Dermatology

Click here to view more from Federal Health Care Data Trends 2025.

Click here to view more from Federal Health Care Data Trends 2025.

Click here to view more from Federal Health Care Data Trends 2025.

Pseudofolliculitis barbae (PFB), also known as razor bumps, is a common inflammatory condition characterized by papules and pustules that typically appear in the beard and cheek regions. It occurs when shaved hair regrows and penetrates the skin, leading to irritation and inflammation. While anyone who shaves can develop PFB, it is more prevalent and severe in individuals with naturally tightly coiled, coarse-textured hair.^1,2 PFB is common in individuals who shave frequently due to personal choice or profession, such as members of the US military^3,4 and firefighters, who are required to remain clean shaven for safety (eg, ensuring proper fit of a respirator mask).⁵ Early diagnosis and treatment of PFB are essential to prevent long-term complications such as scarring or hyperpigmentation, which may be more severe in those with darker skin tones.

Epidemiology

PFB is most common in Black men, affecting 45% to 83% of men of African ancestry.^1,2 This condition also can affect individuals of various ethnicities with coarse or curly hair. The spiral shape of the hair increases the likelihood that it will regrow into the skin after shaving.⁶ Women with hirsutism who shave also can develop PFB.

Key Clinical Features

The papules and pustules seen in PFB may be flesh colored, erythematous, hyperpigmented, brown, or violaceous. Erythema may be less pronounced in darker vs lighter skin tones. Persistent and severe postinflammatory hyperpigmentation may occur, and hypertrophic or keloidal scars may develop in affected areas. Dermoscopy may reveal extrafollicular hair penetration as well as follicular or perifollicular pustules accompanied by hyperkeratosis.

Worth Noting

The most effective management for PFB is to discontinue shaving.¹ If shaving is desired or necessary, it is recommended that patients apply lukewarm water to the affected area followed by a generous amount of shaving foam or gel to create a protective antifriction layer that allows the razor to glide more smoothly over the skin and reduces subsequent irritation.² Using the right razor technology also may help alleviate symptoms. Research has shown that multiblade razors used in conjunction with preshave hair hydration and postshave moisturization do not worsen PFB.² A recent study found that multiblade razor technology paired with use of a shave foam or gel actually improved skin appearance in patients with PFB.⁷

It is important to direct patients to shave in the direction of hair growth; however, this may not be possible for individuals with curly or coarse hair, as the hair may grow in many directions.^8,9 Patients also should avoid pulling the skin taut while shaving, as doing so allows the hair to be clipped below the surface, where it can repenetrate the skin and cause further irritation. As an alternative to shaving with a razor, patients can use hair clippers to trim beard hair, which leaves behind stubble and interrupts the cycle of retracted hairs under the skin. Nd:YAG laser therapy has demonstrated efficacy in reduction of PFB papules and pustules.^9-12 Greater mean improvement in inflammatory papules and reduction in hair density was noted in participants who received Nd:YAG laser plus eflornithine compared with those who received the laser or eflornithine alone.¹¹ Patients should not pluck or dig into the skin to remove any ingrown hairs. If a tweezer is used, the patient should gently lift the tip of the ingrown hair with the tweezer to dislodge it from the skin and prevent plucking out the hair completely.

To help manage inflammation after shaving, topical treatments such as benzoyl peroxide 5%/clindamycin 1% gel can be used.^3,13 A low-potency steroid such as topical hydrocortisone 2.5% applied once or twice daily for up to 2 to 3 days may be helpful.^1,14 Adjunctive treatments including keratolytics (eg, topical retinoids, hydroxy acids) reduce perifollicular hyperkeratosis.^14,15 Agents containing alpha hydroxy acids (eg, glycolic acid) also can decrease the curvature of the hair itself by reducing the sulfhydryl bonds.⁶ If secondary bacterial infections occur, oral antibiotics (eg, doxycycline) may be necessary.

Health Disparity Highlight

Individuals with darker skin tones are at higher risk for PFB and associated complications. Limited access to dermatology services may further exacerbate these challenges. Individuals with PFB may not seek medical treatment until the condition becomes severe. Clinicians also may underestimate the severity of PFB—particularly in those with darker skin tones—based on erythema alone because it may be less pronounced in darker vs lighter skin tones.¹⁶

While permanent hair reduction with laser therapy is a treatment option for PFB, it may be inaccessible to some patients because it can be expensive and is coded as a cosmetic procedure. Additionally, patients may not have access to specialists who are experienced in performing the procedure in those with darker skin tones.⁹ Some patients also may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons.¹⁷

Pseudofolliculitis barbae also has been linked to professional disparities. One study found that members of the US Air Force who had medical shaving waivers experienced longer times to promotion than those with no waiver.¹⁸ Delays in promotion may be linked to perceptions of unprofessionalism, exclusion from high-profile duties, and concerns about career progression. While this delay was similar for individuals of all races, the majority of those in the waiver group were Black/African American. In 2021, 4 Black firefighters with PFB were unsuccessful in their bid to get a medical accommodation regarding a New York City Fire Department policy requiring them to be clean shaven where the oxygen mask seals against the skin.⁵ More research is needed on mask safety and efficiency relative to the length of facial hair. Accommodations or tailored masks for facial hair conditions also are necessary so individuals with PFB can meet job requirements while managing their condition.

Pseudofolliculitis barbae (PFB), also known as razor bumps, is a common inflammatory condition characterized by papules and pustules that typically appear in the beard and cheek regions. It occurs when shaved hair regrows and penetrates the skin, leading to irritation and inflammation. While anyone who shaves can develop PFB, it is more prevalent and severe in individuals with naturally tightly coiled, coarse-textured hair.^1,2 PFB is common in individuals who shave frequently due to personal choice or profession, such as members of the US military^3,4 and firefighters, who are required to remain clean shaven for safety (eg, ensuring proper fit of a respirator mask).⁵ Early diagnosis and treatment of PFB are essential to prevent long-term complications such as scarring or hyperpigmentation, which may be more severe in those with darker skin tones.

Epidemiology

PFB is most common in Black men, affecting 45% to 83% of men of African ancestry.^1,2 This condition also can affect individuals of various ethnicities with coarse or curly hair. The spiral shape of the hair increases the likelihood that it will regrow into the skin after shaving.⁶ Women with hirsutism who shave also can develop PFB.

Key Clinical Features

The papules and pustules seen in PFB may be flesh colored, erythematous, hyperpigmented, brown, or violaceous. Erythema may be less pronounced in darker vs lighter skin tones. Persistent and severe postinflammatory hyperpigmentation may occur, and hypertrophic or keloidal scars may develop in affected areas. Dermoscopy may reveal extrafollicular hair penetration as well as follicular or perifollicular pustules accompanied by hyperkeratosis.

Worth Noting

The most effective management for PFB is to discontinue shaving.¹ If shaving is desired or necessary, it is recommended that patients apply lukewarm water to the affected area followed by a generous amount of shaving foam or gel to create a protective antifriction layer that allows the razor to glide more smoothly over the skin and reduces subsequent irritation.² Using the right razor technology also may help alleviate symptoms. Research has shown that multiblade razors used in conjunction with preshave hair hydration and postshave moisturization do not worsen PFB.² A recent study found that multiblade razor technology paired with use of a shave foam or gel actually improved skin appearance in patients with PFB.⁷

It is important to direct patients to shave in the direction of hair growth; however, this may not be possible for individuals with curly or coarse hair, as the hair may grow in many directions.^8,9 Patients also should avoid pulling the skin taut while shaving, as doing so allows the hair to be clipped below the surface, where it can repenetrate the skin and cause further irritation. As an alternative to shaving with a razor, patients can use hair clippers to trim beard hair, which leaves behind stubble and interrupts the cycle of retracted hairs under the skin. Nd:YAG laser therapy has demonstrated efficacy in reduction of PFB papules and pustules.^9-12 Greater mean improvement in inflammatory papules and reduction in hair density was noted in participants who received Nd:YAG laser plus eflornithine compared with those who received the laser or eflornithine alone.¹¹ Patients should not pluck or dig into the skin to remove any ingrown hairs. If a tweezer is used, the patient should gently lift the tip of the ingrown hair with the tweezer to dislodge it from the skin and prevent plucking out the hair completely.

To help manage inflammation after shaving, topical treatments such as benzoyl peroxide 5%/clindamycin 1% gel can be used.^3,13 A low-potency steroid such as topical hydrocortisone 2.5% applied once or twice daily for up to 2 to 3 days may be helpful.^1,14 Adjunctive treatments including keratolytics (eg, topical retinoids, hydroxy acids) reduce perifollicular hyperkeratosis.^14,15 Agents containing alpha hydroxy acids (eg, glycolic acid) also can decrease the curvature of the hair itself by reducing the sulfhydryl bonds.⁶ If secondary bacterial infections occur, oral antibiotics (eg, doxycycline) may be necessary.

Health Disparity Highlight

Individuals with darker skin tones are at higher risk for PFB and associated complications. Limited access to dermatology services may further exacerbate these challenges. Individuals with PFB may not seek medical treatment until the condition becomes severe. Clinicians also may underestimate the severity of PFB—particularly in those with darker skin tones—based on erythema alone because it may be less pronounced in darker vs lighter skin tones.¹⁶

While permanent hair reduction with laser therapy is a treatment option for PFB, it may be inaccessible to some patients because it can be expensive and is coded as a cosmetic procedure. Additionally, patients may not have access to specialists who are experienced in performing the procedure in those with darker skin tones.⁹ Some patients also may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons.¹⁷

Pseudofolliculitis barbae also has been linked to professional disparities. One study found that members of the US Air Force who had medical shaving waivers experienced longer times to promotion than those with no waiver.¹⁸ Delays in promotion may be linked to perceptions of unprofessionalism, exclusion from high-profile duties, and concerns about career progression. While this delay was similar for individuals of all races, the majority of those in the waiver group were Black/African American. In 2021, 4 Black firefighters with PFB were unsuccessful in their bid to get a medical accommodation regarding a New York City Fire Department policy requiring them to be clean shaven where the oxygen mask seals against the skin.⁵ More research is needed on mask safety and efficiency relative to the length of facial hair. Accommodations or tailored masks for facial hair conditions also are necessary so individuals with PFB can meet job requirements while managing their condition.

Pseudofolliculitis barbae (PFB), also known as razor bumps, is a common inflammatory condition characterized by papules and pustules that typically appear in the beard and cheek regions. It occurs when shaved hair regrows and penetrates the skin, leading to irritation and inflammation. While anyone who shaves can develop PFB, it is more prevalent and severe in individuals with naturally tightly coiled, coarse-textured hair.^1,2 PFB is common in individuals who shave frequently due to personal choice or profession, such as members of the US military^3,4 and firefighters, who are required to remain clean shaven for safety (eg, ensuring proper fit of a respirator mask).⁵ Early diagnosis and treatment of PFB are essential to prevent long-term complications such as scarring or hyperpigmentation, which may be more severe in those with darker skin tones.

Epidemiology

PFB is most common in Black men, affecting 45% to 83% of men of African ancestry.^1,2 This condition also can affect individuals of various ethnicities with coarse or curly hair. The spiral shape of the hair increases the likelihood that it will regrow into the skin after shaving.⁶ Women with hirsutism who shave also can develop PFB.

Key Clinical Features

The papules and pustules seen in PFB may be flesh colored, erythematous, hyperpigmented, brown, or violaceous. Erythema may be less pronounced in darker vs lighter skin tones. Persistent and severe postinflammatory hyperpigmentation may occur, and hypertrophic or keloidal scars may develop in affected areas. Dermoscopy may reveal extrafollicular hair penetration as well as follicular or perifollicular pustules accompanied by hyperkeratosis.

Worth Noting

The most effective management for PFB is to discontinue shaving.¹ If shaving is desired or necessary, it is recommended that patients apply lukewarm water to the affected area followed by a generous amount of shaving foam or gel to create a protective antifriction layer that allows the razor to glide more smoothly over the skin and reduces subsequent irritation.² Using the right razor technology also may help alleviate symptoms. Research has shown that multiblade razors used in conjunction with preshave hair hydration and postshave moisturization do not worsen PFB.² A recent study found that multiblade razor technology paired with use of a shave foam or gel actually improved skin appearance in patients with PFB.⁷

It is important to direct patients to shave in the direction of hair growth; however, this may not be possible for individuals with curly or coarse hair, as the hair may grow in many directions.^8,9 Patients also should avoid pulling the skin taut while shaving, as doing so allows the hair to be clipped below the surface, where it can repenetrate the skin and cause further irritation. As an alternative to shaving with a razor, patients can use hair clippers to trim beard hair, which leaves behind stubble and interrupts the cycle of retracted hairs under the skin. Nd:YAG laser therapy has demonstrated efficacy in reduction of PFB papules and pustules.^9-12 Greater mean improvement in inflammatory papules and reduction in hair density was noted in participants who received Nd:YAG laser plus eflornithine compared with those who received the laser or eflornithine alone.¹¹ Patients should not pluck or dig into the skin to remove any ingrown hairs. If a tweezer is used, the patient should gently lift the tip of the ingrown hair with the tweezer to dislodge it from the skin and prevent plucking out the hair completely.

To help manage inflammation after shaving, topical treatments such as benzoyl peroxide 5%/clindamycin 1% gel can be used.^3,13 A low-potency steroid such as topical hydrocortisone 2.5% applied once or twice daily for up to 2 to 3 days may be helpful.^1,14 Adjunctive treatments including keratolytics (eg, topical retinoids, hydroxy acids) reduce perifollicular hyperkeratosis.^14,15 Agents containing alpha hydroxy acids (eg, glycolic acid) also can decrease the curvature of the hair itself by reducing the sulfhydryl bonds.⁶ If secondary bacterial infections occur, oral antibiotics (eg, doxycycline) may be necessary.

Health Disparity Highlight

Individuals with darker skin tones are at higher risk for PFB and associated complications. Limited access to dermatology services may further exacerbate these challenges. Individuals with PFB may not seek medical treatment until the condition becomes severe. Clinicians also may underestimate the severity of PFB—particularly in those with darker skin tones—based on erythema alone because it may be less pronounced in darker vs lighter skin tones.¹⁶

While permanent hair reduction with laser therapy is a treatment option for PFB, it may be inaccessible to some patients because it can be expensive and is coded as a cosmetic procedure. Additionally, patients may not have access to specialists who are experienced in performing the procedure in those with darker skin tones.⁹ Some patients also may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons.¹⁷

Pseudofolliculitis barbae also has been linked to professional disparities. One study found that members of the US Air Force who had medical shaving waivers experienced longer times to promotion than those with no waiver.¹⁸ Delays in promotion may be linked to perceptions of unprofessionalism, exclusion from high-profile duties, and concerns about career progression. While this delay was similar for individuals of all races, the majority of those in the waiver group were Black/African American. In 2021, 4 Black firefighters with PFB were unsuccessful in their bid to get a medical accommodation regarding a New York City Fire Department policy requiring them to be clean shaven where the oxygen mask seals against the skin.⁵ More research is needed on mask safety and efficiency relative to the length of facial hair. Accommodations or tailored masks for facial hair conditions also are necessary so individuals with PFB can meet job requirements while managing their condition.

The US military has revised its grooming standards to remove medical exemptions for male facial hair, a policy change that may put careers at risk for thousands of service members. According to the updated guidelines, all soldiers must be clean-shaven on duty when in uniform or civilian clothes, with temporary exemptions for medical reasons and permanent exemptions for religious accommodations. 

The Army is the latest service branch to update its guidelines about beards: Soldiers with skin conditions will no longer be granted permanent medical waivers that allow them to avoid shaving. The Air Force and Space Force updated their guidance on grooming waivers in January, as did the Marine Corps in March. 

Defense Secretary Pete Hegseth, who ordered the guideline review, focused on grooming and appearance. In a Feb. 7 townhall with troops and department employees, he said, “It starts with the basic stuff, right? It’s grooming standards and uniform standards and training standards, fitness standards, all of that matters.”

Hegseth compared not enforcing grooming standards to the “broken windows” theory of policing: “I’m not saying if you violate grooming standards, you’re a criminal. The analogy is incomplete. But if you violate the small stuff and you allow it to happen, it creates a culture where the big stuff, you’re not held accountable for.”

The policy changes are particularly significant for soldiers who grow beards because they suffer from pseudofolliculitis barbae (PFB), an often-painful genetic condition that causes ingrown hairs. PFB produces flesh-colored or red follicular papules, which can be itchy, tender, and may bleed when shaved. Even if they heal, the lesions may lead to postinflammatory hyperpigmentation, scarring (including keloid scarring), and abscess. 

Although the updated standards affect all service members with beards, they draw ire from those who claim the rules disproportionately affect men of African descent. Up to 60% of Black men have PFB, according to the American Osteopathic College of Dermatology. According to the US Department of Defense (DoD) 2023 Demographics: Profile of the Military Community, service members who self-identify as Black or African American make up 17% of the total DoD military force (N = 2,034,426). Of 1,273,382 active-duty members, 18% are Black. Of 1,038,909 active-duty enlisted members, 20% are Black, and 9% of 234,473 active-duty officers are Black.

“Almost 65% of the US Air Force shaving waivers are held by Black men. And PFB is one of the most common reasons,” DanTasia Welch, MS, told Federal Practitioner. She, along with Richard P. Usatine, MD, and Candrice R. Heath, MD, wrote a recent review of the impact of PFB that was published in Federal Practitioner. 

“It is almost exclusively found in men of African descent,” Usatine said. “That just means if you have a policy that affects people with this condition, you are basically aiming that policy directly at Black men.”

“Pseudofolliculitis barbae, a lot of that just has to do with your shaving technique is what we’ve determined,” Steve Warren, an Army spokesman, told reporters in early July. “A vast majority of minority soldiers, African American soldiers, are within the standards all the time.” 

Usatine disagreed: “[PFB] is genetic, and whether you shave with or against the direction of the hairs, the problem is still there, and you can't just shave it away by ‘shaving correctly.’ They're going after one racial/ethnic group who has this problem, because almost everyone that has the problem is of African descent.”

The most effective management for PFB is to discontinue shaving. Grooming techniques and topical medications can be effective in treating mild-to-moderate cases of PFB, but more severe cases respond best to laser therapy. The Army, Navy, and Marine Corps advise laser therapy as a treatment option, but it has drawbacks. It is expensive and coded as a cosmetic procedure, and patients also may not have access to specialists experienced in performing the procedure in people with darker skin tones. Some patients may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons. 

A survey of Air Force members with 10,383 responses suggested that the men who had medical shaving waivers experienced longer times to promotion than those with no waiver. Most in the waiver group were Black or African American. 

The branches have handled the rule change in different ways. The Air Force, for example, which began tightening its standards on uniform and shaving waivers in January 2025, grants long-term shaving waivers only to airmen or guardians who have severe cases of PFB following consultation with medical practitioners. Air Force Surgeon General Lt. Gen. John DeGoes said in a video that the department’s 2020 (now expired) policy allowing 5-year shaving waivers did not give clinicians enough clarity on diagnosis by not differentiating between PFB and shaving irritation.

“They are 2 different things,” DeGoes said. “Ensuring a standardized approach to managing PFB is essential. And it is crucial that we provide consistent and effective care to our service members, enabling them to meet grooming standards while managing their condition.”

The new grooming policies leave many service members in an uncomfortable quandary: Keep the beard, run the risk of getting kicked out; keep shaving and put your skin and health at risk for complications; or receive laser treatment and have to deal with lack of beard hair after leaving the military.

Simply changing the rules isn’t enough. Candrice Heath, MD, told Federal Practitioner, “You need to always strike a balance. One of those points that’s always raised is about the facial equipment that's needed to protect during times of war.”

Heath called for more research funding to develop equipment, so people can have some facial hair if needed. “There is an opportunity to not just say, hey, this is an issue, but there's an opportunity for innovation here, to really think about it this problem in a different way, so that we are solution-focused.”

The US military has revised its grooming standards to remove medical exemptions for male facial hair, a policy change that may put careers at risk for thousands of service members. According to the updated guidelines, all soldiers must be clean-shaven on duty when in uniform or civilian clothes, with temporary exemptions for medical reasons and permanent exemptions for religious accommodations. 

The Army is the latest service branch to update its guidelines about beards: Soldiers with skin conditions will no longer be granted permanent medical waivers that allow them to avoid shaving. The Air Force and Space Force updated their guidance on grooming waivers in January, as did the Marine Corps in March. 

Defense Secretary Pete Hegseth, who ordered the guideline review, focused on grooming and appearance. In a Feb. 7 townhall with troops and department employees, he said, “It starts with the basic stuff, right? It’s grooming standards and uniform standards and training standards, fitness standards, all of that matters.”

Hegseth compared not enforcing grooming standards to the “broken windows” theory of policing: “I’m not saying if you violate grooming standards, you’re a criminal. The analogy is incomplete. But if you violate the small stuff and you allow it to happen, it creates a culture where the big stuff, you’re not held accountable for.”

The policy changes are particularly significant for soldiers who grow beards because they suffer from pseudofolliculitis barbae (PFB), an often-painful genetic condition that causes ingrown hairs. PFB produces flesh-colored or red follicular papules, which can be itchy, tender, and may bleed when shaved. Even if they heal, the lesions may lead to postinflammatory hyperpigmentation, scarring (including keloid scarring), and abscess. 

Although the updated standards affect all service members with beards, they draw ire from those who claim the rules disproportionately affect men of African descent. Up to 60% of Black men have PFB, according to the American Osteopathic College of Dermatology. According to the US Department of Defense (DoD) 2023 Demographics: Profile of the Military Community, service members who self-identify as Black or African American make up 17% of the total DoD military force (N = 2,034,426). Of 1,273,382 active-duty members, 18% are Black. Of 1,038,909 active-duty enlisted members, 20% are Black, and 9% of 234,473 active-duty officers are Black.

“Almost 65% of the US Air Force shaving waivers are held by Black men. And PFB is one of the most common reasons,” DanTasia Welch, MS, told Federal Practitioner. She, along with Richard P. Usatine, MD, and Candrice R. Heath, MD, wrote a recent review of the impact of PFB that was published in Federal Practitioner. 

“It is almost exclusively found in men of African descent,” Usatine said. “That just means if you have a policy that affects people with this condition, you are basically aiming that policy directly at Black men.”

“Pseudofolliculitis barbae, a lot of that just has to do with your shaving technique is what we’ve determined,” Steve Warren, an Army spokesman, told reporters in early July. “A vast majority of minority soldiers, African American soldiers, are within the standards all the time.” 

Usatine disagreed: “[PFB] is genetic, and whether you shave with or against the direction of the hairs, the problem is still there, and you can't just shave it away by ‘shaving correctly.’ They're going after one racial/ethnic group who has this problem, because almost everyone that has the problem is of African descent.”

The most effective management for PFB is to discontinue shaving. Grooming techniques and topical medications can be effective in treating mild-to-moderate cases of PFB, but more severe cases respond best to laser therapy. The Army, Navy, and Marine Corps advise laser therapy as a treatment option, but it has drawbacks. It is expensive and coded as a cosmetic procedure, and patients also may not have access to specialists experienced in performing the procedure in people with darker skin tones. Some patients may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons. 

A survey of Air Force members with 10,383 responses suggested that the men who had medical shaving waivers experienced longer times to promotion than those with no waiver. Most in the waiver group were Black or African American. 

The branches have handled the rule change in different ways. The Air Force, for example, which began tightening its standards on uniform and shaving waivers in January 2025, grants long-term shaving waivers only to airmen or guardians who have severe cases of PFB following consultation with medical practitioners. Air Force Surgeon General Lt. Gen. John DeGoes said in a video that the department’s 2020 (now expired) policy allowing 5-year shaving waivers did not give clinicians enough clarity on diagnosis by not differentiating between PFB and shaving irritation.

“They are 2 different things,” DeGoes said. “Ensuring a standardized approach to managing PFB is essential. And it is crucial that we provide consistent and effective care to our service members, enabling them to meet grooming standards while managing their condition.”

The new grooming policies leave many service members in an uncomfortable quandary: Keep the beard, run the risk of getting kicked out; keep shaving and put your skin and health at risk for complications; or receive laser treatment and have to deal with lack of beard hair after leaving the military.

Simply changing the rules isn’t enough. Candrice Heath, MD, told Federal Practitioner, “You need to always strike a balance. One of those points that’s always raised is about the facial equipment that's needed to protect during times of war.”

Heath called for more research funding to develop equipment, so people can have some facial hair if needed. “There is an opportunity to not just say, hey, this is an issue, but there's an opportunity for innovation here, to really think about it this problem in a different way, so that we are solution-focused.”

The US military has revised its grooming standards to remove medical exemptions for male facial hair, a policy change that may put careers at risk for thousands of service members. According to the updated guidelines, all soldiers must be clean-shaven on duty when in uniform or civilian clothes, with temporary exemptions for medical reasons and permanent exemptions for religious accommodations. 

The Army is the latest service branch to update its guidelines about beards: Soldiers with skin conditions will no longer be granted permanent medical waivers that allow them to avoid shaving. The Air Force and Space Force updated their guidance on grooming waivers in January, as did the Marine Corps in March. 

Defense Secretary Pete Hegseth, who ordered the guideline review, focused on grooming and appearance. In a Feb. 7 townhall with troops and department employees, he said, “It starts with the basic stuff, right? It’s grooming standards and uniform standards and training standards, fitness standards, all of that matters.”

Hegseth compared not enforcing grooming standards to the “broken windows” theory of policing: “I’m not saying if you violate grooming standards, you’re a criminal. The analogy is incomplete. But if you violate the small stuff and you allow it to happen, it creates a culture where the big stuff, you’re not held accountable for.”

The policy changes are particularly significant for soldiers who grow beards because they suffer from pseudofolliculitis barbae (PFB), an often-painful genetic condition that causes ingrown hairs. PFB produces flesh-colored or red follicular papules, which can be itchy, tender, and may bleed when shaved. Even if they heal, the lesions may lead to postinflammatory hyperpigmentation, scarring (including keloid scarring), and abscess. 

Although the updated standards affect all service members with beards, they draw ire from those who claim the rules disproportionately affect men of African descent. Up to 60% of Black men have PFB, according to the American Osteopathic College of Dermatology. According to the US Department of Defense (DoD) 2023 Demographics: Profile of the Military Community, service members who self-identify as Black or African American make up 17% of the total DoD military force (N = 2,034,426). Of 1,273,382 active-duty members, 18% are Black. Of 1,038,909 active-duty enlisted members, 20% are Black, and 9% of 234,473 active-duty officers are Black.

“Almost 65% of the US Air Force shaving waivers are held by Black men. And PFB is one of the most common reasons,” DanTasia Welch, MS, told Federal Practitioner. She, along with Richard P. Usatine, MD, and Candrice R. Heath, MD, wrote a recent review of the impact of PFB that was published in Federal Practitioner. 

“It is almost exclusively found in men of African descent,” Usatine said. “That just means if you have a policy that affects people with this condition, you are basically aiming that policy directly at Black men.”

“Pseudofolliculitis barbae, a lot of that just has to do with your shaving technique is what we’ve determined,” Steve Warren, an Army spokesman, told reporters in early July. “A vast majority of minority soldiers, African American soldiers, are within the standards all the time.” 

Usatine disagreed: “[PFB] is genetic, and whether you shave with or against the direction of the hairs, the problem is still there, and you can't just shave it away by ‘shaving correctly.’ They're going after one racial/ethnic group who has this problem, because almost everyone that has the problem is of African descent.”

The most effective management for PFB is to discontinue shaving. Grooming techniques and topical medications can be effective in treating mild-to-moderate cases of PFB, but more severe cases respond best to laser therapy. The Army, Navy, and Marine Corps advise laser therapy as a treatment option, but it has drawbacks. It is expensive and coded as a cosmetic procedure, and patients also may not have access to specialists experienced in performing the procedure in people with darker skin tones. Some patients may not want to permanently reduce the amount of hair that grows in the beard area for personal or religious reasons. 

A survey of Air Force members with 10,383 responses suggested that the men who had medical shaving waivers experienced longer times to promotion than those with no waiver. Most in the waiver group were Black or African American. 

The branches have handled the rule change in different ways. The Air Force, for example, which began tightening its standards on uniform and shaving waivers in January 2025, grants long-term shaving waivers only to airmen or guardians who have severe cases of PFB following consultation with medical practitioners. Air Force Surgeon General Lt. Gen. John DeGoes said in a video that the department’s 2020 (now expired) policy allowing 5-year shaving waivers did not give clinicians enough clarity on diagnosis by not differentiating between PFB and shaving irritation.

“They are 2 different things,” DeGoes said. “Ensuring a standardized approach to managing PFB is essential. And it is crucial that we provide consistent and effective care to our service members, enabling them to meet grooming standards while managing their condition.”

The new grooming policies leave many service members in an uncomfortable quandary: Keep the beard, run the risk of getting kicked out; keep shaving and put your skin and health at risk for complications; or receive laser treatment and have to deal with lack of beard hair after leaving the military.

Simply changing the rules isn’t enough. Candrice Heath, MD, told Federal Practitioner, “You need to always strike a balance. One of those points that’s always raised is about the facial equipment that's needed to protect during times of war.”

Heath called for more research funding to develop equipment, so people can have some facial hair if needed. “There is an opportunity to not just say, hey, this is an issue, but there's an opportunity for innovation here, to really think about it this problem in a different way, so that we are solution-focused.”

DISCUSSION

A diagnosis of familial glomangiomatosis was made based on the clinical history and histopathologic findings from the punch biopsy. Glomus tumors are comprised of glomus cells, or undifferentiated smooth muscle cells responsible for thermoregulation.¹ Glomus tumors are classified into 3 categories: solid (predominantly glomus cells), glomangiomas (predominantly blood vessels), and glomangiomyomas (predominantly smooth muscle cells).² Glomangiomas, which comprise up to 20% of glomus tumors, typically present as bluish-purple, papular or nodular, hyperkeratotic lesions that are 2 to 10 mm in diameter.¹ These lesions are tender to palpation and pain may worsen with exposure to cold. Glomangiomas are associated with a classic triad of symptoms that include hypersensitivity, intermittent pain, and pinpoint pain, but patients rarely present with all 3.³

Glomangiomas tend to occur in areas rich with glomus bodies—the distal extremities—specifically the palms, wrists, forearms, feet, and subungual regions; visceral organ involvement including the GI tract is very rare.^1,4,5 About 38% to 68% of these lesions are hereditary or can be sporadic. If these lesions are hereditary, a patient is said to have familial glomangiomatosis. In familial glomangiomatosis, the glomulin gene is mutated in an autosomal dominant inheritance pattern with incomplete penetrance and variable expressivity. Inherited glomangiomas may present at birth or puberty similar to other vascular anomalies.⁴

Histopathology of glomangiomas shows rows of glomus cells (modified smooth muscle cells) surrounding distorted venous channels.^6,7 These lesions stain positive for CD34, vimentin, calponin, and α-smooth muscle actin, but are negative for desmin, S-100, and von Willebrand factor.^1,8 Although the patient’s medical history and physical examination are important in establishing the diagnosis, histopathology is confirmatory.

While the punch biopsy results were pending, a complete blood count (CBC) and fecal occult blood test (FOBT) were ordered due to concerns for blue rubber bleb nevus syndrome (BRBNS), a rare disorder with about 200 reported cases. Patients present with multiple blue to violaceous compressible nodules that feel rubbery in consistency and may be painful with compression. Lesions may be up to 5 cm in diameter and with time, the GI tract may also become involved.⁹ In the GI tract, the small bowel is the most common site of involvement and patients may present with severe iron deficiency anemia due to hemorrhage.¹⁰ Histopathologic features are nonspecific and have features of venous malformations but may include large, tortuous, dilated vessels with a single endothelial lining with possible smooth muscle in vessel walls or calcifications.¹¹ Due to concerns of BRBNS, laboratory studies (CBC and FOBT) were obtained but did not indicate the patient was experiencing a GI hemorrhage.

The differential diagnosis included Maffucci syndrome, also known as dyschondrodysplasia with hemangiomas, enchondromatosis with cavernous hemangiomas, or hemangiomatosis chondrodystrophic. Patients with Maffucci syndrome present with multiple enchondromas, soft tissue hemangiomas or lymphangiomas, and gliomas. These lesions tend to undergo malignant transformation from enchondromas to chondrosarcomas and hemangiomas to vascular sarcomas.¹² This diagnosis was less likely in the patient in this case as there were no concerns of skeletal involvement upon history and physical examination.

Lastly, Klippel-Trénaunay syndrome can be associated with similar cutaneous vascular manifestations.^13,14 This syndrome occurs due to somatic mutations altering angiogenesis during embryological development. This results in varicosities of superficial and deep venous systems, persistent embryonic veins, and valvular incompetence. However, these patients typically have capillary manifestations such as a flat, red, or purple port-wine stain present at birth and associated limb hypertrophy predominantly affecting a single lower limb.^15,16 The patient reported not having the lesions present at birth and because bilateral upper/lower extremity and trunk involvement is rare in this syndrome, a Klippel-Trénaunay syndrome diagnosis was unlikely even in the absence of biopsy results.

Treatment

Based on pathology results, the patient was diagnosed with familial glomangiomatosis and a discussion of treatment options ensued. Asymptomatic lesions can be periodically managed. In addition, there are several treatments for symptomatic lesions. Symptomatic lesions may be tender to palpation and or hypersensitive to temperature change (cold). Though they exhibit slow growth, they can invade surrounding tissues including nerve sheaths which can worsen pain.

Surgical resection, sclerotherapy, laser therapy, and electron beam radiation have been used on patients with symptomatic lesions.^8,17 Sclerotherapy involves introducing sterile solutions into a blood vessel’s lumen or into the vascular lesion itself to induce permanent endofibrosis and ablation.¹⁷ Hypertonic saline, sodium tetradecyl sulfate (STS), and absolute alcohol have been used to treat vascular anomalies as well as glomangiomas.¹⁷ Though case reports have noticed significant improvement in symptomatic lesions, sclerotherapy has been shown to be more effective in treating venous malformations than glomangiomas.^18,19

A long-pulsed 1064-nm neodymium-doped yttrium aluminum garnet (Nd:YAG) laser has also been effective in treating larger glomangiomas that would otherwise be difficult to excise.²⁰ The Nd:YAG laser has successfully treated lesions in patients with familial glomangiomatosis.^21,22

Our patient opted for sclerotherapy with STS on symptomatic lesions of the bilateral upper extremities and trunk. The patient reported moderate improvement of some lesions at a 4-week follow-up appointment and sclerotherapy with STS was repeated.

It is important to note that if a glomangioma is fully excised, the prognosis is favorable; however, recurrence after surgical excision is seen in 10% to 33% of cases.^23,24 Our patient had symptomatic lesions excised on the face, but they recurred. Glomangiomas confer a low risk of malignancy but some risk factors include lesions > 2 cm in size, deep lesions, muscle and/or bone invasion, and high mitotic activity.^17,25 If left untreated, high-risk glomangiomas can potentially be life-threatening due to growth, bleeding, or vital organ obstruction.²⁶

Primary Care Role

This patient was referred by his PCP assuming that these were symptomatic vascular lesions or telangiectasias (spider veins). Glomus cell tumors are classified as neurovascular neoplasms which may appear similar to vascular malformations or hemangiomas. ²⁷ PCPs serve an important role in performing cutaneous biopsies to increase patient access to dermatologic care, increase patient awareness of skin conditions including skin cancer, and to potentially diagnose a malignant lesion.²⁸ However, the PCP ultimately referred the patient to dermatology due to the number of growing, painful lesions. If the patient had a single lesion, it may have been appropriate to biopsy for diagnostic clarity.

A retrospective review found that the clinical diagnosis of glomus tumor showed concordance with histopathological diagnosis in 45.4% of cases. The most common alternate histopathological diagnoses were vascular tumors (25.9%) followed by other skin or soft tissue tumors like neuromas, leiomyomas, lipomas, or nevi.²⁹ Even if the PCP performed an initial biopsy with high clinical suspicion of a vascular malformation, some glomus cell tumors may be vascular tumors and vice versa.

Though the patient’s history was consistent with the classic triad of glomangiomas including hypersensitivity, intermittent pain, and pinpoint pain, histopathology was necessary to confirm the diagnosis. Given that these appeared to be similar to telangiectasias to the PCP, a rare condition like BRBNS was likely not considered upon initial presentation. Furthermore, the patient had a negative review of systems to include GI symptoms like melena or hematochezia. The PCP had no concern of GI hemorrhage as these lesions can involve the GI tract. If the patient were to endorse additional symptoms, a CBC to evaluate for anemia as well as a GI referral would be warranted.

CONCLUSIONS

This case exhibits the importance of differentiating glomus cell tumors from other more common vascular anomalies via a patient’s history and histopathological findings. Diagnosis and treatment may be difficult depending on the extent of lesions.

DISCUSSION

A diagnosis of familial glomangiomatosis was made based on the clinical history and histopathologic findings from the punch biopsy. Glomus tumors are comprised of glomus cells, or undifferentiated smooth muscle cells responsible for thermoregulation.¹ Glomus tumors are classified into 3 categories: solid (predominantly glomus cells), glomangiomas (predominantly blood vessels), and glomangiomyomas (predominantly smooth muscle cells).² Glomangiomas, which comprise up to 20% of glomus tumors, typically present as bluish-purple, papular or nodular, hyperkeratotic lesions that are 2 to 10 mm in diameter.¹ These lesions are tender to palpation and pain may worsen with exposure to cold. Glomangiomas are associated with a classic triad of symptoms that include hypersensitivity, intermittent pain, and pinpoint pain, but patients rarely present with all 3.³

Glomangiomas tend to occur in areas rich with glomus bodies—the distal extremities—specifically the palms, wrists, forearms, feet, and subungual regions; visceral organ involvement including the GI tract is very rare.^1,4,5 About 38% to 68% of these lesions are hereditary or can be sporadic. If these lesions are hereditary, a patient is said to have familial glomangiomatosis. In familial glomangiomatosis, the glomulin gene is mutated in an autosomal dominant inheritance pattern with incomplete penetrance and variable expressivity. Inherited glomangiomas may present at birth or puberty similar to other vascular anomalies.⁴

Histopathology of glomangiomas shows rows of glomus cells (modified smooth muscle cells) surrounding distorted venous channels.^6,7 These lesions stain positive for CD34, vimentin, calponin, and α-smooth muscle actin, but are negative for desmin, S-100, and von Willebrand factor.^1,8 Although the patient’s medical history and physical examination are important in establishing the diagnosis, histopathology is confirmatory.

While the punch biopsy results were pending, a complete blood count (CBC) and fecal occult blood test (FOBT) were ordered due to concerns for blue rubber bleb nevus syndrome (BRBNS), a rare disorder with about 200 reported cases. Patients present with multiple blue to violaceous compressible nodules that feel rubbery in consistency and may be painful with compression. Lesions may be up to 5 cm in diameter and with time, the GI tract may also become involved.⁹ In the GI tract, the small bowel is the most common site of involvement and patients may present with severe iron deficiency anemia due to hemorrhage.¹⁰ Histopathologic features are nonspecific and have features of venous malformations but may include large, tortuous, dilated vessels with a single endothelial lining with possible smooth muscle in vessel walls or calcifications.¹¹ Due to concerns of BRBNS, laboratory studies (CBC and FOBT) were obtained but did not indicate the patient was experiencing a GI hemorrhage.

The differential diagnosis included Maffucci syndrome, also known as dyschondrodysplasia with hemangiomas, enchondromatosis with cavernous hemangiomas, or hemangiomatosis chondrodystrophic. Patients with Maffucci syndrome present with multiple enchondromas, soft tissue hemangiomas or lymphangiomas, and gliomas. These lesions tend to undergo malignant transformation from enchondromas to chondrosarcomas and hemangiomas to vascular sarcomas.¹² This diagnosis was less likely in the patient in this case as there were no concerns of skeletal involvement upon history and physical examination.

Lastly, Klippel-Trénaunay syndrome can be associated with similar cutaneous vascular manifestations.^13,14 This syndrome occurs due to somatic mutations altering angiogenesis during embryological development. This results in varicosities of superficial and deep venous systems, persistent embryonic veins, and valvular incompetence. However, these patients typically have capillary manifestations such as a flat, red, or purple port-wine stain present at birth and associated limb hypertrophy predominantly affecting a single lower limb.^15,16 The patient reported not having the lesions present at birth and because bilateral upper/lower extremity and trunk involvement is rare in this syndrome, a Klippel-Trénaunay syndrome diagnosis was unlikely even in the absence of biopsy results.

Treatment

Based on pathology results, the patient was diagnosed with familial glomangiomatosis and a discussion of treatment options ensued. Asymptomatic lesions can be periodically managed. In addition, there are several treatments for symptomatic lesions. Symptomatic lesions may be tender to palpation and or hypersensitive to temperature change (cold). Though they exhibit slow growth, they can invade surrounding tissues including nerve sheaths which can worsen pain.

Surgical resection, sclerotherapy, laser therapy, and electron beam radiation have been used on patients with symptomatic lesions.^8,17 Sclerotherapy involves introducing sterile solutions into a blood vessel’s lumen or into the vascular lesion itself to induce permanent endofibrosis and ablation.¹⁷ Hypertonic saline, sodium tetradecyl sulfate (STS), and absolute alcohol have been used to treat vascular anomalies as well as glomangiomas.¹⁷ Though case reports have noticed significant improvement in symptomatic lesions, sclerotherapy has been shown to be more effective in treating venous malformations than glomangiomas.^18,19

A long-pulsed 1064-nm neodymium-doped yttrium aluminum garnet (Nd:YAG) laser has also been effective in treating larger glomangiomas that would otherwise be difficult to excise.²⁰ The Nd:YAG laser has successfully treated lesions in patients with familial glomangiomatosis.^21,22

Our patient opted for sclerotherapy with STS on symptomatic lesions of the bilateral upper extremities and trunk. The patient reported moderate improvement of some lesions at a 4-week follow-up appointment and sclerotherapy with STS was repeated.

It is important to note that if a glomangioma is fully excised, the prognosis is favorable; however, recurrence after surgical excision is seen in 10% to 33% of cases.^23,24 Our patient had symptomatic lesions excised on the face, but they recurred. Glomangiomas confer a low risk of malignancy but some risk factors include lesions > 2 cm in size, deep lesions, muscle and/or bone invasion, and high mitotic activity.^17,25 If left untreated, high-risk glomangiomas can potentially be life-threatening due to growth, bleeding, or vital organ obstruction.²⁶

Primary Care Role

This patient was referred by his PCP assuming that these were symptomatic vascular lesions or telangiectasias (spider veins). Glomus cell tumors are classified as neurovascular neoplasms which may appear similar to vascular malformations or hemangiomas. ²⁷ PCPs serve an important role in performing cutaneous biopsies to increase patient access to dermatologic care, increase patient awareness of skin conditions including skin cancer, and to potentially diagnose a malignant lesion.²⁸ However, the PCP ultimately referred the patient to dermatology due to the number of growing, painful lesions. If the patient had a single lesion, it may have been appropriate to biopsy for diagnostic clarity.

A retrospective review found that the clinical diagnosis of glomus tumor showed concordance with histopathological diagnosis in 45.4% of cases. The most common alternate histopathological diagnoses were vascular tumors (25.9%) followed by other skin or soft tissue tumors like neuromas, leiomyomas, lipomas, or nevi.²⁹ Even if the PCP performed an initial biopsy with high clinical suspicion of a vascular malformation, some glomus cell tumors may be vascular tumors and vice versa.

Though the patient’s history was consistent with the classic triad of glomangiomas including hypersensitivity, intermittent pain, and pinpoint pain, histopathology was necessary to confirm the diagnosis. Given that these appeared to be similar to telangiectasias to the PCP, a rare condition like BRBNS was likely not considered upon initial presentation. Furthermore, the patient had a negative review of systems to include GI symptoms like melena or hematochezia. The PCP had no concern of GI hemorrhage as these lesions can involve the GI tract. If the patient were to endorse additional symptoms, a CBC to evaluate for anemia as well as a GI referral would be warranted.

CONCLUSIONS

This case exhibits the importance of differentiating glomus cell tumors from other more common vascular anomalies via a patient’s history and histopathological findings. Diagnosis and treatment may be difficult depending on the extent of lesions.

DISCUSSION

A diagnosis of familial glomangiomatosis was made based on the clinical history and histopathologic findings from the punch biopsy. Glomus tumors are comprised of glomus cells, or undifferentiated smooth muscle cells responsible for thermoregulation.¹ Glomus tumors are classified into 3 categories: solid (predominantly glomus cells), glomangiomas (predominantly blood vessels), and glomangiomyomas (predominantly smooth muscle cells).² Glomangiomas, which comprise up to 20% of glomus tumors, typically present as bluish-purple, papular or nodular, hyperkeratotic lesions that are 2 to 10 mm in diameter.¹ These lesions are tender to palpation and pain may worsen with exposure to cold. Glomangiomas are associated with a classic triad of symptoms that include hypersensitivity, intermittent pain, and pinpoint pain, but patients rarely present with all 3.³

Glomangiomas tend to occur in areas rich with glomus bodies—the distal extremities—specifically the palms, wrists, forearms, feet, and subungual regions; visceral organ involvement including the GI tract is very rare.^1,4,5 About 38% to 68% of these lesions are hereditary or can be sporadic. If these lesions are hereditary, a patient is said to have familial glomangiomatosis. In familial glomangiomatosis, the glomulin gene is mutated in an autosomal dominant inheritance pattern with incomplete penetrance and variable expressivity. Inherited glomangiomas may present at birth or puberty similar to other vascular anomalies.⁴

Histopathology of glomangiomas shows rows of glomus cells (modified smooth muscle cells) surrounding distorted venous channels.^6,7 These lesions stain positive for CD34, vimentin, calponin, and α-smooth muscle actin, but are negative for desmin, S-100, and von Willebrand factor.^1,8 Although the patient’s medical history and physical examination are important in establishing the diagnosis, histopathology is confirmatory.

While the punch biopsy results were pending, a complete blood count (CBC) and fecal occult blood test (FOBT) were ordered due to concerns for blue rubber bleb nevus syndrome (BRBNS), a rare disorder with about 200 reported cases. Patients present with multiple blue to violaceous compressible nodules that feel rubbery in consistency and may be painful with compression. Lesions may be up to 5 cm in diameter and with time, the GI tract may also become involved.⁹ In the GI tract, the small bowel is the most common site of involvement and patients may present with severe iron deficiency anemia due to hemorrhage.¹⁰ Histopathologic features are nonspecific and have features of venous malformations but may include large, tortuous, dilated vessels with a single endothelial lining with possible smooth muscle in vessel walls or calcifications.¹¹ Due to concerns of BRBNS, laboratory studies (CBC and FOBT) were obtained but did not indicate the patient was experiencing a GI hemorrhage.

The differential diagnosis included Maffucci syndrome, also known as dyschondrodysplasia with hemangiomas, enchondromatosis with cavernous hemangiomas, or hemangiomatosis chondrodystrophic. Patients with Maffucci syndrome present with multiple enchondromas, soft tissue hemangiomas or lymphangiomas, and gliomas. These lesions tend to undergo malignant transformation from enchondromas to chondrosarcomas and hemangiomas to vascular sarcomas.¹² This diagnosis was less likely in the patient in this case as there were no concerns of skeletal involvement upon history and physical examination.

Lastly, Klippel-Trénaunay syndrome can be associated with similar cutaneous vascular manifestations.^13,14 This syndrome occurs due to somatic mutations altering angiogenesis during embryological development. This results in varicosities of superficial and deep venous systems, persistent embryonic veins, and valvular incompetence. However, these patients typically have capillary manifestations such as a flat, red, or purple port-wine stain present at birth and associated limb hypertrophy predominantly affecting a single lower limb.^15,16 The patient reported not having the lesions present at birth and because bilateral upper/lower extremity and trunk involvement is rare in this syndrome, a Klippel-Trénaunay syndrome diagnosis was unlikely even in the absence of biopsy results.

Treatment

Based on pathology results, the patient was diagnosed with familial glomangiomatosis and a discussion of treatment options ensued. Asymptomatic lesions can be periodically managed. In addition, there are several treatments for symptomatic lesions. Symptomatic lesions may be tender to palpation and or hypersensitive to temperature change (cold). Though they exhibit slow growth, they can invade surrounding tissues including nerve sheaths which can worsen pain.

Surgical resection, sclerotherapy, laser therapy, and electron beam radiation have been used on patients with symptomatic lesions.^8,17 Sclerotherapy involves introducing sterile solutions into a blood vessel’s lumen or into the vascular lesion itself to induce permanent endofibrosis and ablation.¹⁷ Hypertonic saline, sodium tetradecyl sulfate (STS), and absolute alcohol have been used to treat vascular anomalies as well as glomangiomas.¹⁷ Though case reports have noticed significant improvement in symptomatic lesions, sclerotherapy has been shown to be more effective in treating venous malformations than glomangiomas.^18,19

A long-pulsed 1064-nm neodymium-doped yttrium aluminum garnet (Nd:YAG) laser has also been effective in treating larger glomangiomas that would otherwise be difficult to excise.²⁰ The Nd:YAG laser has successfully treated lesions in patients with familial glomangiomatosis.^21,22

Our patient opted for sclerotherapy with STS on symptomatic lesions of the bilateral upper extremities and trunk. The patient reported moderate improvement of some lesions at a 4-week follow-up appointment and sclerotherapy with STS was repeated.

It is important to note that if a glomangioma is fully excised, the prognosis is favorable; however, recurrence after surgical excision is seen in 10% to 33% of cases.^23,24 Our patient had symptomatic lesions excised on the face, but they recurred. Glomangiomas confer a low risk of malignancy but some risk factors include lesions > 2 cm in size, deep lesions, muscle and/or bone invasion, and high mitotic activity.^17,25 If left untreated, high-risk glomangiomas can potentially be life-threatening due to growth, bleeding, or vital organ obstruction.²⁶

Primary Care Role

This patient was referred by his PCP assuming that these were symptomatic vascular lesions or telangiectasias (spider veins). Glomus cell tumors are classified as neurovascular neoplasms which may appear similar to vascular malformations or hemangiomas. ²⁷ PCPs serve an important role in performing cutaneous biopsies to increase patient access to dermatologic care, increase patient awareness of skin conditions including skin cancer, and to potentially diagnose a malignant lesion.²⁸ However, the PCP ultimately referred the patient to dermatology due to the number of growing, painful lesions. If the patient had a single lesion, it may have been appropriate to biopsy for diagnostic clarity.

A retrospective review found that the clinical diagnosis of glomus tumor showed concordance with histopathological diagnosis in 45.4% of cases. The most common alternate histopathological diagnoses were vascular tumors (25.9%) followed by other skin or soft tissue tumors like neuromas, leiomyomas, lipomas, or nevi.²⁹ Even if the PCP performed an initial biopsy with high clinical suspicion of a vascular malformation, some glomus cell tumors may be vascular tumors and vice versa.

Though the patient’s history was consistent with the classic triad of glomangiomas including hypersensitivity, intermittent pain, and pinpoint pain, histopathology was necessary to confirm the diagnosis. Given that these appeared to be similar to telangiectasias to the PCP, a rare condition like BRBNS was likely not considered upon initial presentation. Furthermore, the patient had a negative review of systems to include GI symptoms like melena or hematochezia. The PCP had no concern of GI hemorrhage as these lesions can involve the GI tract. If the patient were to endorse additional symptoms, a CBC to evaluate for anemia as well as a GI referral would be warranted.

CONCLUSIONS

This case exhibits the importance of differentiating glomus cell tumors from other more common vascular anomalies via a patient’s history and histopathological findings. Diagnosis and treatment may be difficult depending on the extent of lesions.

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones (Figure).^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided. 

EPIDEMIOLOGY 

The incidence of SKs increases with age.3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹ 

KEY CLINICAL FEATURES 

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules. 2 Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters. ^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4 

WORTH NOTING 

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸ 

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.4 The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶ 

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions. 4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰ 

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigatorblinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P =.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful. 

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹ 

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹² 

HEALTH DISPARITY HIGHLIGHT 

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address— and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden. 

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones (Figure).^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided. 

EPIDEMIOLOGY 

The incidence of SKs increases with age.3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹ 

KEY CLINICAL FEATURES 

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules. 2 Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters. ^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4 

WORTH NOTING 

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸ 

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.4 The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶ 

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions. 4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰ 

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigatorblinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P =.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful. 

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹ 

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹² 

HEALTH DISPARITY HIGHLIGHT 

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address— and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden. 

Dermatosis papulosa nigra (DPN), a subvariant of seborrheic keratosis (SK), is characterized by benign pigmented epidermal neoplasms that typically manifest on the face, neck, and trunk in individuals with darker skin tones (Figure).^1,2 While DPN meets the diagnostic criteria for SK, certain characteristics can help distinguish these lesions from other SK types. Treatment of DPN in patients with skin of color requires caution, particularly regarding the use of abrasive methods as well as cryotherapy, which generally should be avoided. 

EPIDEMIOLOGY 

The incidence of SKs increases with age.3,4 Although it can occur in patients of all skin tones, SK is more common in lighter skin tones, while DPN predominantly is diagnosed in darker skin types.^1,4 The prevalence of DPN in Black patients ranges from 10% to 30%, and Black women are twice as likely to be diagnosed with DPN as men.² One study reported a first-degree relative with DPN in 84% (42/50) of patients.⁵ The number and size of DPN papules increase with age.¹ 

KEY CLINICAL FEATURES 

Dermatosis papulosa nigra and SK have distinctive morphologies: DPN typically manifests as raised, round or filiform, sessile, brown to black, 1- to 5-mm papules. 2 Seborrheic keratoses tend to be larger with a “stuck on” appearance and manifest as well-demarcated, pink to black papules or plaques that can range in size from millimeters to a few centimeters. ^3,4 In DPN, the lesions usually are asymptomatic but may be tender, pruritic, dry, or scaly and may become irritated.^1,2 They develop symmetrically in sun-exposed areas, and the most common sites are the malar face, temporal region, neck, and trunk.^1,2,6,7 Seborrheic keratoses can appear throughout the body, including in sun-exposed areas, but have varying textures (eg, greasy, waxy, verrucous).^3,4 

WORTH NOTING 

Dermatosis papulosa nigra and SK can resemble each other histologically: DPN demonstrates a fibrous stroma, papillomatosis, hyperkeratosis, and acanthosis at the intraepidermal layer, which are diagnostic criteria for SK.^2,4,8 However, other histologic features characteristic of SK that are not seen in DPN include pseudohorn cysts, spindle tumor cells, and basaloid cell nests.⁸ 

Dermoscopy can be useful in ruling out malignant skin cancers when evaluating pigmented lesions. The most common dermoscopic features of SK are cerebriform patterns such as fissures and ridges, comedolike openings, and pigmented fingerprintlike structures.^3,4 To a lesser degree, milialike cysts, sharp demarcation, and hairpin-shaped vascular structures also may be present.4 The dermoscopic findings of DPN have not been well evaluated, but one study revealed that DPN had similar dermoscopic features to SK with some predominant features.⁶ Ridges and fissures were seen in 59% of patients diagnosed with DPN followed by comedolike openings seen in 27% of patients. The coexistence of a cerebriform pattern with comedolike openings was infrequent, and milialike cysts were rare.⁶ 

While DPN and SK are benign, patients often seek treatment for cosmetic reasons. Factors to consider when choosing a treatment modality include location of the lesions, the patient’s skin tone, and postprocedural outcomes (eg, depigmentation, wound healing). In general, treatments for SK include cryotherapy, electrodesiccation and curettage, and topical therapeutics such as hydrogen peroxide 40%, topical vitamin D3, and nitric-zinc 30%-50% solutions. 4,8 Well-established treatment options for DPN include electrodesiccation, laser therapies, scissor excision, and cryotherapy, but topical options such as tazarotene also have been reported.^1,9 Of the treatments for DPN, electrodesiccation and laser therapy routinely are used.¹⁰ 

The efficacy of electrodessication and potassium titanyl phosphate (KTP) laser were assessed in a randomized, investigatorblinded split-face study.¹¹ Both modalities received high improvement ratings, with the results favoring the KTP laser. The patients (most of whom were Black) reported that KTP laser was more effective but more painful than electrodessication (P =.002).¹¹ In another randomized study, patients received 3 treatments—electrodessication, pulsed dye laser, and curettage—for select DPN papules.¹⁰ There was no difference in the degree of clearance, cosmetic outcome, or postinflammatory hyperpigmentation between the 3 modalities, but patients found the laser to be the most painful. 

It is important to exercise caution when using abrasive methods (eg, laser therapy, electrodesiccation, curettage) in patients with darker skin tones because of the increased risk for postinflammatory pigment alteration.^1,2,12 Adverse effects of treatment are a top concern in the management of DPN.^5,13 While cryotherapy is a preferred treatment of SK in lighter skin tones, it generally is avoided for DPN in darker skin types because melanocyte destruction can lead to cosmetically unsatisfactory and easily visible depigmentation.⁹ 

To mitigate postprocedural adverse effects, proper aftercare can promote wound healing and minimize postinflammatory pigment alteration. In one split-face study of Black patients, 2 DPN papules were removed from each side of the face using fine-curved surgical scissors.¹⁴ Next, a petrolatum-based ointment and an antibiotic ointment with polymyxin B sulfate/bacitracin zinc was applied twice daily for 21 days to opposite sides of the face. Patients did not develop infection, tolerated both treatments well, and demonstrated improved general wound appearance according to investigator- rated clinical assessment.¹⁴ Other reported postprocedural approaches include using topical agents with ingredients shown to improve hyperpigmentation (eg, niacinamide, azelaic acid) as well as photoprotection.¹² 

HEALTH DISPARITY HIGHLIGHT 

While DPN is benign, it can have adverse psychosocial effects on patients. A study in Senegal revealed that 60% (19/30) of patients with DPN experienced anxiety related to their condition, while others noted that DPN hindered their social relationships.¹³ In one US study of 50 Black patients with DPN, there was a moderate effect on quality of life, and 36% (18/50) of patients had the lesions removed. However, of the treated patients, 67% (12/18) reported few—if any—symptoms prior to removal.⁵ Although treatment of DPN is widely considered a cosmetic procedure, therapeutic management can address— and may improve—mental health in patients with skin of color.^1,5,13 Despite the high prevalence of DPN in patients with darker skin tones, data on treatment frequency and insurance coverage are not widely available, thus limiting our understanding of treatment accessibility and economic burden. 

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Recently one of my keep-up-to-date apps alerted me to a study in Pediatric Dermatology on sleep and atopic dermatitis. When I chased down the abstract it was a shoulder-shrugging-so-what encounter. The authors reported that having a child with atopic dermatitis decreased the odds of a parent getting 7 hours of sleep a night and increased the odds that the parent was also taking sleep-aiding medications. The authors felt their data was meaningful enough to publish based on the size and the cross-sectional nature of their sample. However, anyone who has worked with families with atopic dermatitis shouldn’t be surprised at their findings.

Curious about what other investigators had discovered about the anecdotally obvious relationship between sleep and atopic dermatitis, I dug until I found a rather thorough discussion of the literature published in The Journal of Clinical Immunology Practice. These authors from the University of Rochester Medical School in New York begin by pointing out that, although 47%-80% of children with atopic dermatitis and 33%-90% of adults with atopic dermatitis have disturbed sleep, “literature on this topic remains sparse with most studies evaluating sleep as a secondary outcome using subjective measures.” They further note that sleep is one of the three most problematic symptoms for children with atopic dermatitis and their families. 

 

Characterizing the Sleep Loss

Difficulty falling asleep, frequent and long waking, and excessive daytime sleepiness are the most common symptoms reported. In the few sleep laboratory studies that have been done there has been no significant decrease in sleep duration, which is a bit of a surprise. However, as expected, sleep-onset latency, more wake time after sleep onset, sleep fragmentation, and decreased sleep efficiency have been observed in the atopic dermatitis patients. In other studies of younger children, female gender and lower socioeconomic status seem to be associated with poor sleep quality.

Most studies found that in general the prevalence and severity of sleep disturbances increases with the severity of the disease. As the disease flares, increased bedtime resistance, nocturnal wakings and daytime sleepiness become more likely. These parentally reported associations have also been confirmed by sleep laboratory observations. 

The sleep disturbances quickly become a family affair with 60% of siblings and parents reporting disturbed sleep. When the child with atopic dermatitis is having a flareup, nearly 90% of their parents report losing up to 2.5 hours of sleep. Not surprisingly sleep disturbances have been associated with behavioral and emotional problems including decreased happiness, poor cognitive performance, hyperactivity, and inattention. Mothers seem to bear the brunt of the problem and interpersonal conflicts and exhaustion are unfortunately not uncommon.

 

Probing the Causes

So why are atopic dermatitis patients and their families so prone to the ill effects of disturbed sleep? Although you might think it should be obvious, this review of the “sparse” literature doesn’t provide a satisfying answer. However, the authors provide three possible explanations.

The one with the least supporting evidence is circadian variations in the products of inflammation such as cytokines and their effect on melatonin production. The explanation which I think most of us have already considered is that pruritus disrupts sleep. This is the often-quoted itch-scratch feedback cycle which can release inflammatory mediators (“pruritogens”). However, the investigators have found that many studies report “conflicting results or only weak correlations.”

The third alternative posed by the authors is by far the most appealing and hinges on the assumption that, as with many other chronic conditions, atopic dermatitis renders the patient vulnerable to insomnia. “Nocturnal scratching disrupts sleep and sets the stage for cognitive and behavioral factors that reinforce insomnia as a conditioned response.” In other words, even after the “co-concurring condition” resolves insomnia related sleep behaviors continue. The investigators point to a study supporting this explanation which found that, even after a child’s skin cleared, his/her sleep arousals failed to return to normal suggesting that learned behavior patterns might be playing a role.

It may be a stretch to suggest that poor sleep hygiene might in and of itself cause atopic dermatitis, but it can’t be ruled out. At a minimum the current research suggests that there is a bidirectional relationship between sleep disturbances and atopic dermatitis. 

 

Next Steps

The authors of this study urge that we be more creative in using already-existing portable and relatively low-cost sleep monitoring technology to better define this relationship. While that is a worthwhile avenue for research, I think we who see children (both primary care providers and dermatologists) now have enough evidence to move managing the sleep hygiene of our atopic dermatitis patients to the front burner, along with moisturizers and topical medications, without needing to do costly and time-consuming studies.

This means taking a thorough sleep history. If, in the rare cases where the child’s sleep habits are normal, the parents should be warned that falling off the sleep wagon is likely to exacerbate the child’s skin. If the history reveals an inefficient and dysfunctional bedtime routine or other symptoms of insomnia, advise the parents on how it can be improved. Then follow up at each visit if there has been no improvement. Sleep management can be time-consuming as well but it should be part of every primary care pediatrician’s toolbox. For the dermatologist who doesn’t feel comfortable managing sleep problems, a consultation with a pediatrician or a sleep specialist is in order.

The adult with atopic dermatitis is a somewhat different animal and a formal sleep study may be indicated. Cognitive-behavioral therapy might be helpful for adult population but the investigators could find no trials of its use in patients with atopic dermatitis.

Convincing the parents of an atopic dermatitis patient that their family’s disturbed sleep may not only be the result of his/her itchy skin but may be a preexisting compounding problem may not be an easy sell. I hope if you can be open to the strong possibility that disordered sleep is not just the effect but in some ways may be a likely contributor to your patients’ atopic dermatitis, you may become more effective in managing the disease.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Advances in understanding the pathophysiology of vitiligo are transforming patient management, offering new hope for individuals with mild, moderate, and even severe forms of the disease, delegates heard at a recent conference, the Dermatology Days of Paris 2024, organized by the French Society of Dermatology.

A Distinct Disease

An estimated 65% of patients with vitiligo in Europe have been told that their disease is untreatable, according to a recent international study, and this figure rises to 75% in France, Julien Seneschal, MD, PhD, professor of dermatology at Bordeaux University Hospital in Bordeaux, France, told the audience during his presentation. 

“This is a message we must change,” he said.

The survey also revealed that in France, even when treatment is offered, 80% of patients do not receive appropriate care. However, treatments do exist, and novel approaches are revolutionizing the management of patients, whatever the degree of severity, he explained.

As a specialist in inflammatory and autoimmune skin diseases, he stressed that these advances are important because vitiligo is a distinct disease and not merely a cosmetic issue. When widespread, it has a significant impact on quality of life and can lead to depression, anxiety, and even suicidal thoughts, even though it does not affect life expectancy.

 

Updated Guidelines

Since October 2023, new international guidelines for vitiligo management have defined a therapeutic algorithm.

“Nowadays, we place the patient at the center of therapeutic decision-making,” Seneschal said. It is essential to educate patients about the disease and take the time to understand their treatment goals.

For patients with mild vitiligo that does not affect quality of life, simple monitoring may suffice.

However, when a decision is made to pursue treatment, its goals should be:

• Halting disease progression and melanocyte loss 
• Achieving repigmentation (a process that can take 6-24 months) 
• Preventing relapse after treatment discontinuation 

For moderate cases affecting less than 10% of the skin surface, localized treatment is recommended. Previously, topical corticosteroids were used for body lesions, while tacrolimus 0.1% (off-label) was often prescribed for the face and neck. However, as of March 2024, tacrolimus has been officially approved for use in patients aged ≥ 2 years.

In more severe, generalized, and/or active cases, oral treatments such as corticosteroids taken twice weekly for 12-24 weeks can stabilize the disease in 80% of cases (off-label use). Other off-label options include methotrexate, cyclosporine, and tetracyclines.

 

Targeted Therapies

Recent targeted therapies have significantly advanced the treatment of moderate to severe vitiligo. Since January 2024, the Janus kinase 1 (JAK1)/JAK2 inhibitor ruxolitinib cream has been available in community pharmacies after previously being restricted to hospital use, Seneschal said, and can have spectacular results if previous treatments have failed.

Ruxolitinib is approved for patients aged > 12 years with nonsegmental vitiligo and facial involvement, covering up to 10% of the body surface area. Treatment typically lasts 6 months to 1 year.

 

Key Findings

The cream-formulated drug has been demonstrated effective in reducing inflammation in two phase 3 clinical trials published in the New England Journal of Medicine that demonstrated its efficacy and safety in patients aged ≥ 12 years. The treatment was well tolerated despite some mild acne-like reactions in 8% of patients. It was shown to be very effective on the face, with a reduction of over 75% in facial lesions in more than 50% of patients, and had good effectiveness on the body, with a 50% decrease in lesions in more than 50% of patients on the body, trunk, arms, and legs, excluding hands and feet.

“Areas like the underarms, hands, and feet are more resistant to treatment,” Seneschal noted.

Although some improvement continues after 1 year, disease recurrence is common if treatment is stopped: Only 40% of patients maintain therapeutic benefits in the year following discontinuation.

“It is therefore important to consider the value of continuing treatment in order to achieve better efficacy or to maintain the repigmentation obtained,” Seneschal said.

He stressed that all treatments should be paired with phototherapy, typically narrowband UVB, to accelerate repigmentation. “There is no increased skin cancer risk in vitiligo patients treated with narrowband UVB,” Seneschal said.

 

New Therapies

Emerging treatments under development, including injectable biologics alone or in combination with phototherapy, show great promise, he said. Oral JAK inhibitors such as ritlecitinib, upadacitinib, and povorcitinib are also under investigation.

In particular, ritlecitinib, a JAK3/TEC pathway inhibitor, has shown significant reductions in affected skin area in severely affected patients in a phase 2b trial. Phase 3 trials are now underway.

On the safety profile of JAK inhibitors, Seneschal said that studies are reassuring but highlighted the need to monitor cardiovascular, thromboembolic, and infectious risks.

“The question of safety is important because vitiligo is a visible but nonsevere condition, and we do not want to expose patients to unnecessary risks,” added Gaëlle Quéreux, MD, PhD, president of the French Society of Dermatology.

This story was translated from Medscape’s French edition using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Advances in understanding the pathophysiology of vitiligo are transforming patient management, offering new hope for individuals with mild, moderate, and even severe forms of the disease, delegates heard at a recent conference, the Dermatology Days of Paris 2024, organized by the French Society of Dermatology.

A Distinct Disease

An estimated 65% of patients with vitiligo in Europe have been told that their disease is untreatable, according to a recent international study, and this figure rises to 75% in France, Julien Seneschal, MD, PhD, professor of dermatology at Bordeaux University Hospital in Bordeaux, France, told the audience during his presentation. 

“This is a message we must change,” he said.

The survey also revealed that in France, even when treatment is offered, 80% of patients do not receive appropriate care. However, treatments do exist, and novel approaches are revolutionizing the management of patients, whatever the degree of severity, he explained.

As a specialist in inflammatory and autoimmune skin diseases, he stressed that these advances are important because vitiligo is a distinct disease and not merely a cosmetic issue. When widespread, it has a significant impact on quality of life and can lead to depression, anxiety, and even suicidal thoughts, even though it does not affect life expectancy.

 

Updated Guidelines

Since October 2023, new international guidelines for vitiligo management have defined a therapeutic algorithm.

“Nowadays, we place the patient at the center of therapeutic decision-making,” Seneschal said. It is essential to educate patients about the disease and take the time to understand their treatment goals.

For patients with mild vitiligo that does not affect quality of life, simple monitoring may suffice.

However, when a decision is made to pursue treatment, its goals should be:

• Halting disease progression and melanocyte loss 
• Achieving repigmentation (a process that can take 6-24 months) 
• Preventing relapse after treatment discontinuation 

For moderate cases affecting less than 10% of the skin surface, localized treatment is recommended. Previously, topical corticosteroids were used for body lesions, while tacrolimus 0.1% (off-label) was often prescribed for the face and neck. However, as of March 2024, tacrolimus has been officially approved for use in patients aged ≥ 2 years.

In more severe, generalized, and/or active cases, oral treatments such as corticosteroids taken twice weekly for 12-24 weeks can stabilize the disease in 80% of cases (off-label use). Other off-label options include methotrexate, cyclosporine, and tetracyclines.

 

Targeted Therapies

Recent targeted therapies have significantly advanced the treatment of moderate to severe vitiligo. Since January 2024, the Janus kinase 1 (JAK1)/JAK2 inhibitor ruxolitinib cream has been available in community pharmacies after previously being restricted to hospital use, Seneschal said, and can have spectacular results if previous treatments have failed.

Ruxolitinib is approved for patients aged > 12 years with nonsegmental vitiligo and facial involvement, covering up to 10% of the body surface area. Treatment typically lasts 6 months to 1 year.

 

Key Findings

The cream-formulated drug has been demonstrated effective in reducing inflammation in two phase 3 clinical trials published in the New England Journal of Medicine that demonstrated its efficacy and safety in patients aged ≥ 12 years. The treatment was well tolerated despite some mild acne-like reactions in 8% of patients. It was shown to be very effective on the face, with a reduction of over 75% in facial lesions in more than 50% of patients, and had good effectiveness on the body, with a 50% decrease in lesions in more than 50% of patients on the body, trunk, arms, and legs, excluding hands and feet.

“Areas like the underarms, hands, and feet are more resistant to treatment,” Seneschal noted.

Although some improvement continues after 1 year, disease recurrence is common if treatment is stopped: Only 40% of patients maintain therapeutic benefits in the year following discontinuation.

“It is therefore important to consider the value of continuing treatment in order to achieve better efficacy or to maintain the repigmentation obtained,” Seneschal said.

He stressed that all treatments should be paired with phototherapy, typically narrowband UVB, to accelerate repigmentation. “There is no increased skin cancer risk in vitiligo patients treated with narrowband UVB,” Seneschal said.

 

New Therapies

Emerging treatments under development, including injectable biologics alone or in combination with phototherapy, show great promise, he said. Oral JAK inhibitors such as ritlecitinib, upadacitinib, and povorcitinib are also under investigation.

In particular, ritlecitinib, a JAK3/TEC pathway inhibitor, has shown significant reductions in affected skin area in severely affected patients in a phase 2b trial. Phase 3 trials are now underway.

On the safety profile of JAK inhibitors, Seneschal said that studies are reassuring but highlighted the need to monitor cardiovascular, thromboembolic, and infectious risks.

“The question of safety is important because vitiligo is a visible but nonsevere condition, and we do not want to expose patients to unnecessary risks,” added Gaëlle Quéreux, MD, PhD, president of the French Society of Dermatology.

This story was translated from Medscape’s French edition using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Advances in understanding the pathophysiology of vitiligo are transforming patient management, offering new hope for individuals with mild, moderate, and even severe forms of the disease, delegates heard at a recent conference, the Dermatology Days of Paris 2024, organized by the French Society of Dermatology.

A Distinct Disease

An estimated 65% of patients with vitiligo in Europe have been told that their disease is untreatable, according to a recent international study, and this figure rises to 75% in France, Julien Seneschal, MD, PhD, professor of dermatology at Bordeaux University Hospital in Bordeaux, France, told the audience during his presentation. 

“This is a message we must change,” he said.

The survey also revealed that in France, even when treatment is offered, 80% of patients do not receive appropriate care. However, treatments do exist, and novel approaches are revolutionizing the management of patients, whatever the degree of severity, he explained.

As a specialist in inflammatory and autoimmune skin diseases, he stressed that these advances are important because vitiligo is a distinct disease and not merely a cosmetic issue. When widespread, it has a significant impact on quality of life and can lead to depression, anxiety, and even suicidal thoughts, even though it does not affect life expectancy.

 

Updated Guidelines

Since October 2023, new international guidelines for vitiligo management have defined a therapeutic algorithm.

“Nowadays, we place the patient at the center of therapeutic decision-making,” Seneschal said. It is essential to educate patients about the disease and take the time to understand their treatment goals.

For patients with mild vitiligo that does not affect quality of life, simple monitoring may suffice.

However, when a decision is made to pursue treatment, its goals should be:

• Halting disease progression and melanocyte loss 
• Achieving repigmentation (a process that can take 6-24 months) 
• Preventing relapse after treatment discontinuation 

For moderate cases affecting less than 10% of the skin surface, localized treatment is recommended. Previously, topical corticosteroids were used for body lesions, while tacrolimus 0.1% (off-label) was often prescribed for the face and neck. However, as of March 2024, tacrolimus has been officially approved for use in patients aged ≥ 2 years.

In more severe, generalized, and/or active cases, oral treatments such as corticosteroids taken twice weekly for 12-24 weeks can stabilize the disease in 80% of cases (off-label use). Other off-label options include methotrexate, cyclosporine, and tetracyclines.

 

Targeted Therapies

Recent targeted therapies have significantly advanced the treatment of moderate to severe vitiligo. Since January 2024, the Janus kinase 1 (JAK1)/JAK2 inhibitor ruxolitinib cream has been available in community pharmacies after previously being restricted to hospital use, Seneschal said, and can have spectacular results if previous treatments have failed.

Ruxolitinib is approved for patients aged > 12 years with nonsegmental vitiligo and facial involvement, covering up to 10% of the body surface area. Treatment typically lasts 6 months to 1 year.

 

Key Findings

The cream-formulated drug has been demonstrated effective in reducing inflammation in two phase 3 clinical trials published in the New England Journal of Medicine that demonstrated its efficacy and safety in patients aged ≥ 12 years. The treatment was well tolerated despite some mild acne-like reactions in 8% of patients. It was shown to be very effective on the face, with a reduction of over 75% in facial lesions in more than 50% of patients, and had good effectiveness on the body, with a 50% decrease in lesions in more than 50% of patients on the body, trunk, arms, and legs, excluding hands and feet.

“Areas like the underarms, hands, and feet are more resistant to treatment,” Seneschal noted.

Although some improvement continues after 1 year, disease recurrence is common if treatment is stopped: Only 40% of patients maintain therapeutic benefits in the year following discontinuation.

“It is therefore important to consider the value of continuing treatment in order to achieve better efficacy or to maintain the repigmentation obtained,” Seneschal said.

He stressed that all treatments should be paired with phototherapy, typically narrowband UVB, to accelerate repigmentation. “There is no increased skin cancer risk in vitiligo patients treated with narrowband UVB,” Seneschal said.

 

New Therapies

Emerging treatments under development, including injectable biologics alone or in combination with phototherapy, show great promise, he said. Oral JAK inhibitors such as ritlecitinib, upadacitinib, and povorcitinib are also under investigation.

In particular, ritlecitinib, a JAK3/TEC pathway inhibitor, has shown significant reductions in affected skin area in severely affected patients in a phase 2b trial. Phase 3 trials are now underway.

On the safety profile of JAK inhibitors, Seneschal said that studies are reassuring but highlighted the need to monitor cardiovascular, thromboembolic, and infectious risks.

“The question of safety is important because vitiligo is a visible but nonsevere condition, and we do not want to expose patients to unnecessary risks,” added Gaëlle Quéreux, MD, PhD, president of the French Society of Dermatology.

This story was translated from Medscape’s French edition using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Merkel cell carcinoma (MCC) is less common and is associated with higher mortality rates than melanoma, according to a study that also reported that male gender, older age, and exposure to ultraviolet radiation (UVR) are significant risk factors.

METHODOLOGY:

• Researchers identified 19,444 MCC cases and 646,619 melanoma cases diagnosed between 2000 and 2021 using data from the Surveillance, Epidemiology, and End Results (SEER) Program.
• Ambient UVR exposure data were obtained from the National Aeronautics and Space Administration’s total ozone mapping spectrometer database.
• Risk factors and cancer-specific mortality rates were evaluated for both cancers.

TAKEAWAY:

• Incidence rates per 100,000 person-years of MCC and melanoma were 0.8 and 27.3, respectively.
• Men (adjusted incidence rate ratio [IRR], 1.72 for MCC and 1.23 for melanoma), older age groups (IRR: 2.69 for MCC and 1.62 for melanoma among those 70-79 years; and 5.68 for MCC and 2.26 for melanoma among those 80 years or older) showed higher incidences of MCC and melanoma. Non-Hispanic White individuals were at higher risk for MCC and melanoma than other racial/ethnic groups.
• Exposure to UVR was associated with higher incidences of melanoma (IRR, 1.24-1.49) and MCC (IRR, 1.15-1.20) in non-Hispanic White individuals, particularly on the head and neck. These associations were unclear among racial/ethnic groups.
• Individuals with MCC had a higher risk for cancer-specific mortality than those with melanoma (adjusted hazard ratio [HR], 2.33; 95% CI, 2.26-2.42). Cancer-specific survival for both cancers improved for cases diagnosed during 2012-2021 vs 2004-2011 (MCC: HR, 0.83; 95% CI, 0.78-0.89; melanoma: HR, 0.75; 95% CI, 0.74-0.76).

IN PRACTICE:

“MCC and melanoma are aggressive skin cancers with similar risk factors including male sex, older age, and UV radiation exposure. Clinicians should be alert to diagnosis of these cancers to allow for prompt treatment,” the authors wrote, adding: “It is encouraging that survival for both cancers has increased in recent years, with the largest gains in survival seen in distant stage melanoma, coinciding with the approval of BRAF and PD-1 inhibitors used for distant stage disease,” although mortality for advanced stage tumors “continues to be very high.”

SOURCE:

The study was led by Jacob T. Tribble, BA, National Cancer Institute, Rockville, Maryland. It was published online on January 5 in the Journal of Investigative Dermatology.

LIMITATIONS:

The study relied on SEER’s general staging system rather than the American Joint Committee on Cancer standard, and UVR exposure estimates did not account for individual sun protection behaviors or prior residential history. Race and ethnicity served as a proxy for UVR sensitivity, which may introduce misclassification bias.

DISCLOSURES:

The research was supported by the Intramural Research Program of the National Cancer Institute, the National Institutes of Health, the American Association for Dental Research, and the Colgate-Palmolive Company. The authors reported no conflict of interests.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Merkel cell carcinoma (MCC) is less common and is associated with higher mortality rates than melanoma, according to a study that also reported that male gender, older age, and exposure to ultraviolet radiation (UVR) are significant risk factors.

METHODOLOGY:

• Researchers identified 19,444 MCC cases and 646,619 melanoma cases diagnosed between 2000 and 2021 using data from the Surveillance, Epidemiology, and End Results (SEER) Program.
• Ambient UVR exposure data were obtained from the National Aeronautics and Space Administration’s total ozone mapping spectrometer database.
• Risk factors and cancer-specific mortality rates were evaluated for both cancers.

TAKEAWAY:

• Incidence rates per 100,000 person-years of MCC and melanoma were 0.8 and 27.3, respectively.
• Men (adjusted incidence rate ratio [IRR], 1.72 for MCC and 1.23 for melanoma), older age groups (IRR: 2.69 for MCC and 1.62 for melanoma among those 70-79 years; and 5.68 for MCC and 2.26 for melanoma among those 80 years or older) showed higher incidences of MCC and melanoma. Non-Hispanic White individuals were at higher risk for MCC and melanoma than other racial/ethnic groups.
• Exposure to UVR was associated with higher incidences of melanoma (IRR, 1.24-1.49) and MCC (IRR, 1.15-1.20) in non-Hispanic White individuals, particularly on the head and neck. These associations were unclear among racial/ethnic groups.
• Individuals with MCC had a higher risk for cancer-specific mortality than those with melanoma (adjusted hazard ratio [HR], 2.33; 95% CI, 2.26-2.42). Cancer-specific survival for both cancers improved for cases diagnosed during 2012-2021 vs 2004-2011 (MCC: HR, 0.83; 95% CI, 0.78-0.89; melanoma: HR, 0.75; 95% CI, 0.74-0.76).

IN PRACTICE:

“MCC and melanoma are aggressive skin cancers with similar risk factors including male sex, older age, and UV radiation exposure. Clinicians should be alert to diagnosis of these cancers to allow for prompt treatment,” the authors wrote, adding: “It is encouraging that survival for both cancers has increased in recent years, with the largest gains in survival seen in distant stage melanoma, coinciding with the approval of BRAF and PD-1 inhibitors used for distant stage disease,” although mortality for advanced stage tumors “continues to be very high.”

SOURCE:

The study was led by Jacob T. Tribble, BA, National Cancer Institute, Rockville, Maryland. It was published online on January 5 in the Journal of Investigative Dermatology.

LIMITATIONS:

The study relied on SEER’s general staging system rather than the American Joint Committee on Cancer standard, and UVR exposure estimates did not account for individual sun protection behaviors or prior residential history. Race and ethnicity served as a proxy for UVR sensitivity, which may introduce misclassification bias.

DISCLOSURES:

The research was supported by the Intramural Research Program of the National Cancer Institute, the National Institutes of Health, the American Association for Dental Research, and the Colgate-Palmolive Company. The authors reported no conflict of interests.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Merkel cell carcinoma (MCC) is less common and is associated with higher mortality rates than melanoma, according to a study that also reported that male gender, older age, and exposure to ultraviolet radiation (UVR) are significant risk factors.

METHODOLOGY:

• Researchers identified 19,444 MCC cases and 646,619 melanoma cases diagnosed between 2000 and 2021 using data from the Surveillance, Epidemiology, and End Results (SEER) Program.
• Ambient UVR exposure data were obtained from the National Aeronautics and Space Administration’s total ozone mapping spectrometer database.
• Risk factors and cancer-specific mortality rates were evaluated for both cancers.

TAKEAWAY:

• Incidence rates per 100,000 person-years of MCC and melanoma were 0.8 and 27.3, respectively.
• Men (adjusted incidence rate ratio [IRR], 1.72 for MCC and 1.23 for melanoma), older age groups (IRR: 2.69 for MCC and 1.62 for melanoma among those 70-79 years; and 5.68 for MCC and 2.26 for melanoma among those 80 years or older) showed higher incidences of MCC and melanoma. Non-Hispanic White individuals were at higher risk for MCC and melanoma than other racial/ethnic groups.
• Exposure to UVR was associated with higher incidences of melanoma (IRR, 1.24-1.49) and MCC (IRR, 1.15-1.20) in non-Hispanic White individuals, particularly on the head and neck. These associations were unclear among racial/ethnic groups.
• Individuals with MCC had a higher risk for cancer-specific mortality than those with melanoma (adjusted hazard ratio [HR], 2.33; 95% CI, 2.26-2.42). Cancer-specific survival for both cancers improved for cases diagnosed during 2012-2021 vs 2004-2011 (MCC: HR, 0.83; 95% CI, 0.78-0.89; melanoma: HR, 0.75; 95% CI, 0.74-0.76).

IN PRACTICE:

“MCC and melanoma are aggressive skin cancers with similar risk factors including male sex, older age, and UV radiation exposure. Clinicians should be alert to diagnosis of these cancers to allow for prompt treatment,” the authors wrote, adding: “It is encouraging that survival for both cancers has increased in recent years, with the largest gains in survival seen in distant stage melanoma, coinciding with the approval of BRAF and PD-1 inhibitors used for distant stage disease,” although mortality for advanced stage tumors “continues to be very high.”

SOURCE:

The study was led by Jacob T. Tribble, BA, National Cancer Institute, Rockville, Maryland. It was published online on January 5 in the Journal of Investigative Dermatology.

LIMITATIONS:

The study relied on SEER’s general staging system rather than the American Joint Committee on Cancer standard, and UVR exposure estimates did not account for individual sun protection behaviors or prior residential history. Race and ethnicity served as a proxy for UVR sensitivity, which may introduce misclassification bias.

DISCLOSURES:

The research was supported by the Intramural Research Program of the National Cancer Institute, the National Institutes of Health, the American Association for Dental Research, and the Colgate-Palmolive Company. The authors reported no conflict of interests.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.