an inotrope by blocking the Na+/K+ ATPase pump. These effects in a patient who is already taking digoxin can cause notable cardiotoxicity because the 2 drugs share a mechanism of action.14

 

 

Chelerythrine blocks production of cyclooxygenase 2 and prostaglandin E2.15 This pathway modification results in anti-inflammatory effects that can help treat arthritis, edema, and other inflammatory conditions.16 Moreover, sanguinarine has demonstrated efficacy in numerous anticancer pathways,17 including downregulation of intercellular adhesion molecules, vascular cell adhesion molecules, and vascular endothelial growth factor (VEGF).18-20 Blocking VEGF is one way to inhibit angiogenesis,21 which is upregulated in tumor formation, thus sanguinarine can have an antiproliferative anticancer effect.22 Sanguinarine also upregulates molecules such as nuclear factor–κB and the protease enzymes known as caspases to cause proapoptotic effects, furthering its antitumor potential.23,24

Treatment of Dermatologic Conditions

The initial technique of Mohs micrographic surgery employed a chemopaste that utilized an extract of S canadensis to preserve tissue.25 Outside the dermatologist’s office, bloodroot is used as a topical home remedy for a variety of cutaneous conditions, including cancer, skin tags, and warts.26 Bloodroot is advertised as black salve, an alternative anticancer treatment.27,28

As useful as this natural agent sounds, it has a pitfall: The alkaloids of S canadensis are nonspecific in their cytotoxicity, damaging neoplastic and healthy tissue.29 This cytotoxic effect can cause escharification through diffuse tissue destruction and has been observed to result in formation of a keloid scar.30 The alkaloids in black salve also have been shown to cause skin erosions and cellular atypia.28,31 Therefore, the utility of this escharotic in medical treatment is limited.32 Fortuitously, oral antibiotics and wound care can help address this adverse effect.28

Bloodroot was once used as a mouth rinse and toothpaste to treat gingivitis, but this application was later associated with oral leukoplakia, a premalignant condition.33 Leukoplakia associated with S canadensis extract often is unremitting. Immediate discontinuation of the offending agent produces little regression, suggesting that cellular damage is irreversible.34

Final Thoughts

Although bloodroot demonstrates efficacy as a phytotherapeutic, it does come with notable toxicity. Physicians should warn patients of the unwanted cosmetic effects of black salve, especially oral products that incorporate sanguinarine. Adverse effects on the oropharynx can be irreversible, though the eschar associated with black salve can be treated with a topical or oral corticosteroid.29

References
  1. Vogel M, Lawson M, Sippl W, et al. Structure and mechanism of sanguinarine reductase, an enzyme of alkaloid detoxification. J Biol Chem. 2010;285:18397-18406. doi:10.1074/jbc.M109.088989
  2. Maranda EL, Wang MX, Cortizo J, et al. Flower power—the versatility of bloodroot. JAMA Dermatol. 2016;152:824. doi:10.1001/jamadermatol.2015.5522
  3. Setzer WN. The phytochemistry of Cherokee aromatic medicinal plants. Medicines (Basel). 2018;5:121. doi:10.3390/medicines5040121
  4. Croaker A, King GJ, Pyne JH, et al. Sanguinaria canadensis: traditional medicine, phytochemical composition, biological activities and current uses. Int J Mol Sci. 2016;17:1414. doi:10.3390/ijms17091414
  5. Graf TN, Levine KE, Andrews ME, et al. Variability in the yield of benzophenanthridine alkaloids in wildcrafted vs cultivated bloodroot (Sanguinaria canadensis L.) J Agric Food Chem. 2007; 55:1205-1211. doi:10.1021/jf062498f
  6. Bennett BC, Bell CR, Boulware RT. Geographic variation in alkaloid content of Sanguinaria canadensis (Papaveraceae). Rhodora. 1990;92:57-69.
  7. Leaver CA, Yuan H, Wallen GR. Apoptotic activities of Sanguinaria canadensis: primary human keratinocytes, C-33A, and human papillomavirus HeLa cervical cancer lines. Integr Med (Encinitas). 2018;17:32-37.
  8. Kutchan TM. Molecular genetics of plant alkaloid biosynthesis. In: Cordell GA, ed. The Alkaloids. Vol 50. Elsevier Science Publishing Co, Inc; 1997:257-316.
  9. Obiang-Obounou BW, Kang O-H, Choi J-G, et al. The mechanism of action of sanguinarine against methicillin-resistant Staphylococcus aureus. J Toxicol Sci. 2011;36:277-283. doi:10.2131/jts.36.277
  10. Z˙abka A, Winnicki K, Polit JT, et al. Sanguinarine-induced oxidative stress and apoptosis-like programmed cell death (AL-PCD) in root meristem cells of Allium cepa. Plant Physiol Biochem. 2017;112:193-206. doi:10.1016/j.plaphy.2017.01.004
  11. Kumar GS, Hazra S. Sanguinarine, a promising anticancer therapeutic: photochemical and nucleic acid binding properties. RSC Advances. 2014;4:56518-56531.
  12. Ping G, Wang Y, Shen L, et al. Highly efficient complexation of sanguinarine alkaloid by carboxylatopillar[6]arene: pKa shift, increased solubility and enhanced antibacterial activity. Chemical Commun (Camb). 2017;53:7381-7384. doi:10.1039/c7cc02799k
  13. Caballero-George C, Vanderheyden PM, Solis PN, et al. Biological screening of selected medicinal Panamanian plants by radioligand-binding techniques. Phytomedicine. 2001;8:59-70. doi:10.1078/0944-7113-00011
  14. Seifen E, Adams RJ, Riemer RK. Sanguinarine: a positive inotropic alkaloid which inhibits cardiac Na+, K+-ATPase. Eur J Pharmacol. 1979;60:373-377. doi:10.1016/0014-2999(79)90245-0
  15. Debprasad C, Hemanta M, Paromita B, et al. Inhibition of NO2, PGE2, TNF-α, and iNOS EXpression by Shorea robusta L.: an ethnomedicine used for anti-inflammatory and analgesic activity. Evid Based Complement Alternat Med. 2012; 2012:254849. doi:10.1155/2012/254849
  16. Melov S, Ravenscroft J, Malik S, et al. Extension of life-span with superoxide dismutase/catalase mimetics. Science. 2000;289:1567-1569. doi:10.1126/science.289.5484.1567
  17. Basu P, Kumar GS. Sanguinarine and its role in chronic diseases. In: Gupta SC, Prasad S, Aggarwal BB, eds. Advances in Experimental Medicine and Biology: Anti-inflammatory Nutraceuticals and Chronic Diseases. Vol 928. Springer International Publishing; 2016:155-172.
  18. Alasvand M, Assadollahi V, Ambra R, et al. Antiangiogenic effect of alkaloids. Oxid Med Cell Longev. 2019;2019:9475908. doi:10.1155/2019/9475908
  19. Basini G, Santini SE, Bussolati S, et al. The plant alkaloid sanguinarine is a potential inhibitor of follicular angiogenesis. J Reprod Dev. 2007;53:573-579. doi:10.1262/jrd.18126
  20. Xu J-Y, Meng Q-H, Chong Y, et al. Sanguinarine is a novel VEGF inhibitor involved in the suppression of angiogenesis and cell migration. Mol Clin Oncol. 2013;1:331-336. doi:10.3892/mco.2012.41
  21. Lu K, Bhat M, Basu S. Plants and their active compounds: natural molecules to target angiogenesis. Angiogenesis. 2016;19:287-295. doi:10.1007/s10456-016-9512-y
  22. Achkar IW, Mraiche F, Mohammad RM, et al. Anticancer potential of sanguinarine for various human malignancies. Future Med Chem. 2017;9:933-950. doi:10.4155/fmc-2017-0041
  23. Lee TK, Park C, Jeong S-J, et al. Sanguinarine induces apoptosis of human oral squamous cell carcinoma KB cells via inactivation of the PI3K/Akt signaling pathway. Drug Dev Res. 2016;77:227-240. doi:10.1002/ddr.21315
  24. Gaziano R, Moroni G, Buè C, et al. Antitumor effects of the benzophenanthridine alkaloid sanguinarine: evidence and perspectives. World J Gastrointest Oncol. 2016;8:30-39. doi:10.4251/wjgo.v8.i1.30
  25. Mohs FE. Chemosurgery for skin cancer: fixed tissue and fresh tissue techniques. Arch Dermatol. 1976;112:211-215.
  26. Affleck AG, Varma S. A case of do-it-yourself Mohs’ surgery using bloodroot obtained from the internet. Br J Dermatol. 2007;157:1078-1079. doi:10.1111/j.1365-2133.2007.08180.x
  27. Eastman KL, McFarland LV, Raugi GJ. Buyer beware: a black salve caution. J Am Acad Dermatol. 2011;65:E154-E155. doi:10.1016/j.jaad.2011.07.031
  28. Osswald SS, Elston DM, Farley MF, et al. Self-treatment of a basal cell carcinoma with “black and yellow salve.” J Am Acad Dermatol. 2005;53:508-510. doi:10.1016/j.jaad.2005.04.007
  29. Schlichte MJ, Downing CP, Ramirez-Fort M, et al. Bloodroot associated eschar. Dermatol Online J. 2015;20:13030/qt05r0r2wr.
  30. Wang MZ, Warshaw EM. Bloodroot. Dermatitis. 2012;23:281-283. doi:10.1097/DER.0b013e318273a4dd
  31. Tan JM, Peters P, Ong N, et al. Histopathological features after topical black salve application. Australas J Dermatol. 2015;56:75-76.
  32. Hou JL, Brewer JD. Black salve and bloodroot extract in dermatologic conditions. Cutis. 2015;95:309-311.
  33. Eversole LR, Eversole GM, Kopcik J. Sanguinaria-associated oral leukoplakia: comparison with other benign and dysplastic leukoplakic lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89:455-464. doi:10.1016/s1079-2104(00)70125-9
  34. Mascarenhas AK, Allen CM, Moeschberger ML. The association between Viadent® use and oral leukoplakia—results of a matched case-control study. J Public Health Dent. 2002;62:158-162. doi:10.1111/j.1752-7325.2002.tb03437.x
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Author and Disclosure Information

Dr. Schwartzberg is from the Department of Medicine, Lehigh Valley Health Network, Allentown, Pennsylvania. Dr. Osswald is from the Department of Dermatology and Cutaneous Surgery, UT Health San Antonio, Texas. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, 135 Rutledge Ave, MSC 578, Charleston, SC 29425 ([email protected]).

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Dr. Schwartzberg is from the Department of Medicine, Lehigh Valley Health Network, Allentown, Pennsylvania. Dr. Osswald is from the Department of Dermatology and Cutaneous Surgery, UT Health San Antonio, Texas. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, 135 Rutledge Ave, MSC 578, Charleston, SC 29425 ([email protected]).

Author and Disclosure Information

Dr. Schwartzberg is from the Department of Medicine, Lehigh Valley Health Network, Allentown, Pennsylvania. Dr. Osswald is from the Department of Dermatology and Cutaneous Surgery, UT Health San Antonio, Texas. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, 135 Rutledge Ave, MSC 578, Charleston, SC 29425 ([email protected]).

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Bloodroot (Sanguinaria canadensis) is a member of the family Papaveraceae.1 This North American plant commonly is found in widespread distribution from Nova Scotia, Canada, to Florida and from the Great Lakes to Mississippi.2 Historically, Native Americans used bloodroot as a skin dye and as a medicine for many ailments.3

Bloodroot blooms for only a few days, starting in March, and fruits in June. The flowers comprise 8 to 10 white petals, surrounding a bed of yellow stamens (Figure). The plant thrives in wooded areas and grows to 12 inches tall. In its off-season, the plant remains dormant and can survive below-freezing temperatures.4

Flowered bloodroot (Sanguinaria canadensis).

Chemical Constituents

Bloodroot gets its colloquial name from its red sap, which is released when the plant’s rhizome is cut. This sap contains a high concentration of alkaloids that are used for protection against predators. The rhizome itself has a rusty, red-brown color; the roots are a brighter red-orange.4

The rhizome of S canadensis contains the highest concentration of active alkaloids; the roots also contain these chemicals, though to a lesser degree; and the leaves, flowers, and fruits harvest approximately 1% of the alkaloids found in the roots.4 The concentration of alkaloids can vary from one plant to the next, depending on environmental conditions.5,6

The major alkaloids in S canadensis include both quaternary benzophenanthridine alkaloids (eg, sanguinarine, chelerythrine, sanguilutine, chelilutine, sanguirubine, chelirubine) and protopin alkaloids (eg, protopine, allocryptopine).3,7 Of these, sanguinarine and chelerythrine typically are the most potent.1 Oral ingestion or topical application of these molecules can have therapeutic and toxic effects.8

Biophysiological Effects

Bloodroot has been shown to have remarkable antimicrobial effects.9 The plant produces hydrogen peroxide and superoxide anion.10 These mediators cause oxidative stress, thus inducing destruction of cellular DNA and the cell membrane.11 Although these effects can be helpful when fighting infection, they are not necessarily selective against healthy cells.12

Alkaloids of bloodroot also have cardiovascular therapeutic effects. Sanguinarine blocks angiotensin II and causes vasodilation, thus helping treat hypertension.13 It also acts as an inotrope by blocking the Na+/K+ ATPase pump. These effects in a patient who is already taking digoxin can cause notable cardiotoxicity because the 2 drugs share a mechanism of action.14

 

 

Chelerythrine blocks production of cyclooxygenase 2 and prostaglandin E2.15 This pathway modification results in anti-inflammatory effects that can help treat arthritis, edema, and other inflammatory conditions.16 Moreover, sanguinarine has demonstrated efficacy in numerous anticancer pathways,17 including downregulation of intercellular adhesion molecules, vascular cell adhesion molecules, and vascular endothelial growth factor (VEGF).18-20 Blocking VEGF is one way to inhibit angiogenesis,21 which is upregulated in tumor formation, thus sanguinarine can have an antiproliferative anticancer effect.22 Sanguinarine also upregulates molecules such as nuclear factor–κB and the protease enzymes known as caspases to cause proapoptotic effects, furthering its antitumor potential.23,24

Treatment of Dermatologic Conditions

The initial technique of Mohs micrographic surgery employed a chemopaste that utilized an extract of S canadensis to preserve tissue.25 Outside the dermatologist’s office, bloodroot is used as a topical home remedy for a variety of cutaneous conditions, including cancer, skin tags, and warts.26 Bloodroot is advertised as black salve, an alternative anticancer treatment.27,28

As useful as this natural agent sounds, it has a pitfall: The alkaloids of S canadensis are nonspecific in their cytotoxicity, damaging neoplastic and healthy tissue.29 This cytotoxic effect can cause escharification through diffuse tissue destruction and has been observed to result in formation of a keloid scar.30 The alkaloids in black salve also have been shown to cause skin erosions and cellular atypia.28,31 Therefore, the utility of this escharotic in medical treatment is limited.32 Fortuitously, oral antibiotics and wound care can help address this adverse effect.28

Bloodroot was once used as a mouth rinse and toothpaste to treat gingivitis, but this application was later associated with oral leukoplakia, a premalignant condition.33 Leukoplakia associated with S canadensis extract often is unremitting. Immediate discontinuation of the offending agent produces little regression, suggesting that cellular damage is irreversible.34

Final Thoughts

Although bloodroot demonstrates efficacy as a phytotherapeutic, it does come with notable toxicity. Physicians should warn patients of the unwanted cosmetic effects of black salve, especially oral products that incorporate sanguinarine. Adverse effects on the oropharynx can be irreversible, though the eschar associated with black salve can be treated with a topical or oral corticosteroid.29

Bloodroot (Sanguinaria canadensis) is a member of the family Papaveraceae.1 This North American plant commonly is found in widespread distribution from Nova Scotia, Canada, to Florida and from the Great Lakes to Mississippi.2 Historically, Native Americans used bloodroot as a skin dye and as a medicine for many ailments.3

Bloodroot blooms for only a few days, starting in March, and fruits in June. The flowers comprise 8 to 10 white petals, surrounding a bed of yellow stamens (Figure). The plant thrives in wooded areas and grows to 12 inches tall. In its off-season, the plant remains dormant and can survive below-freezing temperatures.4

Flowered bloodroot (Sanguinaria canadensis).

Chemical Constituents

Bloodroot gets its colloquial name from its red sap, which is released when the plant’s rhizome is cut. This sap contains a high concentration of alkaloids that are used for protection against predators. The rhizome itself has a rusty, red-brown color; the roots are a brighter red-orange.4

The rhizome of S canadensis contains the highest concentration of active alkaloids; the roots also contain these chemicals, though to a lesser degree; and the leaves, flowers, and fruits harvest approximately 1% of the alkaloids found in the roots.4 The concentration of alkaloids can vary from one plant to the next, depending on environmental conditions.5,6

The major alkaloids in S canadensis include both quaternary benzophenanthridine alkaloids (eg, sanguinarine, chelerythrine, sanguilutine, chelilutine, sanguirubine, chelirubine) and protopin alkaloids (eg, protopine, allocryptopine).3,7 Of these, sanguinarine and chelerythrine typically are the most potent.1 Oral ingestion or topical application of these molecules can have therapeutic and toxic effects.8

Biophysiological Effects

Bloodroot has been shown to have remarkable antimicrobial effects.9 The plant produces hydrogen peroxide and superoxide anion.10 These mediators cause oxidative stress, thus inducing destruction of cellular DNA and the cell membrane.11 Although these effects can be helpful when fighting infection, they are not necessarily selective against healthy cells.12

Alkaloids of bloodroot also have cardiovascular therapeutic effects. Sanguinarine blocks angiotensin II and causes vasodilation, thus helping treat hypertension.13 It also acts as an inotrope by blocking the Na+/K+ ATPase pump. These effects in a patient who is already taking digoxin can cause notable cardiotoxicity because the 2 drugs share a mechanism of action.14

 

 

Chelerythrine blocks production of cyclooxygenase 2 and prostaglandin E2.15 This pathway modification results in anti-inflammatory effects that can help treat arthritis, edema, and other inflammatory conditions.16 Moreover, sanguinarine has demonstrated efficacy in numerous anticancer pathways,17 including downregulation of intercellular adhesion molecules, vascular cell adhesion molecules, and vascular endothelial growth factor (VEGF).18-20 Blocking VEGF is one way to inhibit angiogenesis,21 which is upregulated in tumor formation, thus sanguinarine can have an antiproliferative anticancer effect.22 Sanguinarine also upregulates molecules such as nuclear factor–κB and the protease enzymes known as caspases to cause proapoptotic effects, furthering its antitumor potential.23,24

Treatment of Dermatologic Conditions

The initial technique of Mohs micrographic surgery employed a chemopaste that utilized an extract of S canadensis to preserve tissue.25 Outside the dermatologist’s office, bloodroot is used as a topical home remedy for a variety of cutaneous conditions, including cancer, skin tags, and warts.26 Bloodroot is advertised as black salve, an alternative anticancer treatment.27,28

As useful as this natural agent sounds, it has a pitfall: The alkaloids of S canadensis are nonspecific in their cytotoxicity, damaging neoplastic and healthy tissue.29 This cytotoxic effect can cause escharification through diffuse tissue destruction and has been observed to result in formation of a keloid scar.30 The alkaloids in black salve also have been shown to cause skin erosions and cellular atypia.28,31 Therefore, the utility of this escharotic in medical treatment is limited.32 Fortuitously, oral antibiotics and wound care can help address this adverse effect.28

Bloodroot was once used as a mouth rinse and toothpaste to treat gingivitis, but this application was later associated with oral leukoplakia, a premalignant condition.33 Leukoplakia associated with S canadensis extract often is unremitting. Immediate discontinuation of the offending agent produces little regression, suggesting that cellular damage is irreversible.34

Final Thoughts

Although bloodroot demonstrates efficacy as a phytotherapeutic, it does come with notable toxicity. Physicians should warn patients of the unwanted cosmetic effects of black salve, especially oral products that incorporate sanguinarine. Adverse effects on the oropharynx can be irreversible, though the eschar associated with black salve can be treated with a topical or oral corticosteroid.29

References
  1. Vogel M, Lawson M, Sippl W, et al. Structure and mechanism of sanguinarine reductase, an enzyme of alkaloid detoxification. J Biol Chem. 2010;285:18397-18406. doi:10.1074/jbc.M109.088989
  2. Maranda EL, Wang MX, Cortizo J, et al. Flower power—the versatility of bloodroot. JAMA Dermatol. 2016;152:824. doi:10.1001/jamadermatol.2015.5522
  3. Setzer WN. The phytochemistry of Cherokee aromatic medicinal plants. Medicines (Basel). 2018;5:121. doi:10.3390/medicines5040121
  4. Croaker A, King GJ, Pyne JH, et al. Sanguinaria canadensis: traditional medicine, phytochemical composition, biological activities and current uses. Int J Mol Sci. 2016;17:1414. doi:10.3390/ijms17091414
  5. Graf TN, Levine KE, Andrews ME, et al. Variability in the yield of benzophenanthridine alkaloids in wildcrafted vs cultivated bloodroot (Sanguinaria canadensis L.) J Agric Food Chem. 2007; 55:1205-1211. doi:10.1021/jf062498f
  6. Bennett BC, Bell CR, Boulware RT. Geographic variation in alkaloid content of Sanguinaria canadensis (Papaveraceae). Rhodora. 1990;92:57-69.
  7. Leaver CA, Yuan H, Wallen GR. Apoptotic activities of Sanguinaria canadensis: primary human keratinocytes, C-33A, and human papillomavirus HeLa cervical cancer lines. Integr Med (Encinitas). 2018;17:32-37.
  8. Kutchan TM. Molecular genetics of plant alkaloid biosynthesis. In: Cordell GA, ed. The Alkaloids. Vol 50. Elsevier Science Publishing Co, Inc; 1997:257-316.
  9. Obiang-Obounou BW, Kang O-H, Choi J-G, et al. The mechanism of action of sanguinarine against methicillin-resistant Staphylococcus aureus. J Toxicol Sci. 2011;36:277-283. doi:10.2131/jts.36.277
  10. Z˙abka A, Winnicki K, Polit JT, et al. Sanguinarine-induced oxidative stress and apoptosis-like programmed cell death (AL-PCD) in root meristem cells of Allium cepa. Plant Physiol Biochem. 2017;112:193-206. doi:10.1016/j.plaphy.2017.01.004
  11. Kumar GS, Hazra S. Sanguinarine, a promising anticancer therapeutic: photochemical and nucleic acid binding properties. RSC Advances. 2014;4:56518-56531.
  12. Ping G, Wang Y, Shen L, et al. Highly efficient complexation of sanguinarine alkaloid by carboxylatopillar[6]arene: pKa shift, increased solubility and enhanced antibacterial activity. Chemical Commun (Camb). 2017;53:7381-7384. doi:10.1039/c7cc02799k
  13. Caballero-George C, Vanderheyden PM, Solis PN, et al. Biological screening of selected medicinal Panamanian plants by radioligand-binding techniques. Phytomedicine. 2001;8:59-70. doi:10.1078/0944-7113-00011
  14. Seifen E, Adams RJ, Riemer RK. Sanguinarine: a positive inotropic alkaloid which inhibits cardiac Na+, K+-ATPase. Eur J Pharmacol. 1979;60:373-377. doi:10.1016/0014-2999(79)90245-0
  15. Debprasad C, Hemanta M, Paromita B, et al. Inhibition of NO2, PGE2, TNF-α, and iNOS EXpression by Shorea robusta L.: an ethnomedicine used for anti-inflammatory and analgesic activity. Evid Based Complement Alternat Med. 2012; 2012:254849. doi:10.1155/2012/254849
  16. Melov S, Ravenscroft J, Malik S, et al. Extension of life-span with superoxide dismutase/catalase mimetics. Science. 2000;289:1567-1569. doi:10.1126/science.289.5484.1567
  17. Basu P, Kumar GS. Sanguinarine and its role in chronic diseases. In: Gupta SC, Prasad S, Aggarwal BB, eds. Advances in Experimental Medicine and Biology: Anti-inflammatory Nutraceuticals and Chronic Diseases. Vol 928. Springer International Publishing; 2016:155-172.
  18. Alasvand M, Assadollahi V, Ambra R, et al. Antiangiogenic effect of alkaloids. Oxid Med Cell Longev. 2019;2019:9475908. doi:10.1155/2019/9475908
  19. Basini G, Santini SE, Bussolati S, et al. The plant alkaloid sanguinarine is a potential inhibitor of follicular angiogenesis. J Reprod Dev. 2007;53:573-579. doi:10.1262/jrd.18126
  20. Xu J-Y, Meng Q-H, Chong Y, et al. Sanguinarine is a novel VEGF inhibitor involved in the suppression of angiogenesis and cell migration. Mol Clin Oncol. 2013;1:331-336. doi:10.3892/mco.2012.41
  21. Lu K, Bhat M, Basu S. Plants and their active compounds: natural molecules to target angiogenesis. Angiogenesis. 2016;19:287-295. doi:10.1007/s10456-016-9512-y
  22. Achkar IW, Mraiche F, Mohammad RM, et al. Anticancer potential of sanguinarine for various human malignancies. Future Med Chem. 2017;9:933-950. doi:10.4155/fmc-2017-0041
  23. Lee TK, Park C, Jeong S-J, et al. Sanguinarine induces apoptosis of human oral squamous cell carcinoma KB cells via inactivation of the PI3K/Akt signaling pathway. Drug Dev Res. 2016;77:227-240. doi:10.1002/ddr.21315
  24. Gaziano R, Moroni G, Buè C, et al. Antitumor effects of the benzophenanthridine alkaloid sanguinarine: evidence and perspectives. World J Gastrointest Oncol. 2016;8:30-39. doi:10.4251/wjgo.v8.i1.30
  25. Mohs FE. Chemosurgery for skin cancer: fixed tissue and fresh tissue techniques. Arch Dermatol. 1976;112:211-215.
  26. Affleck AG, Varma S. A case of do-it-yourself Mohs’ surgery using bloodroot obtained from the internet. Br J Dermatol. 2007;157:1078-1079. doi:10.1111/j.1365-2133.2007.08180.x
  27. Eastman KL, McFarland LV, Raugi GJ. Buyer beware: a black salve caution. J Am Acad Dermatol. 2011;65:E154-E155. doi:10.1016/j.jaad.2011.07.031
  28. Osswald SS, Elston DM, Farley MF, et al. Self-treatment of a basal cell carcinoma with “black and yellow salve.” J Am Acad Dermatol. 2005;53:508-510. doi:10.1016/j.jaad.2005.04.007
  29. Schlichte MJ, Downing CP, Ramirez-Fort M, et al. Bloodroot associated eschar. Dermatol Online J. 2015;20:13030/qt05r0r2wr.
  30. Wang MZ, Warshaw EM. Bloodroot. Dermatitis. 2012;23:281-283. doi:10.1097/DER.0b013e318273a4dd
  31. Tan JM, Peters P, Ong N, et al. Histopathological features after topical black salve application. Australas J Dermatol. 2015;56:75-76.
  32. Hou JL, Brewer JD. Black salve and bloodroot extract in dermatologic conditions. Cutis. 2015;95:309-311.
  33. Eversole LR, Eversole GM, Kopcik J. Sanguinaria-associated oral leukoplakia: comparison with other benign and dysplastic leukoplakic lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89:455-464. doi:10.1016/s1079-2104(00)70125-9
  34. Mascarenhas AK, Allen CM, Moeschberger ML. The association between Viadent® use and oral leukoplakia—results of a matched case-control study. J Public Health Dent. 2002;62:158-162. doi:10.1111/j.1752-7325.2002.tb03437.x
References
  1. Vogel M, Lawson M, Sippl W, et al. Structure and mechanism of sanguinarine reductase, an enzyme of alkaloid detoxification. J Biol Chem. 2010;285:18397-18406. doi:10.1074/jbc.M109.088989
  2. Maranda EL, Wang MX, Cortizo J, et al. Flower power—the versatility of bloodroot. JAMA Dermatol. 2016;152:824. doi:10.1001/jamadermatol.2015.5522
  3. Setzer WN. The phytochemistry of Cherokee aromatic medicinal plants. Medicines (Basel). 2018;5:121. doi:10.3390/medicines5040121
  4. Croaker A, King GJ, Pyne JH, et al. Sanguinaria canadensis: traditional medicine, phytochemical composition, biological activities and current uses. Int J Mol Sci. 2016;17:1414. doi:10.3390/ijms17091414
  5. Graf TN, Levine KE, Andrews ME, et al. Variability in the yield of benzophenanthridine alkaloids in wildcrafted vs cultivated bloodroot (Sanguinaria canadensis L.) J Agric Food Chem. 2007; 55:1205-1211. doi:10.1021/jf062498f
  6. Bennett BC, Bell CR, Boulware RT. Geographic variation in alkaloid content of Sanguinaria canadensis (Papaveraceae). Rhodora. 1990;92:57-69.
  7. Leaver CA, Yuan H, Wallen GR. Apoptotic activities of Sanguinaria canadensis: primary human keratinocytes, C-33A, and human papillomavirus HeLa cervical cancer lines. Integr Med (Encinitas). 2018;17:32-37.
  8. Kutchan TM. Molecular genetics of plant alkaloid biosynthesis. In: Cordell GA, ed. The Alkaloids. Vol 50. Elsevier Science Publishing Co, Inc; 1997:257-316.
  9. Obiang-Obounou BW, Kang O-H, Choi J-G, et al. The mechanism of action of sanguinarine against methicillin-resistant Staphylococcus aureus. J Toxicol Sci. 2011;36:277-283. doi:10.2131/jts.36.277
  10. Z˙abka A, Winnicki K, Polit JT, et al. Sanguinarine-induced oxidative stress and apoptosis-like programmed cell death (AL-PCD) in root meristem cells of Allium cepa. Plant Physiol Biochem. 2017;112:193-206. doi:10.1016/j.plaphy.2017.01.004
  11. Kumar GS, Hazra S. Sanguinarine, a promising anticancer therapeutic: photochemical and nucleic acid binding properties. RSC Advances. 2014;4:56518-56531.
  12. Ping G, Wang Y, Shen L, et al. Highly efficient complexation of sanguinarine alkaloid by carboxylatopillar[6]arene: pKa shift, increased solubility and enhanced antibacterial activity. Chemical Commun (Camb). 2017;53:7381-7384. doi:10.1039/c7cc02799k
  13. Caballero-George C, Vanderheyden PM, Solis PN, et al. Biological screening of selected medicinal Panamanian plants by radioligand-binding techniques. Phytomedicine. 2001;8:59-70. doi:10.1078/0944-7113-00011
  14. Seifen E, Adams RJ, Riemer RK. Sanguinarine: a positive inotropic alkaloid which inhibits cardiac Na+, K+-ATPase. Eur J Pharmacol. 1979;60:373-377. doi:10.1016/0014-2999(79)90245-0
  15. Debprasad C, Hemanta M, Paromita B, et al. Inhibition of NO2, PGE2, TNF-α, and iNOS EXpression by Shorea robusta L.: an ethnomedicine used for anti-inflammatory and analgesic activity. Evid Based Complement Alternat Med. 2012; 2012:254849. doi:10.1155/2012/254849
  16. Melov S, Ravenscroft J, Malik S, et al. Extension of life-span with superoxide dismutase/catalase mimetics. Science. 2000;289:1567-1569. doi:10.1126/science.289.5484.1567
  17. Basu P, Kumar GS. Sanguinarine and its role in chronic diseases. In: Gupta SC, Prasad S, Aggarwal BB, eds. Advances in Experimental Medicine and Biology: Anti-inflammatory Nutraceuticals and Chronic Diseases. Vol 928. Springer International Publishing; 2016:155-172.
  18. Alasvand M, Assadollahi V, Ambra R, et al. Antiangiogenic effect of alkaloids. Oxid Med Cell Longev. 2019;2019:9475908. doi:10.1155/2019/9475908
  19. Basini G, Santini SE, Bussolati S, et al. The plant alkaloid sanguinarine is a potential inhibitor of follicular angiogenesis. J Reprod Dev. 2007;53:573-579. doi:10.1262/jrd.18126
  20. Xu J-Y, Meng Q-H, Chong Y, et al. Sanguinarine is a novel VEGF inhibitor involved in the suppression of angiogenesis and cell migration. Mol Clin Oncol. 2013;1:331-336. doi:10.3892/mco.2012.41
  21. Lu K, Bhat M, Basu S. Plants and their active compounds: natural molecules to target angiogenesis. Angiogenesis. 2016;19:287-295. doi:10.1007/s10456-016-9512-y
  22. Achkar IW, Mraiche F, Mohammad RM, et al. Anticancer potential of sanguinarine for various human malignancies. Future Med Chem. 2017;9:933-950. doi:10.4155/fmc-2017-0041
  23. Lee TK, Park C, Jeong S-J, et al. Sanguinarine induces apoptosis of human oral squamous cell carcinoma KB cells via inactivation of the PI3K/Akt signaling pathway. Drug Dev Res. 2016;77:227-240. doi:10.1002/ddr.21315
  24. Gaziano R, Moroni G, Buè C, et al. Antitumor effects of the benzophenanthridine alkaloid sanguinarine: evidence and perspectives. World J Gastrointest Oncol. 2016;8:30-39. doi:10.4251/wjgo.v8.i1.30
  25. Mohs FE. Chemosurgery for skin cancer: fixed tissue and fresh tissue techniques. Arch Dermatol. 1976;112:211-215.
  26. Affleck AG, Varma S. A case of do-it-yourself Mohs’ surgery using bloodroot obtained from the internet. Br J Dermatol. 2007;157:1078-1079. doi:10.1111/j.1365-2133.2007.08180.x
  27. Eastman KL, McFarland LV, Raugi GJ. Buyer beware: a black salve caution. J Am Acad Dermatol. 2011;65:E154-E155. doi:10.1016/j.jaad.2011.07.031
  28. Osswald SS, Elston DM, Farley MF, et al. Self-treatment of a basal cell carcinoma with “black and yellow salve.” J Am Acad Dermatol. 2005;53:508-510. doi:10.1016/j.jaad.2005.04.007
  29. Schlichte MJ, Downing CP, Ramirez-Fort M, et al. Bloodroot associated eschar. Dermatol Online J. 2015;20:13030/qt05r0r2wr.
  30. Wang MZ, Warshaw EM. Bloodroot. Dermatitis. 2012;23:281-283. doi:10.1097/DER.0b013e318273a4dd
  31. Tan JM, Peters P, Ong N, et al. Histopathological features after topical black salve application. Australas J Dermatol. 2015;56:75-76.
  32. Hou JL, Brewer JD. Black salve and bloodroot extract in dermatologic conditions. Cutis. 2015;95:309-311.
  33. Eversole LR, Eversole GM, Kopcik J. Sanguinaria-associated oral leukoplakia: comparison with other benign and dysplastic leukoplakic lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;89:455-464. doi:10.1016/s1079-2104(00)70125-9
  34. Mascarenhas AK, Allen CM, Moeschberger ML. The association between Viadent® use and oral leukoplakia—results of a matched case-control study. J Public Health Dent. 2002;62:158-162. doi:10.1111/j.1752-7325.2002.tb03437.x
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  • Bloodroot (Sanguinaria canadensis) is a plant historically used in Mohs micrographic surgery as chemopaste.
  • Bloodroot has been shown to have remarkable antimicrobial effects.
  • The alkaloids of S canadensis are nonspecific in their cytotoxicity, damaging both neoplastic and healthy tissue. They have been shown to cause skin erosions and cellular atypia.
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Skin of Color in Preclinical Medical Education: A Cross-Institutional Comparison and A Call to Action

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Skin of Color in Preclinical Medical Education: A Cross-Institutional Comparison and A Call to Action
In Collaboration With the Skin of Color Society

A ccording to the US Census Bureau, more than half of all Americans are projected to belong to a minority group, defined as any group other than non-Hispanic White alone, by 2044. 1 Consequently, the United States rapidly is becoming a country in which the majority of citizens will have skin of color. Individuals with skin of color are of diverse ethnic backgrounds and include people of African, Latin American, Native American, Pacific Islander, and Asian descent, as well as interethnic backgrounds. 2 Throughout the country, dermatologists along with primary care practitioners may be confronted with certain cutaneous conditions that have varying disease presentations or processes in patients with skin of color. It also is important to note that racial categories are socially rather than biologically constructed, and the term skin of color includes a wide variety of diverse skin types. Nevertheless, the current literature thoroughly supports unique pathophysiologic differences in skin of color as well as variations in disease manifestation compared to White patients. 3-5 For example, the increased lability of melanosomes in skin of color patients, which increases their risk for postinflammatory hyperpigmentation, has been well documented. 5-7 There are various dermatologic conditions that also occur with higher frequency and manifest uniquely in people with darker, more pigmented skin, 7-9 and dermatologists, along with primary care physicians, should feel prepared to recognize and address them.

Extensive evidence also indicates that there are unique aspects to consider while managing certain skin diseases in patients with skin of color.8,10,11 Consequently, as noted on the Skin of Color Society (SOCS) website, “[a]n increase in the body of dermatological literature concerning skin of color as well as the advancement of both basic science and clinical investigational research is necessary to meet the needs of the expanding skin of color population.”2 In the meantime, current knowledge regarding cutaneous conditions that diversely or disproportionately affect skin of color should be actively disseminated to physicians in training. Although patients with skin of color should always have access to comprehensive care and knowledgeable practitioners, the current changes in national and regional demographics further underscore the need for a more thorough understanding of skin of color with regard to disease pathogenesis, diagnosis, and treatment.

Several studies have found that medical students in the United States are minimally exposed to dermatology in general compared to other clinical specialties,12-14 which can easily lead to the underrecognition of disorders that may uniquely or disproportionately affect individuals with pigmented skin. Recent data showed that medical schools typically required fewer than 10 hours of dermatology instruction,12 and on average, dermatologic training made up less than 1% of a medical student’s undergraduate medical education.13,15,16 Consequently, less than 40% of primary care residents felt that their medical school curriculum adequately prepared them to manage common skin conditions.14 Although not all physicians should be expected to fully grasp the complexities of skin of color and its diagnostic and therapeutic implications, both practicing and training dermatologists have acknowledged a lack of exposure to skin of color. In one study, approximately 47% of dermatologists and dermatology residents reported that their medical training (medical school and/or residency) was inadequate in training them on skin conditions in Black patients. Furthermore, many who felt their training was lacking in skin of color identified the need for greater exposure to Black patients and training materials.15 The absence of comprehensive medical education regarding skin of color ultimately can be a disadvantage for both practitioners and patients, resulting in poorer outcomes. Furthermore, underrepresentation of skin of color may persist beyond undergraduate and graduate medical education. There also is evidence to suggest that noninclusion of skin of color pervades foundational dermatologic educational resources, including commonly used textbooks as well as continuing medical education disseminated at national conferences and meetings.17 Taken together, these findings highlight the need for more diverse and representative exposure to skin of color throughout medical training, which begins with a diverse inclusive undergraduate medical education in dermatology.

The objective of this study was to determine if the preclinical dermatology curriculum at 3 US medical schools provided adequate representation of skin of color patients in their didactic presentation slides.

Methods

Participants—Three US medical schools, a blend of private and public medical schools located across different geographic boundaries, agreed to participate in the study. All 3 institutions were current members of the American Medical Association (AMA) Accelerating Change in Medical Education consortium, whose primary goal is to create the medical school of the future and transform physician training.18 All 32 member institutions of the AMA consortium were contacted to request their participation in the study. As part of the consortium, these institutions have vowed to collectively work to develop and share the best models for educational advancement to improve care for patients, populations, and communities18 and would expectedly provide a more racially and ethnically inclusive curriculum than an institution not accountable to a group dedicated to identifying the best ways to deliver care for increasingly diverse communities.

Data Collection—Lectures were included if they were presented during dermatology preclinical courses in the 2015 to 2016 academic year. An uninvolved third party removed the names and identities of instructors to preserve anonymity. Two independent coders from different institutions extracted the data—lecture title, total number of clinical and histologic images, and number of skin of color images—from each of the anonymized lectures using a standardized coding form. We documented differences in skin of color noted in lectures and the disease context for the discussed differences, such as variations in clinical presentation, disease process, epidemiology/risk, and treatment between different skin phenotypes or ethnic groups. Photographs in which the coders were unable to differentiate whether the patient had skin of color were designated as indeterminate or unclear. Photographs appearing to represent Fitzpatrick skin types IV, V, and VI19 were categorically designated as skin of color, and those appearing to represent Fitzpatrick skin types I and II were described as not skin of color; however, images appearing to represent Fitzpatrick skin type III often were classified as not skin of color or indeterminate and occasionally skin of color. The Figure shows examples of images classified as skin of color, indeterminate, and not skin of color. Photographs often were classified as indeterminate due to poor lighting, close-up view photographs, or highlighted pathology obscuring the surrounding skin. We excluded duplicate photographs and histologic images from the analyses.

A–C, Examples of images classified as skin of color, indeterminate, and not skin of color, respectively

We also reviewed 19 conditions previously highlighted by the SOCS as areas of importance to skin of color patients.20 The coders tracked how many of these conditions were noted in each lecture. Duplicate discussion of these conditions was not included in the analyses. Any discrepancies between coders were resolved through additional slide review and discussion. The final coded data with the agreed upon changes were used for statistical analyses. Recent national demographic data from the US Census Bureau in 2019 describe approximately 39.9% of the population as belonging to racial/ethnic groups other than non-Hispanic/Latinx White.21 Consequently, the standard for adequate representation for skin of color photographs was set at 35% for the purpose of this study.

 

 

Results

Across all 3 institutions included in the study, the proportion of the total number of clinical photographs showing skin of color was 16% (290/1812). Eight percent of the total photographs (145/1812) were noted to be indeterminate (Table). For institution 1, 23.6% of photographs (155/658) showed skin of color, and 12.6% (83/658) were indeterminate. For institution 2, 13.1% (76/578) showed skin of color and 7.8% (45/578) were indeterminate. For institution 3, 10.2% (59/576) showed skin of color and 3% (17/576) were indeterminate.

Institutions 1, 2, and 3 had 18, 8, and 17 total dermatology lectures, respectively. Of the 19 conditions designated as areas of importance to skin of color patients by the SOCS, 16 (84.2%) were discussed by institution 1, 11 (57.9%) by institution 2, and 9 (47.4%) by institution 3 (eTable 1). Institution 3 did not include photographs of skin of color patients in its acne, psoriasis, or cutaneous malignancy lectures. Institution 1 also did not include any skin of color patients in its malignancy lecture. Lectures that focused on pigmentary disorders, atopic dermatitis, infectious conditions, and benign cutaneous neoplasms were more likely to display photographs of skin of color patients; for example, lectures that discussed infectious conditions, such as superficial mycoses, herpes viruses, human papillomavirus, syphilis, and atypical mycobacterial infections, were consistently among those with higher proportions of photographs of skin of color patients.

Throughout the entire preclinical dermatology course at all 3 institutions, of 2945 lecture slides, only 24 (0.8%) unique differences were noted between skin color and non–skin of color patients, with 10 total differences noted by institution 1, 6 by institution 2, and 8 by institution 3 (Table). The majority of these differences (19/24) were related to epidemiologic differences in prevalence among varying racial/ethnic groups, with only 5 instances highlighting differences in clinical presentation. There was only a single instance that elaborated on the underlying pathophysiologic mechanisms of the discussed difference. Of all 24 unique differences discussed, 8 were related to skin cancer, 3 were related to dermatitis, and 2 were related to the difference in manifestation of erythema in patients with darker skin (eTable 2).

 

Comment

The results of this study demonstrated that skin of color is underrepresented in the preclinical dermatology curriculum at these 3 institutions. Although only 16% of all included clinical photographs were of skin of color, individuals with skin of color will soon represent more than half of the total US population within the next 2 decades.1 To increase representation of skin of color patients, teaching faculty should consciously and deliberately include more photographs of skin of color patients for a wider variety of common conditions, including atopic dermatitis and psoriasis, in addition to those that tend to disparately affect skin of color patients, such as pseudofolliculitis barbae or melasma. Furthermore, they also can incorporate more detailed discussions about important differences seen in skin of color patients.

More Skin of Color Photographs in Psoriasis Lectures—At institution 3, there were no skin of color patients included in the psoriasis lecture, even though there is considerable data in the literature indicating notable differences in the clinical presentation, quality-of-life impact, and treatment of psoriasis in skin of color patients.11,22 There are multiple nuances in psoriasis manifestation in patients with skin of color, including less-conspicuous erythema in darker skin, higher degrees of dyspigmentation, and greater body surface area involvement. For Black patients with scalp psoriasis, the impact of hair texture, styling practices, and washing frequency are additional considerations that may impact disease severity and selection of topical therapy.11 The lack of inclusion of any skin of color patients in the psoriasis lecture at one institution further underscores the pressing need to prioritize communities of color in medical education.

 

 

More Skin of Color Photographs in Cutaneous Malignancy Lectures—Similarly, while a lecturer at institution 2 noted that acral lentiginous melanoma accounts for a considerable proportion of melanoma among skin of color patients,23 there was no mention of how melanoma generally is substantially more deadly in this population, potentially due to decreased awareness and inconsistent screening.24 Furthermore, at institutions 1 and 3, there were no photographs or discussion of skin of color patients during the cutaneous malignancy lectures. Evidence shows that more emphasis is needed for melanoma screening and awareness in skin of color populations to improve survival outcomes,24 and this begins with educating not only future dermatologists but all future physicians as well. The failure to include photographs of skin of color patients in discussions or lectures regarding cutaneous malignancies may serve to further perpetuate the harmful misperception that individuals with skin of color are unaffected by skin cancer.25,26

Analysis of Skin of Color Photographs in Infectious Disease Lectures—In addition, lectures discussing infectious etiologies were among those with the highest proportion of skin of color photographs. This relatively disproportionate representation of skin of color compared to the other lectures may contribute to the development of harmful stereotypes or the stigmatization of skin of color patients. Although skin of color should continue to be represented in similar lectures, teaching faculty should remain mindful of the potential unintended impact from lectures including relatively disproportionate amounts of skin of color, particularly when other lectures may have sparse to absent representation of skin of color.

More Photographs Available for Education—Overall, our findings may help to inform changes to preclinical dermatology medical education at other institutions to create more inclusive and representative curricula for skin of color patients. The ability of instructors to provide visual representation of various dermatologic conditions may be limited by the photographs available in certain textbooks with few examples of patients with skin of color; however, concerns regarding the lack of skin of color representation in dermatology training is not a novel discussion.17 Although it is the responsibility of all dermatologists to advocate for the inclusion of skin of color, many dermatologists of color have been leading the way in this movement for decades, publishing several textbooks to document various skin conditions in those with darker skin types and discuss unique considerations for patients with skin of color.27-29 Images from these textbooks can be utilized by programs to increase representation of skin of color in dermatology training. There also are multiple expanding online dermatologic databases, such as VisualDx, with an increasing focus on skin of color patients, some of which allow users to filter images by degree of skin pigmentation.30 Moreover, instructors also can work to diversify their curricula by highlighting more of the SOCS conditions of importance to skin of color patients, which have since been renamed and highlighted on the Patient Dermatology Education section of the SOCS website.20 These conditions, while not completely comprehensive, provide a useful starting point for medical educators to reevaluate for potential areas of improvement and inclusion.

There are several potential strategies that can be used to better represent skin of color in dermatologic preclinical medical education, including increasing awareness, especially among dermatology teaching faculty, of existing disparities in the representation of skin of color in the preclinical curricula. Additionally, all dermatology teaching materials could be reviewed at the department level prior to being disseminated to medical students to assess for instances in which skin of color could be prioritized for discussion or varying disease presentations in skin of color could be demonstrated. Finally, teaching faculty may consider photographing more clinical images of their skin of color patients to further develop a catalog of diverse images that can be used to teach students.

Study Limitations—Our study was unable to account for verbal discussion of skin of color not otherwise denoted or captured in lecture slides. Additional limitations include the utilization of Fitzpatrick skin types to describe and differentiate varying skin tones, as the Fitzpatrick scale originally was developed as a method to describe an individual’s response to UV exposure.19 The inability to further delineate the representation of darker skin types, such as those that may be classified as Fitzpatrick skin types V or VI,19 compared to those with lighter skin of color also was a limiting factor. This study was unable to assess for discussion of other common conditions affecting skin of color patients that were not listed as one of the priority conditions by SOCS. Photographs that were designated as indeterminate were difficult to elucidate as skin of color; however, it is possible that instructors may have verbally described these images as skin of color during lectures. Nonetheless, it may be beneficial for learners if teaching faculty were to clearly label instances where skin of color patients are shown or when notable differences are present.

 

 

Conclusion

Future studies would benefit from the inclusion of audio data from lectures, syllabi, and small group teaching materials from preclinical courses to more accurately assess representation of skin of color in dermatology training. Additionally, future studies also may expand to include images from lectures of overlapping clinical specialties, particularly infectious disease and rheumatology, to provide a broader assessment of skin of color exposure. Furthermore, repeat assessment may be beneficial to assess the longitudinal effectiveness of curricular changes at the institutions included in this study, comparing older lectures to more recent, updated lectures. This study also may be replicated at other medical schools to allow for wider comparison of curricula.

Acknowledgment—The authors wish to thank the institutions that offered and agreed to participate in this study with the hopes of improving medical education.

References
  1. Colby SL, Ortman JM. Projections of the size and composition of the US population: 2014 to 2060. United States Census Bureau website. Published March 2015. Accessed September 14, 2021. https://www.census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf
  2. Learn more about SOCS. Skin of Color Society website. Accessed September 14, 2021. http://skinofcolorsociety.org/about-socs/
  3. Taylor SC. Skin of color: biology, structure, function, and implications for dermatologic disease. J Am Acad Dermatol. 2002;46(suppl 2):S41-S62.
  4. Berardesca E, Maibach H. Ethnic skin: overview of structure and function. J Am Acad Dermatol. 2003;48(suppl 6):S139-S142.
  5. Callender VD, Surin-Lord SS, Davis EC, et al. Postinflammatory hyperpigmentation. Am J Clin Dermatol. 2011;12:87-99.
  6. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
  7. Grimes PE, Stockton T. Pigmentary disorders in blacks. Dermatol Clin. 1988;6:271-281.
  8. Halder RM, Nootheti PK. Ethnic skin disorders overview. J Am Acad Dermatol. 2003;48(suppl 6):S143-S148.
  9. Alexis AF, Sergay AB, Taylor SC. Common dermatologic disorders in skin of color: a comparative practice survey. Cutis. 2007;80:387-394.
  10. Callender VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  11. Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7:16-24.
  12. McCleskey PE, Gilson RT, DeVillez RL. Medical student core curriculum in dermatology survey. J Am Acad Dermatol. 2009;61:30-35.
  13. Ramsay DL, Mayer F. National survey of undergraduate dermatologic medical education. Arch Dermatol.1985;121:1529-1530.
  14. Hansra NK, O’Sullivan P, Chen CL, et al. Medical school dermatology curriculum: are we adequately preparing primary care physicians? J Am Acad Dermatol. 2009;61:23-29.
  15. Buster KJ, Stevens EI, Elmets CA. Dermatologic health disparities. Dermatol Clin. 2012;30:53-59, viii.
  16. Knable A, Hood AF, Pearson TG. Undergraduate medical education in dermatology: report from the AAD Interdisciplinary Education Committee, Subcommittee on Undergraduate Medical Education. J Am Acad Dermatol. 1997;36:467-470.
  17. Ebede T, Papier A. Disparities in dermatology educational resources. J Am Acad Dermatol. 2006;55:687-690.
  18. Skochelak SE, Stack SJ. Creating the medical schools of the future. Acad Med. 2017;92:16-19.
  19. Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol. 1988;124:869-871.
  20. Skin of Color Society. Patient dermatology education. Accessed September 22, 2021. https://skinofcolorsociety.org/patient-dermatology-education
  21. QuickFacts: United States. US Census Bureau website. Updated July 1, 2019. Accessed September 14, 2021. https://www.census.gov/quickfacts/fact/table/US#
  22. Kaufman BP, Alexis AF. Psoriasis in skin of color: insights into the epidemiology, clinical presentation, genetics, quality-of-life impact, and treatment of psoriasis in non-white racial/ethnic groups. Am J Clin Dermatol. 2018;19:405-423.
  23. Bradford PT, Goldstein AM, McMaster ML, et al. Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Arch Dermatol. 2009;145:427-434.
  24. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dermatol. 2016;75:983-991.
  25. Pipitone M, Robinson JK, Camara C, et al. Skin cancer awareness in suburban employees: a Hispanic perspective. J Am Acad Dermatol. 2002;47:118-123.
  26. Imahiyerobo-Ip J, Ip I, Jamal S, et al. Skin cancer awareness in communities of color. J Am Acad Dermatol. 2011;64:198-200.
  27. Taylor SSC, Serrano AMA, Kelly AP, et al, eds. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. McGraw-Hill Education; 2016.
  28. Dadzie OE, Petit A, Alexis AF, eds. Ethnic Dermatology: Principles and Practice. Wiley-Blackwell; 2013.
  29. Jackson-Richards D, Pandya AG, eds. Dermatology Atlas for Skin of Color. Springer; 2014.
  30. VisualDx. New VisualDx feature: skin of color sort. Published October 14, 2020. Accessed September 22, 2021. https://www.visualdx.com/blog/new-visualdx-feature-skin-of-color-sort/
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Author and Disclosure Information

Dr. Okoro is from the Transitional Year Residency Program, Dwight D. Eisenhower Army Medical Center, Fort Gordon, Georgia. Drs. Chau, Kawaoka, and Quereshi are from the Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, Rhode Island. Dr. Wong is from the Department of Dermatology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.

The authors report no conflict of interest.

The views expressed are those of the authors and do not reflect the official policy of the Army, the Department of Defense, or the US Government.

The eTables appear in the Appendix online at www.mdedge.com/dermatology.

Correspondence: Uzoamaka Okoro, MD, MSc, Dwight D. Eisenhower Army Medical Center, 300 E Hospital Rd, Fort Gordon, GA 30905 ([email protected]).

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Author and Disclosure Information

Dr. Okoro is from the Transitional Year Residency Program, Dwight D. Eisenhower Army Medical Center, Fort Gordon, Georgia. Drs. Chau, Kawaoka, and Quereshi are from the Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, Rhode Island. Dr. Wong is from the Department of Dermatology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.

The authors report no conflict of interest.

The views expressed are those of the authors and do not reflect the official policy of the Army, the Department of Defense, or the US Government.

The eTables appear in the Appendix online at www.mdedge.com/dermatology.

Correspondence: Uzoamaka Okoro, MD, MSc, Dwight D. Eisenhower Army Medical Center, 300 E Hospital Rd, Fort Gordon, GA 30905 ([email protected]).

Author and Disclosure Information

Dr. Okoro is from the Transitional Year Residency Program, Dwight D. Eisenhower Army Medical Center, Fort Gordon, Georgia. Drs. Chau, Kawaoka, and Quereshi are from the Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, Rhode Island. Dr. Wong is from the Department of Dermatology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.

The authors report no conflict of interest.

The views expressed are those of the authors and do not reflect the official policy of the Army, the Department of Defense, or the US Government.

The eTables appear in the Appendix online at www.mdedge.com/dermatology.

Correspondence: Uzoamaka Okoro, MD, MSc, Dwight D. Eisenhower Army Medical Center, 300 E Hospital Rd, Fort Gordon, GA 30905 ([email protected]).

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In Collaboration With the Skin of Color Society
In Collaboration With the Skin of Color Society

A ccording to the US Census Bureau, more than half of all Americans are projected to belong to a minority group, defined as any group other than non-Hispanic White alone, by 2044. 1 Consequently, the United States rapidly is becoming a country in which the majority of citizens will have skin of color. Individuals with skin of color are of diverse ethnic backgrounds and include people of African, Latin American, Native American, Pacific Islander, and Asian descent, as well as interethnic backgrounds. 2 Throughout the country, dermatologists along with primary care practitioners may be confronted with certain cutaneous conditions that have varying disease presentations or processes in patients with skin of color. It also is important to note that racial categories are socially rather than biologically constructed, and the term skin of color includes a wide variety of diverse skin types. Nevertheless, the current literature thoroughly supports unique pathophysiologic differences in skin of color as well as variations in disease manifestation compared to White patients. 3-5 For example, the increased lability of melanosomes in skin of color patients, which increases their risk for postinflammatory hyperpigmentation, has been well documented. 5-7 There are various dermatologic conditions that also occur with higher frequency and manifest uniquely in people with darker, more pigmented skin, 7-9 and dermatologists, along with primary care physicians, should feel prepared to recognize and address them.

Extensive evidence also indicates that there are unique aspects to consider while managing certain skin diseases in patients with skin of color.8,10,11 Consequently, as noted on the Skin of Color Society (SOCS) website, “[a]n increase in the body of dermatological literature concerning skin of color as well as the advancement of both basic science and clinical investigational research is necessary to meet the needs of the expanding skin of color population.”2 In the meantime, current knowledge regarding cutaneous conditions that diversely or disproportionately affect skin of color should be actively disseminated to physicians in training. Although patients with skin of color should always have access to comprehensive care and knowledgeable practitioners, the current changes in national and regional demographics further underscore the need for a more thorough understanding of skin of color with regard to disease pathogenesis, diagnosis, and treatment.

Several studies have found that medical students in the United States are minimally exposed to dermatology in general compared to other clinical specialties,12-14 which can easily lead to the underrecognition of disorders that may uniquely or disproportionately affect individuals with pigmented skin. Recent data showed that medical schools typically required fewer than 10 hours of dermatology instruction,12 and on average, dermatologic training made up less than 1% of a medical student’s undergraduate medical education.13,15,16 Consequently, less than 40% of primary care residents felt that their medical school curriculum adequately prepared them to manage common skin conditions.14 Although not all physicians should be expected to fully grasp the complexities of skin of color and its diagnostic and therapeutic implications, both practicing and training dermatologists have acknowledged a lack of exposure to skin of color. In one study, approximately 47% of dermatologists and dermatology residents reported that their medical training (medical school and/or residency) was inadequate in training them on skin conditions in Black patients. Furthermore, many who felt their training was lacking in skin of color identified the need for greater exposure to Black patients and training materials.15 The absence of comprehensive medical education regarding skin of color ultimately can be a disadvantage for both practitioners and patients, resulting in poorer outcomes. Furthermore, underrepresentation of skin of color may persist beyond undergraduate and graduate medical education. There also is evidence to suggest that noninclusion of skin of color pervades foundational dermatologic educational resources, including commonly used textbooks as well as continuing medical education disseminated at national conferences and meetings.17 Taken together, these findings highlight the need for more diverse and representative exposure to skin of color throughout medical training, which begins with a diverse inclusive undergraduate medical education in dermatology.

The objective of this study was to determine if the preclinical dermatology curriculum at 3 US medical schools provided adequate representation of skin of color patients in their didactic presentation slides.

Methods

Participants—Three US medical schools, a blend of private and public medical schools located across different geographic boundaries, agreed to participate in the study. All 3 institutions were current members of the American Medical Association (AMA) Accelerating Change in Medical Education consortium, whose primary goal is to create the medical school of the future and transform physician training.18 All 32 member institutions of the AMA consortium were contacted to request their participation in the study. As part of the consortium, these institutions have vowed to collectively work to develop and share the best models for educational advancement to improve care for patients, populations, and communities18 and would expectedly provide a more racially and ethnically inclusive curriculum than an institution not accountable to a group dedicated to identifying the best ways to deliver care for increasingly diverse communities.

Data Collection—Lectures were included if they were presented during dermatology preclinical courses in the 2015 to 2016 academic year. An uninvolved third party removed the names and identities of instructors to preserve anonymity. Two independent coders from different institutions extracted the data—lecture title, total number of clinical and histologic images, and number of skin of color images—from each of the anonymized lectures using a standardized coding form. We documented differences in skin of color noted in lectures and the disease context for the discussed differences, such as variations in clinical presentation, disease process, epidemiology/risk, and treatment between different skin phenotypes or ethnic groups. Photographs in which the coders were unable to differentiate whether the patient had skin of color were designated as indeterminate or unclear. Photographs appearing to represent Fitzpatrick skin types IV, V, and VI19 were categorically designated as skin of color, and those appearing to represent Fitzpatrick skin types I and II were described as not skin of color; however, images appearing to represent Fitzpatrick skin type III often were classified as not skin of color or indeterminate and occasionally skin of color. The Figure shows examples of images classified as skin of color, indeterminate, and not skin of color. Photographs often were classified as indeterminate due to poor lighting, close-up view photographs, or highlighted pathology obscuring the surrounding skin. We excluded duplicate photographs and histologic images from the analyses.

A–C, Examples of images classified as skin of color, indeterminate, and not skin of color, respectively

We also reviewed 19 conditions previously highlighted by the SOCS as areas of importance to skin of color patients.20 The coders tracked how many of these conditions were noted in each lecture. Duplicate discussion of these conditions was not included in the analyses. Any discrepancies between coders were resolved through additional slide review and discussion. The final coded data with the agreed upon changes were used for statistical analyses. Recent national demographic data from the US Census Bureau in 2019 describe approximately 39.9% of the population as belonging to racial/ethnic groups other than non-Hispanic/Latinx White.21 Consequently, the standard for adequate representation for skin of color photographs was set at 35% for the purpose of this study.

 

 

Results

Across all 3 institutions included in the study, the proportion of the total number of clinical photographs showing skin of color was 16% (290/1812). Eight percent of the total photographs (145/1812) were noted to be indeterminate (Table). For institution 1, 23.6% of photographs (155/658) showed skin of color, and 12.6% (83/658) were indeterminate. For institution 2, 13.1% (76/578) showed skin of color and 7.8% (45/578) were indeterminate. For institution 3, 10.2% (59/576) showed skin of color and 3% (17/576) were indeterminate.

Institutions 1, 2, and 3 had 18, 8, and 17 total dermatology lectures, respectively. Of the 19 conditions designated as areas of importance to skin of color patients by the SOCS, 16 (84.2%) were discussed by institution 1, 11 (57.9%) by institution 2, and 9 (47.4%) by institution 3 (eTable 1). Institution 3 did not include photographs of skin of color patients in its acne, psoriasis, or cutaneous malignancy lectures. Institution 1 also did not include any skin of color patients in its malignancy lecture. Lectures that focused on pigmentary disorders, atopic dermatitis, infectious conditions, and benign cutaneous neoplasms were more likely to display photographs of skin of color patients; for example, lectures that discussed infectious conditions, such as superficial mycoses, herpes viruses, human papillomavirus, syphilis, and atypical mycobacterial infections, were consistently among those with higher proportions of photographs of skin of color patients.

Throughout the entire preclinical dermatology course at all 3 institutions, of 2945 lecture slides, only 24 (0.8%) unique differences were noted between skin color and non–skin of color patients, with 10 total differences noted by institution 1, 6 by institution 2, and 8 by institution 3 (Table). The majority of these differences (19/24) were related to epidemiologic differences in prevalence among varying racial/ethnic groups, with only 5 instances highlighting differences in clinical presentation. There was only a single instance that elaborated on the underlying pathophysiologic mechanisms of the discussed difference. Of all 24 unique differences discussed, 8 were related to skin cancer, 3 were related to dermatitis, and 2 were related to the difference in manifestation of erythema in patients with darker skin (eTable 2).

 

Comment

The results of this study demonstrated that skin of color is underrepresented in the preclinical dermatology curriculum at these 3 institutions. Although only 16% of all included clinical photographs were of skin of color, individuals with skin of color will soon represent more than half of the total US population within the next 2 decades.1 To increase representation of skin of color patients, teaching faculty should consciously and deliberately include more photographs of skin of color patients for a wider variety of common conditions, including atopic dermatitis and psoriasis, in addition to those that tend to disparately affect skin of color patients, such as pseudofolliculitis barbae or melasma. Furthermore, they also can incorporate more detailed discussions about important differences seen in skin of color patients.

More Skin of Color Photographs in Psoriasis Lectures—At institution 3, there were no skin of color patients included in the psoriasis lecture, even though there is considerable data in the literature indicating notable differences in the clinical presentation, quality-of-life impact, and treatment of psoriasis in skin of color patients.11,22 There are multiple nuances in psoriasis manifestation in patients with skin of color, including less-conspicuous erythema in darker skin, higher degrees of dyspigmentation, and greater body surface area involvement. For Black patients with scalp psoriasis, the impact of hair texture, styling practices, and washing frequency are additional considerations that may impact disease severity and selection of topical therapy.11 The lack of inclusion of any skin of color patients in the psoriasis lecture at one institution further underscores the pressing need to prioritize communities of color in medical education.

 

 

More Skin of Color Photographs in Cutaneous Malignancy Lectures—Similarly, while a lecturer at institution 2 noted that acral lentiginous melanoma accounts for a considerable proportion of melanoma among skin of color patients,23 there was no mention of how melanoma generally is substantially more deadly in this population, potentially due to decreased awareness and inconsistent screening.24 Furthermore, at institutions 1 and 3, there were no photographs or discussion of skin of color patients during the cutaneous malignancy lectures. Evidence shows that more emphasis is needed for melanoma screening and awareness in skin of color populations to improve survival outcomes,24 and this begins with educating not only future dermatologists but all future physicians as well. The failure to include photographs of skin of color patients in discussions or lectures regarding cutaneous malignancies may serve to further perpetuate the harmful misperception that individuals with skin of color are unaffected by skin cancer.25,26

Analysis of Skin of Color Photographs in Infectious Disease Lectures—In addition, lectures discussing infectious etiologies were among those with the highest proportion of skin of color photographs. This relatively disproportionate representation of skin of color compared to the other lectures may contribute to the development of harmful stereotypes or the stigmatization of skin of color patients. Although skin of color should continue to be represented in similar lectures, teaching faculty should remain mindful of the potential unintended impact from lectures including relatively disproportionate amounts of skin of color, particularly when other lectures may have sparse to absent representation of skin of color.

More Photographs Available for Education—Overall, our findings may help to inform changes to preclinical dermatology medical education at other institutions to create more inclusive and representative curricula for skin of color patients. The ability of instructors to provide visual representation of various dermatologic conditions may be limited by the photographs available in certain textbooks with few examples of patients with skin of color; however, concerns regarding the lack of skin of color representation in dermatology training is not a novel discussion.17 Although it is the responsibility of all dermatologists to advocate for the inclusion of skin of color, many dermatologists of color have been leading the way in this movement for decades, publishing several textbooks to document various skin conditions in those with darker skin types and discuss unique considerations for patients with skin of color.27-29 Images from these textbooks can be utilized by programs to increase representation of skin of color in dermatology training. There also are multiple expanding online dermatologic databases, such as VisualDx, with an increasing focus on skin of color patients, some of which allow users to filter images by degree of skin pigmentation.30 Moreover, instructors also can work to diversify their curricula by highlighting more of the SOCS conditions of importance to skin of color patients, which have since been renamed and highlighted on the Patient Dermatology Education section of the SOCS website.20 These conditions, while not completely comprehensive, provide a useful starting point for medical educators to reevaluate for potential areas of improvement and inclusion.

There are several potential strategies that can be used to better represent skin of color in dermatologic preclinical medical education, including increasing awareness, especially among dermatology teaching faculty, of existing disparities in the representation of skin of color in the preclinical curricula. Additionally, all dermatology teaching materials could be reviewed at the department level prior to being disseminated to medical students to assess for instances in which skin of color could be prioritized for discussion or varying disease presentations in skin of color could be demonstrated. Finally, teaching faculty may consider photographing more clinical images of their skin of color patients to further develop a catalog of diverse images that can be used to teach students.

Study Limitations—Our study was unable to account for verbal discussion of skin of color not otherwise denoted or captured in lecture slides. Additional limitations include the utilization of Fitzpatrick skin types to describe and differentiate varying skin tones, as the Fitzpatrick scale originally was developed as a method to describe an individual’s response to UV exposure.19 The inability to further delineate the representation of darker skin types, such as those that may be classified as Fitzpatrick skin types V or VI,19 compared to those with lighter skin of color also was a limiting factor. This study was unable to assess for discussion of other common conditions affecting skin of color patients that were not listed as one of the priority conditions by SOCS. Photographs that were designated as indeterminate were difficult to elucidate as skin of color; however, it is possible that instructors may have verbally described these images as skin of color during lectures. Nonetheless, it may be beneficial for learners if teaching faculty were to clearly label instances where skin of color patients are shown or when notable differences are present.

 

 

Conclusion

Future studies would benefit from the inclusion of audio data from lectures, syllabi, and small group teaching materials from preclinical courses to more accurately assess representation of skin of color in dermatology training. Additionally, future studies also may expand to include images from lectures of overlapping clinical specialties, particularly infectious disease and rheumatology, to provide a broader assessment of skin of color exposure. Furthermore, repeat assessment may be beneficial to assess the longitudinal effectiveness of curricular changes at the institutions included in this study, comparing older lectures to more recent, updated lectures. This study also may be replicated at other medical schools to allow for wider comparison of curricula.

Acknowledgment—The authors wish to thank the institutions that offered and agreed to participate in this study with the hopes of improving medical education.

A ccording to the US Census Bureau, more than half of all Americans are projected to belong to a minority group, defined as any group other than non-Hispanic White alone, by 2044. 1 Consequently, the United States rapidly is becoming a country in which the majority of citizens will have skin of color. Individuals with skin of color are of diverse ethnic backgrounds and include people of African, Latin American, Native American, Pacific Islander, and Asian descent, as well as interethnic backgrounds. 2 Throughout the country, dermatologists along with primary care practitioners may be confronted with certain cutaneous conditions that have varying disease presentations or processes in patients with skin of color. It also is important to note that racial categories are socially rather than biologically constructed, and the term skin of color includes a wide variety of diverse skin types. Nevertheless, the current literature thoroughly supports unique pathophysiologic differences in skin of color as well as variations in disease manifestation compared to White patients. 3-5 For example, the increased lability of melanosomes in skin of color patients, which increases their risk for postinflammatory hyperpigmentation, has been well documented. 5-7 There are various dermatologic conditions that also occur with higher frequency and manifest uniquely in people with darker, more pigmented skin, 7-9 and dermatologists, along with primary care physicians, should feel prepared to recognize and address them.

Extensive evidence also indicates that there are unique aspects to consider while managing certain skin diseases in patients with skin of color.8,10,11 Consequently, as noted on the Skin of Color Society (SOCS) website, “[a]n increase in the body of dermatological literature concerning skin of color as well as the advancement of both basic science and clinical investigational research is necessary to meet the needs of the expanding skin of color population.”2 In the meantime, current knowledge regarding cutaneous conditions that diversely or disproportionately affect skin of color should be actively disseminated to physicians in training. Although patients with skin of color should always have access to comprehensive care and knowledgeable practitioners, the current changes in national and regional demographics further underscore the need for a more thorough understanding of skin of color with regard to disease pathogenesis, diagnosis, and treatment.

Several studies have found that medical students in the United States are minimally exposed to dermatology in general compared to other clinical specialties,12-14 which can easily lead to the underrecognition of disorders that may uniquely or disproportionately affect individuals with pigmented skin. Recent data showed that medical schools typically required fewer than 10 hours of dermatology instruction,12 and on average, dermatologic training made up less than 1% of a medical student’s undergraduate medical education.13,15,16 Consequently, less than 40% of primary care residents felt that their medical school curriculum adequately prepared them to manage common skin conditions.14 Although not all physicians should be expected to fully grasp the complexities of skin of color and its diagnostic and therapeutic implications, both practicing and training dermatologists have acknowledged a lack of exposure to skin of color. In one study, approximately 47% of dermatologists and dermatology residents reported that their medical training (medical school and/or residency) was inadequate in training them on skin conditions in Black patients. Furthermore, many who felt their training was lacking in skin of color identified the need for greater exposure to Black patients and training materials.15 The absence of comprehensive medical education regarding skin of color ultimately can be a disadvantage for both practitioners and patients, resulting in poorer outcomes. Furthermore, underrepresentation of skin of color may persist beyond undergraduate and graduate medical education. There also is evidence to suggest that noninclusion of skin of color pervades foundational dermatologic educational resources, including commonly used textbooks as well as continuing medical education disseminated at national conferences and meetings.17 Taken together, these findings highlight the need for more diverse and representative exposure to skin of color throughout medical training, which begins with a diverse inclusive undergraduate medical education in dermatology.

The objective of this study was to determine if the preclinical dermatology curriculum at 3 US medical schools provided adequate representation of skin of color patients in their didactic presentation slides.

Methods

Participants—Three US medical schools, a blend of private and public medical schools located across different geographic boundaries, agreed to participate in the study. All 3 institutions were current members of the American Medical Association (AMA) Accelerating Change in Medical Education consortium, whose primary goal is to create the medical school of the future and transform physician training.18 All 32 member institutions of the AMA consortium were contacted to request their participation in the study. As part of the consortium, these institutions have vowed to collectively work to develop and share the best models for educational advancement to improve care for patients, populations, and communities18 and would expectedly provide a more racially and ethnically inclusive curriculum than an institution not accountable to a group dedicated to identifying the best ways to deliver care for increasingly diverse communities.

Data Collection—Lectures were included if they were presented during dermatology preclinical courses in the 2015 to 2016 academic year. An uninvolved third party removed the names and identities of instructors to preserve anonymity. Two independent coders from different institutions extracted the data—lecture title, total number of clinical and histologic images, and number of skin of color images—from each of the anonymized lectures using a standardized coding form. We documented differences in skin of color noted in lectures and the disease context for the discussed differences, such as variations in clinical presentation, disease process, epidemiology/risk, and treatment between different skin phenotypes or ethnic groups. Photographs in which the coders were unable to differentiate whether the patient had skin of color were designated as indeterminate or unclear. Photographs appearing to represent Fitzpatrick skin types IV, V, and VI19 were categorically designated as skin of color, and those appearing to represent Fitzpatrick skin types I and II were described as not skin of color; however, images appearing to represent Fitzpatrick skin type III often were classified as not skin of color or indeterminate and occasionally skin of color. The Figure shows examples of images classified as skin of color, indeterminate, and not skin of color. Photographs often were classified as indeterminate due to poor lighting, close-up view photographs, or highlighted pathology obscuring the surrounding skin. We excluded duplicate photographs and histologic images from the analyses.

A–C, Examples of images classified as skin of color, indeterminate, and not skin of color, respectively

We also reviewed 19 conditions previously highlighted by the SOCS as areas of importance to skin of color patients.20 The coders tracked how many of these conditions were noted in each lecture. Duplicate discussion of these conditions was not included in the analyses. Any discrepancies between coders were resolved through additional slide review and discussion. The final coded data with the agreed upon changes were used for statistical analyses. Recent national demographic data from the US Census Bureau in 2019 describe approximately 39.9% of the population as belonging to racial/ethnic groups other than non-Hispanic/Latinx White.21 Consequently, the standard for adequate representation for skin of color photographs was set at 35% for the purpose of this study.

 

 

Results

Across all 3 institutions included in the study, the proportion of the total number of clinical photographs showing skin of color was 16% (290/1812). Eight percent of the total photographs (145/1812) were noted to be indeterminate (Table). For institution 1, 23.6% of photographs (155/658) showed skin of color, and 12.6% (83/658) were indeterminate. For institution 2, 13.1% (76/578) showed skin of color and 7.8% (45/578) were indeterminate. For institution 3, 10.2% (59/576) showed skin of color and 3% (17/576) were indeterminate.

Institutions 1, 2, and 3 had 18, 8, and 17 total dermatology lectures, respectively. Of the 19 conditions designated as areas of importance to skin of color patients by the SOCS, 16 (84.2%) were discussed by institution 1, 11 (57.9%) by institution 2, and 9 (47.4%) by institution 3 (eTable 1). Institution 3 did not include photographs of skin of color patients in its acne, psoriasis, or cutaneous malignancy lectures. Institution 1 also did not include any skin of color patients in its malignancy lecture. Lectures that focused on pigmentary disorders, atopic dermatitis, infectious conditions, and benign cutaneous neoplasms were more likely to display photographs of skin of color patients; for example, lectures that discussed infectious conditions, such as superficial mycoses, herpes viruses, human papillomavirus, syphilis, and atypical mycobacterial infections, were consistently among those with higher proportions of photographs of skin of color patients.

Throughout the entire preclinical dermatology course at all 3 institutions, of 2945 lecture slides, only 24 (0.8%) unique differences were noted between skin color and non–skin of color patients, with 10 total differences noted by institution 1, 6 by institution 2, and 8 by institution 3 (Table). The majority of these differences (19/24) were related to epidemiologic differences in prevalence among varying racial/ethnic groups, with only 5 instances highlighting differences in clinical presentation. There was only a single instance that elaborated on the underlying pathophysiologic mechanisms of the discussed difference. Of all 24 unique differences discussed, 8 were related to skin cancer, 3 were related to dermatitis, and 2 were related to the difference in manifestation of erythema in patients with darker skin (eTable 2).

 

Comment

The results of this study demonstrated that skin of color is underrepresented in the preclinical dermatology curriculum at these 3 institutions. Although only 16% of all included clinical photographs were of skin of color, individuals with skin of color will soon represent more than half of the total US population within the next 2 decades.1 To increase representation of skin of color patients, teaching faculty should consciously and deliberately include more photographs of skin of color patients for a wider variety of common conditions, including atopic dermatitis and psoriasis, in addition to those that tend to disparately affect skin of color patients, such as pseudofolliculitis barbae or melasma. Furthermore, they also can incorporate more detailed discussions about important differences seen in skin of color patients.

More Skin of Color Photographs in Psoriasis Lectures—At institution 3, there were no skin of color patients included in the psoriasis lecture, even though there is considerable data in the literature indicating notable differences in the clinical presentation, quality-of-life impact, and treatment of psoriasis in skin of color patients.11,22 There are multiple nuances in psoriasis manifestation in patients with skin of color, including less-conspicuous erythema in darker skin, higher degrees of dyspigmentation, and greater body surface area involvement. For Black patients with scalp psoriasis, the impact of hair texture, styling practices, and washing frequency are additional considerations that may impact disease severity and selection of topical therapy.11 The lack of inclusion of any skin of color patients in the psoriasis lecture at one institution further underscores the pressing need to prioritize communities of color in medical education.

 

 

More Skin of Color Photographs in Cutaneous Malignancy Lectures—Similarly, while a lecturer at institution 2 noted that acral lentiginous melanoma accounts for a considerable proportion of melanoma among skin of color patients,23 there was no mention of how melanoma generally is substantially more deadly in this population, potentially due to decreased awareness and inconsistent screening.24 Furthermore, at institutions 1 and 3, there were no photographs or discussion of skin of color patients during the cutaneous malignancy lectures. Evidence shows that more emphasis is needed for melanoma screening and awareness in skin of color populations to improve survival outcomes,24 and this begins with educating not only future dermatologists but all future physicians as well. The failure to include photographs of skin of color patients in discussions or lectures regarding cutaneous malignancies may serve to further perpetuate the harmful misperception that individuals with skin of color are unaffected by skin cancer.25,26

Analysis of Skin of Color Photographs in Infectious Disease Lectures—In addition, lectures discussing infectious etiologies were among those with the highest proportion of skin of color photographs. This relatively disproportionate representation of skin of color compared to the other lectures may contribute to the development of harmful stereotypes or the stigmatization of skin of color patients. Although skin of color should continue to be represented in similar lectures, teaching faculty should remain mindful of the potential unintended impact from lectures including relatively disproportionate amounts of skin of color, particularly when other lectures may have sparse to absent representation of skin of color.

More Photographs Available for Education—Overall, our findings may help to inform changes to preclinical dermatology medical education at other institutions to create more inclusive and representative curricula for skin of color patients. The ability of instructors to provide visual representation of various dermatologic conditions may be limited by the photographs available in certain textbooks with few examples of patients with skin of color; however, concerns regarding the lack of skin of color representation in dermatology training is not a novel discussion.17 Although it is the responsibility of all dermatologists to advocate for the inclusion of skin of color, many dermatologists of color have been leading the way in this movement for decades, publishing several textbooks to document various skin conditions in those with darker skin types and discuss unique considerations for patients with skin of color.27-29 Images from these textbooks can be utilized by programs to increase representation of skin of color in dermatology training. There also are multiple expanding online dermatologic databases, such as VisualDx, with an increasing focus on skin of color patients, some of which allow users to filter images by degree of skin pigmentation.30 Moreover, instructors also can work to diversify their curricula by highlighting more of the SOCS conditions of importance to skin of color patients, which have since been renamed and highlighted on the Patient Dermatology Education section of the SOCS website.20 These conditions, while not completely comprehensive, provide a useful starting point for medical educators to reevaluate for potential areas of improvement and inclusion.

There are several potential strategies that can be used to better represent skin of color in dermatologic preclinical medical education, including increasing awareness, especially among dermatology teaching faculty, of existing disparities in the representation of skin of color in the preclinical curricula. Additionally, all dermatology teaching materials could be reviewed at the department level prior to being disseminated to medical students to assess for instances in which skin of color could be prioritized for discussion or varying disease presentations in skin of color could be demonstrated. Finally, teaching faculty may consider photographing more clinical images of their skin of color patients to further develop a catalog of diverse images that can be used to teach students.

Study Limitations—Our study was unable to account for verbal discussion of skin of color not otherwise denoted or captured in lecture slides. Additional limitations include the utilization of Fitzpatrick skin types to describe and differentiate varying skin tones, as the Fitzpatrick scale originally was developed as a method to describe an individual’s response to UV exposure.19 The inability to further delineate the representation of darker skin types, such as those that may be classified as Fitzpatrick skin types V or VI,19 compared to those with lighter skin of color also was a limiting factor. This study was unable to assess for discussion of other common conditions affecting skin of color patients that were not listed as one of the priority conditions by SOCS. Photographs that were designated as indeterminate were difficult to elucidate as skin of color; however, it is possible that instructors may have verbally described these images as skin of color during lectures. Nonetheless, it may be beneficial for learners if teaching faculty were to clearly label instances where skin of color patients are shown or when notable differences are present.

 

 

Conclusion

Future studies would benefit from the inclusion of audio data from lectures, syllabi, and small group teaching materials from preclinical courses to more accurately assess representation of skin of color in dermatology training. Additionally, future studies also may expand to include images from lectures of overlapping clinical specialties, particularly infectious disease and rheumatology, to provide a broader assessment of skin of color exposure. Furthermore, repeat assessment may be beneficial to assess the longitudinal effectiveness of curricular changes at the institutions included in this study, comparing older lectures to more recent, updated lectures. This study also may be replicated at other medical schools to allow for wider comparison of curricula.

Acknowledgment—The authors wish to thank the institutions that offered and agreed to participate in this study with the hopes of improving medical education.

References
  1. Colby SL, Ortman JM. Projections of the size and composition of the US population: 2014 to 2060. United States Census Bureau website. Published March 2015. Accessed September 14, 2021. https://www.census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf
  2. Learn more about SOCS. Skin of Color Society website. Accessed September 14, 2021. http://skinofcolorsociety.org/about-socs/
  3. Taylor SC. Skin of color: biology, structure, function, and implications for dermatologic disease. J Am Acad Dermatol. 2002;46(suppl 2):S41-S62.
  4. Berardesca E, Maibach H. Ethnic skin: overview of structure and function. J Am Acad Dermatol. 2003;48(suppl 6):S139-S142.
  5. Callender VD, Surin-Lord SS, Davis EC, et al. Postinflammatory hyperpigmentation. Am J Clin Dermatol. 2011;12:87-99.
  6. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
  7. Grimes PE, Stockton T. Pigmentary disorders in blacks. Dermatol Clin. 1988;6:271-281.
  8. Halder RM, Nootheti PK. Ethnic skin disorders overview. J Am Acad Dermatol. 2003;48(suppl 6):S143-S148.
  9. Alexis AF, Sergay AB, Taylor SC. Common dermatologic disorders in skin of color: a comparative practice survey. Cutis. 2007;80:387-394.
  10. Callender VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  11. Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7:16-24.
  12. McCleskey PE, Gilson RT, DeVillez RL. Medical student core curriculum in dermatology survey. J Am Acad Dermatol. 2009;61:30-35.
  13. Ramsay DL, Mayer F. National survey of undergraduate dermatologic medical education. Arch Dermatol.1985;121:1529-1530.
  14. Hansra NK, O’Sullivan P, Chen CL, et al. Medical school dermatology curriculum: are we adequately preparing primary care physicians? J Am Acad Dermatol. 2009;61:23-29.
  15. Buster KJ, Stevens EI, Elmets CA. Dermatologic health disparities. Dermatol Clin. 2012;30:53-59, viii.
  16. Knable A, Hood AF, Pearson TG. Undergraduate medical education in dermatology: report from the AAD Interdisciplinary Education Committee, Subcommittee on Undergraduate Medical Education. J Am Acad Dermatol. 1997;36:467-470.
  17. Ebede T, Papier A. Disparities in dermatology educational resources. J Am Acad Dermatol. 2006;55:687-690.
  18. Skochelak SE, Stack SJ. Creating the medical schools of the future. Acad Med. 2017;92:16-19.
  19. Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol. 1988;124:869-871.
  20. Skin of Color Society. Patient dermatology education. Accessed September 22, 2021. https://skinofcolorsociety.org/patient-dermatology-education
  21. QuickFacts: United States. US Census Bureau website. Updated July 1, 2019. Accessed September 14, 2021. https://www.census.gov/quickfacts/fact/table/US#
  22. Kaufman BP, Alexis AF. Psoriasis in skin of color: insights into the epidemiology, clinical presentation, genetics, quality-of-life impact, and treatment of psoriasis in non-white racial/ethnic groups. Am J Clin Dermatol. 2018;19:405-423.
  23. Bradford PT, Goldstein AM, McMaster ML, et al. Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Arch Dermatol. 2009;145:427-434.
  24. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dermatol. 2016;75:983-991.
  25. Pipitone M, Robinson JK, Camara C, et al. Skin cancer awareness in suburban employees: a Hispanic perspective. J Am Acad Dermatol. 2002;47:118-123.
  26. Imahiyerobo-Ip J, Ip I, Jamal S, et al. Skin cancer awareness in communities of color. J Am Acad Dermatol. 2011;64:198-200.
  27. Taylor SSC, Serrano AMA, Kelly AP, et al, eds. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. McGraw-Hill Education; 2016.
  28. Dadzie OE, Petit A, Alexis AF, eds. Ethnic Dermatology: Principles and Practice. Wiley-Blackwell; 2013.
  29. Jackson-Richards D, Pandya AG, eds. Dermatology Atlas for Skin of Color. Springer; 2014.
  30. VisualDx. New VisualDx feature: skin of color sort. Published October 14, 2020. Accessed September 22, 2021. https://www.visualdx.com/blog/new-visualdx-feature-skin-of-color-sort/
References
  1. Colby SL, Ortman JM. Projections of the size and composition of the US population: 2014 to 2060. United States Census Bureau website. Published March 2015. Accessed September 14, 2021. https://www.census.gov/content/dam/Census/library/publications/2015/demo/p25-1143.pdf
  2. Learn more about SOCS. Skin of Color Society website. Accessed September 14, 2021. http://skinofcolorsociety.org/about-socs/
  3. Taylor SC. Skin of color: biology, structure, function, and implications for dermatologic disease. J Am Acad Dermatol. 2002;46(suppl 2):S41-S62.
  4. Berardesca E, Maibach H. Ethnic skin: overview of structure and function. J Am Acad Dermatol. 2003;48(suppl 6):S139-S142.
  5. Callender VD, Surin-Lord SS, Davis EC, et al. Postinflammatory hyperpigmentation. Am J Clin Dermatol. 2011;12:87-99.
  6. Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010;3:20-31.
  7. Grimes PE, Stockton T. Pigmentary disorders in blacks. Dermatol Clin. 1988;6:271-281.
  8. Halder RM, Nootheti PK. Ethnic skin disorders overview. J Am Acad Dermatol. 2003;48(suppl 6):S143-S148.
  9. Alexis AF, Sergay AB, Taylor SC. Common dermatologic disorders in skin of color: a comparative practice survey. Cutis. 2007;80:387-394.
  10. Callender VD. Acne in ethnic skin: special considerations for therapy. Dermatol Ther. 2004;17:184-195.
  11. Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7:16-24.
  12. McCleskey PE, Gilson RT, DeVillez RL. Medical student core curriculum in dermatology survey. J Am Acad Dermatol. 2009;61:30-35.
  13. Ramsay DL, Mayer F. National survey of undergraduate dermatologic medical education. Arch Dermatol.1985;121:1529-1530.
  14. Hansra NK, O’Sullivan P, Chen CL, et al. Medical school dermatology curriculum: are we adequately preparing primary care physicians? J Am Acad Dermatol. 2009;61:23-29.
  15. Buster KJ, Stevens EI, Elmets CA. Dermatologic health disparities. Dermatol Clin. 2012;30:53-59, viii.
  16. Knable A, Hood AF, Pearson TG. Undergraduate medical education in dermatology: report from the AAD Interdisciplinary Education Committee, Subcommittee on Undergraduate Medical Education. J Am Acad Dermatol. 1997;36:467-470.
  17. Ebede T, Papier A. Disparities in dermatology educational resources. J Am Acad Dermatol. 2006;55:687-690.
  18. Skochelak SE, Stack SJ. Creating the medical schools of the future. Acad Med. 2017;92:16-19.
  19. Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol. 1988;124:869-871.
  20. Skin of Color Society. Patient dermatology education. Accessed September 22, 2021. https://skinofcolorsociety.org/patient-dermatology-education
  21. QuickFacts: United States. US Census Bureau website. Updated July 1, 2019. Accessed September 14, 2021. https://www.census.gov/quickfacts/fact/table/US#
  22. Kaufman BP, Alexis AF. Psoriasis in skin of color: insights into the epidemiology, clinical presentation, genetics, quality-of-life impact, and treatment of psoriasis in non-white racial/ethnic groups. Am J Clin Dermatol. 2018;19:405-423.
  23. Bradford PT, Goldstein AM, McMaster ML, et al. Acral lentiginous melanoma: incidence and survival patterns in the United States, 1986-2005. Arch Dermatol. 2009;145:427-434.
  24. Dawes SM, Tsai S, Gittleman H, et al. Racial disparities in melanoma survival. J Am Acad Dermatol. 2016;75:983-991.
  25. Pipitone M, Robinson JK, Camara C, et al. Skin cancer awareness in suburban employees: a Hispanic perspective. J Am Acad Dermatol. 2002;47:118-123.
  26. Imahiyerobo-Ip J, Ip I, Jamal S, et al. Skin cancer awareness in communities of color. J Am Acad Dermatol. 2011;64:198-200.
  27. Taylor SSC, Serrano AMA, Kelly AP, et al, eds. Taylor and Kelly’s Dermatology for Skin of Color. 2nd ed. McGraw-Hill Education; 2016.
  28. Dadzie OE, Petit A, Alexis AF, eds. Ethnic Dermatology: Principles and Practice. Wiley-Blackwell; 2013.
  29. Jackson-Richards D, Pandya AG, eds. Dermatology Atlas for Skin of Color. Springer; 2014.
  30. VisualDx. New VisualDx feature: skin of color sort. Published October 14, 2020. Accessed September 22, 2021. https://www.visualdx.com/blog/new-visualdx-feature-skin-of-color-sort/
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Skin of Color in Preclinical Medical Education: A Cross-Institutional Comparison and A Call to Action
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  • The United States rapidly is becoming a country in which the majority of citizens will have skin of color.
  • Our study results strongly suggest that skin of color may be seriously underrepresented in medical education and can guide modifications to preclinical dermatology medical education to develop a more comprehensive and inclusive curriculum.
  • Efforts should be made to increase images and discussion of skin of color in preclinical didactics.
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