Hair & Nails

Therapeutic use of oral minoxidil in the treatment of androgenetic alopecia (AGA) is a lifeline for dermatologists who treat hair loss. Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.

Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.

Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.

In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3

To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.

Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).

In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.

Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at [email protected]. Dr. Talakoub had no relevant disclosures.

References

Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.

Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.

Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.

Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.

Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.

Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.

Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.

Therapeutic use of oral minoxidil in the treatment of androgenetic alopecia (AGA) is a lifeline for dermatologists who treat hair loss. Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.

Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.

Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.

In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3

To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.

Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).

In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.

Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at [email protected]. Dr. Talakoub had no relevant disclosures.

References

Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.

Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.

Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.

Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.

Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.

Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.

Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.

Therapeutic use of oral minoxidil in the treatment of androgenetic alopecia (AGA) is a lifeline for dermatologists who treat hair loss. Other than oral finasteride, vitamins, and topicals, there has been little advancement in the treatment of AGA leaving many (including me) desperate for anything remotely new.

Oral minoxidil is a peripheral vasodilator approved by the Food and Drug Administration for use in patients with hypertensive disease taken at doses ranging between 10 mg to 40 mg daily. Animal studies have shown that minoxidil affects the hair growth cycle by shortening the telogen phase and prolonging the anagen phase.

Recent case studies have also shown growing evidence for the off-label use of low-dose oral minoxidil (LDOM) for treating different types of alopecia. Topical minoxidil is metabolized into its active metabolite minoxidil sulfate, by sulfotransferase enzymes located in the outer root sheath of hair follicles. The expression of sulfotransferase varies greatly in the scalp of different individuals, and this difference is directly correlated to the wide range of responses to minoxidil treatment. LDOM is, however, more widely effective because it requires decreased follicular enzymatic activity to form its active metabolite as compared with its topical form.

In a retrospective series by Beach and colleagues evaluating the efficacy and tolerability of LDOM for treating AGA, there was increased scalp hair growth in 33 of 51 patients (65%) and decreased hair shedding in 14 of the 51 patients (27%) with LDOM. Patients with nonscarring alopecia were most likely to show improvement. Side effects were dose dependent and infrequent. The most frequent adverse effects were hypertrichosis, lightheadedness, edema, and tachycardia. No life-threatening adverse effects were observed. Although there has been a recently reported case report of severe pericardial effusion, edema, and anasarca in a woman with frontal fibrosing alopecia treated with LDOM, life threatening side effects are rare.3

To compare the efficacy of topical versus oral minoxidil, Ramos and colleagues performed a 24-week prospective study of low-dose (1 mg/day) oral minoxidil, compared with topical 5% minoxidil, in the treatment of 52 women with female pattern hair loss. Blinded analysis of trichoscopic images were evaluated to compare the change in total hair density in a target area from baseline to week 24 by three dermatologists.

Results after 24 weeks of treatment showed an increase in total hair density (12%) among the women taking oral minoxidil, compared with 7.2% in women who applied topical minoxidil (P =.09).

In the armamentarium of hair-loss treatments, dermatologists have limited choices. LDOM can be used in patients with both scarring and nonscarring alopecia if monitored regularly. Treatment doses I recommend are 1.25-5 mg daily titrated up slowly in properly selected patients without contraindications and those who are not taking other vasodilators. Self-reported dizziness, edema, and headache are common and treatments for facial hypertrichosis in women are always discussed. Clinical efficacy can be evaluated after 10-12 months of therapy and concomitant spironolactone can be given to mitigate the side effect of hypertrichosis.Patient selection is crucial as patients with severe scarring alopecia and those with active inflammatory diseases of the scalp may not see similar results. Similar to other hair loss treatments, treatment courses of 10-12 months are often needed to see visible signs of hair growth.

Dr. Talakoub and Naissan O. Wesley, MD, are cocontributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. Write to them at [email protected]. Dr. Talakoub had no relevant disclosures.

References

Beach RA et al. J Am Acad Dermatol. 2021 Mar;84(3):761-3.

Dlova et al. JAAD Case Reports. 2022 Oct;28:94-6.

Jimenez-Cauhe J et al. J Am Acad Dermatol. 2021 Jan;84(1):222-3.

Ramos PM et al. J Eur Acad Dermatol Venereol. 2020 Jan;34(1):e40-1.

Ramos PM et al. J Am Acad Dermatol. 2020 Jan;82(1):252-3.

Randolph M and Tosti A. J Am Acad Dermatol. 2021 Mar;84(3):737-46.

Vañó-Galván S et al. J Am Acad Dermatol. 2021 Jun;84(6):1644-51.

PORTLAND, ORE. – When individuals with skin of color seek help from dermatologists to optimize the treatment and management of scalp and hair disorders, they expect them to understand their concerns, but sometimes their doctors fall short.

“Many times, you may not have race concordant visits with patients of color,” Janiene Luke, MD, said at the annual meeting of the Pacific Dermatologic Association. She referred to a survey of 200 Black women aged 21-83 years, which found that 28% had visited a physician to discuss hair or scalp issues. Of those, 68% felt like their dermatologists did not understand African American hair.

“I recommend trying the best you can to familiarize yourself with various common cultural hair styling methods and practices in patients of color. It’s important to understand what your patients are engaging in and the types of styles they’re using,” said Dr. Luke, associate professor of dermatology at Loma Linda (Calif.) University. “Approach all patients with cultural humility. We know from studies that patients value dermatologists who take time to listen to their concerns, involve them in the decision-making process, and educate them about their conditions,” she added.

National efforts to educate clinicians on treating skin of color have emerged in recent years, including textbooks, CME courses at dermatology conferences, and the American Academy of Dermatology’s Skin of Color Curriculum, which consists of 15-minute modules that can be viewed online.

At the meeting, Dr. Luke, shared her approach to assessing hair and scalp disorders in skin of color. She begins by taking a thorough history, “because not all things that are associated with hair styling will be the reason why your patient comes in,” she said. “Patients of color can have telogen effluvium and seborrheic dermatitis just like anyone else. I ask about the hair styling practices they use. I also ask how often they wash their hair, because sometimes our recommendations for treatment are not realistic based on their current routine.”

Next, she examines the scalp with her hands – which sometimes surprises patients. “I’ve had so many patients come in and say, ‘the dermatologist never touched my scalp,’ or ‘they never even looked at my hair,’ ” said Dr. Luke, who directs the university’s dermatology residency program. She asks patients to remove any hair extensions or weaves prior to the office visit and to remove wigs prior to the exam itself. The lab tests she customarily orders include CBC, TSH, iron, total iron binding capacity, ferritin, vitamin D, and zinc. If there are signs of androgen excess, she may check testosterone, sex hormone binding globulin, and dehydroepiandrosterone sulfate (DHEA-S). She routinely incorporates a dermoscopy-directed biopsy into the evaluation.

Dr. Luke examines the patient from above, the sides, and the back to assess the pattern/distribution of hair loss. A visible scalp at the vertex indicates a 50% reduction in normal hair density. “I’m looking at the hairline, their part width, and the length of their hair,” she said. “I also look at the eyebrows and eyelashes, because these can be involved in alopecia areata, frontal fibrosing alopecia, or congenital hair shaft disorders.”

On closeup examination, she looks for scarring versus non-scarring types of hair loss, and for the presence or absence of follicular ostia. “I also look at hair changes,” she said. “Is the texture of their hair different? Are there signs of breakage or fragility? It’s been noted in studies that breakage can be an early sign of central centrifugal cicatricial alopecia.” (For more tips on examining tightly coiled hair among patients with hair loss in race discordant patient-physician interactions, she recommended a 2021 article in JAMA Dermatology)..

Trichoscopy allows for magnified observation of the hair shafts, hair follicle openings, perifollicular dermis, and blood vessels. Normal trichoscopy findings in skin of color reveal a perifollicular pigment network (honeycomb pattern) and pinpoint white dots that are regularly distributed between follicular units.

Common abnormalities seen on trichoscopy include central centrifugal cicatricial alopecia (CCCA), with one or two hairs emerging together, surrounded by a gray halo; lichen planopilaris/frontal fibrosing alopecia, characterized by hair with peripilar casts and absence of vellus hairs; discoid lupus erythematosus, characterized by keratotic plugs; and traction, characterized by hair casts.

Once a diagnosis is confirmed, Dr. Luke provides other general advice for optimal skin health, including a balanced (whole food) diet to ensure adequate nutrition. “I tend to find a lot of nutrient deficiencies that contribute to and compound their condition,” she said. Other recommendations include avoiding excess tension on the hair, such as hair styles with tight ponytails, buns, braids, and weaves; avoiding or limiting chemical treatments with hair color, relaxers, and permanents; and avoiding or limiting excessive heat styling with blow dryers, flat irons, and curling irons.


 

Photoprotection misconceptions

At the meeting, Dr. Luke also discussed three misconceptions of photoprotection in skin of color, drawn from an article on the topic published in 2021.

• Myth No. 1: Endogenous melanin provides complete photoprotection for Fitzpatrick skin types IV-V. Many people with skin of color may believe sunscreen is not needed given the melanin already present in their skin, but research has shown that the epidermis of dark skin has an intrinsic sun protection factor (SPF) of 13.4, compared with an SPF of 3.3 in light skin. “That may not provide them with full protection,” Dr. Luke said. “Many dermatologists are not counseling their skin of color patients about photoprotection.”
• Myth No. 2: Individuals with skin of color have negligible risks associated with skin cancer. Skin cancer prevalence in patients with skin of color is significantly lower compared with those with light skin. However, people with skin of color tend to be diagnosed with cancers at a more advanced stage, and cancers associated with a worse prognosis and poorer survival rate. An analysis of ethnic differences among patients with cutaneous melanoma that drew from the Surveillance, Epidemiology, and End Results (SEER) program found that Hispanic individuals (odds ratio [OR], 3.6), Black individuals (OR, 4.2), and Asian individuals (OR, 2.4), were more likely than were White individuals to have stage IV melanoma at the time of presentation. “For melanoma in skin of color, UV radiation does not seem to be a major risk factor, as melanoma tends to occur on palmar/plantar and subungual skin as well as mucous membranes,” Dr. Luke said. “For squamous cell carcinoma in skin of color, lesions are more likely to be present in areas that are not sun exposed. The risk factors for this tend to be chronic wounds, nonhealing ulcers, and people with chronic inflammatory conditions.” For basal cell carcinoma, she added, UV radiation seems to play more of a role and tends to occur in sun-exposed areas in patients with lighter Fitzpatrick skin types. Patients are more likely to present with pigmented BCCs.

• Myth No. 3: Broad-spectrum sunscreens provide photoprotection against all wavelengths of light that cause skin damage. To be labeled “broad-spectrum” the Food and Drug Administration requires that sunscreens have a critical wavelength of 370 nm or below, but Dr. Luke noted that broad-spectrum sunscreens do not necessarily protect against visible light (VL) and UV-A1. Research has demonstrated that VL exposure induces both transient and long-term cutaneous pigmentation in a dose-dependent manner.

“This induces free radicals and reactive oxygen species, leading to a cascade of events including the induction of pro-inflammatory cytokines, matrix metalloproteinases, and melanogenesis,” she said. “More intense and persistent VL-induced pigmentation occurs in subjects with darker skin. However, there is increasing evidence that antioxidants may help to mitigate these negative effects, so we are starting to see the addition of antioxidants into sunscreens.”

Dr. Luke recommends a broad-spectrum sunscreen with an SPF of 30 or higher for skin of color patients. Tinted sunscreens, which contain iron oxide pigments, are recommended for the prevention and treatment of pigmentary disorders in patients with Fitzpatrick skin types IV-VI skin. “What about adding antioxidants to prevent formation of reactive oxygen species?” she asked. “It’s possible but we don’t have a lot of research yet. You also want a sunscreen that’s aesthetically elegant, meaning it doesn’t leave a white cast.”

Dr. Luke reported having no relevant disclosures.

PORTLAND, ORE. – When individuals with skin of color seek help from dermatologists to optimize the treatment and management of scalp and hair disorders, they expect them to understand their concerns, but sometimes their doctors fall short.

“Many times, you may not have race concordant visits with patients of color,” Janiene Luke, MD, said at the annual meeting of the Pacific Dermatologic Association. She referred to a survey of 200 Black women aged 21-83 years, which found that 28% had visited a physician to discuss hair or scalp issues. Of those, 68% felt like their dermatologists did not understand African American hair.

“I recommend trying the best you can to familiarize yourself with various common cultural hair styling methods and practices in patients of color. It’s important to understand what your patients are engaging in and the types of styles they’re using,” said Dr. Luke, associate professor of dermatology at Loma Linda (Calif.) University. “Approach all patients with cultural humility. We know from studies that patients value dermatologists who take time to listen to their concerns, involve them in the decision-making process, and educate them about their conditions,” she added.

National efforts to educate clinicians on treating skin of color have emerged in recent years, including textbooks, CME courses at dermatology conferences, and the American Academy of Dermatology’s Skin of Color Curriculum, which consists of 15-minute modules that can be viewed online.

At the meeting, Dr. Luke, shared her approach to assessing hair and scalp disorders in skin of color. She begins by taking a thorough history, “because not all things that are associated with hair styling will be the reason why your patient comes in,” she said. “Patients of color can have telogen effluvium and seborrheic dermatitis just like anyone else. I ask about the hair styling practices they use. I also ask how often they wash their hair, because sometimes our recommendations for treatment are not realistic based on their current routine.”

Next, she examines the scalp with her hands – which sometimes surprises patients. “I’ve had so many patients come in and say, ‘the dermatologist never touched my scalp,’ or ‘they never even looked at my hair,’ ” said Dr. Luke, who directs the university’s dermatology residency program. She asks patients to remove any hair extensions or weaves prior to the office visit and to remove wigs prior to the exam itself. The lab tests she customarily orders include CBC, TSH, iron, total iron binding capacity, ferritin, vitamin D, and zinc. If there are signs of androgen excess, she may check testosterone, sex hormone binding globulin, and dehydroepiandrosterone sulfate (DHEA-S). She routinely incorporates a dermoscopy-directed biopsy into the evaluation.

Dr. Luke examines the patient from above, the sides, and the back to assess the pattern/distribution of hair loss. A visible scalp at the vertex indicates a 50% reduction in normal hair density. “I’m looking at the hairline, their part width, and the length of their hair,” she said. “I also look at the eyebrows and eyelashes, because these can be involved in alopecia areata, frontal fibrosing alopecia, or congenital hair shaft disorders.”

On closeup examination, she looks for scarring versus non-scarring types of hair loss, and for the presence or absence of follicular ostia. “I also look at hair changes,” she said. “Is the texture of their hair different? Are there signs of breakage or fragility? It’s been noted in studies that breakage can be an early sign of central centrifugal cicatricial alopecia.” (For more tips on examining tightly coiled hair among patients with hair loss in race discordant patient-physician interactions, she recommended a 2021 article in JAMA Dermatology)..

Trichoscopy allows for magnified observation of the hair shafts, hair follicle openings, perifollicular dermis, and blood vessels. Normal trichoscopy findings in skin of color reveal a perifollicular pigment network (honeycomb pattern) and pinpoint white dots that are regularly distributed between follicular units.

Common abnormalities seen on trichoscopy include central centrifugal cicatricial alopecia (CCCA), with one or two hairs emerging together, surrounded by a gray halo; lichen planopilaris/frontal fibrosing alopecia, characterized by hair with peripilar casts and absence of vellus hairs; discoid lupus erythematosus, characterized by keratotic plugs; and traction, characterized by hair casts.

Once a diagnosis is confirmed, Dr. Luke provides other general advice for optimal skin health, including a balanced (whole food) diet to ensure adequate nutrition. “I tend to find a lot of nutrient deficiencies that contribute to and compound their condition,” she said. Other recommendations include avoiding excess tension on the hair, such as hair styles with tight ponytails, buns, braids, and weaves; avoiding or limiting chemical treatments with hair color, relaxers, and permanents; and avoiding or limiting excessive heat styling with blow dryers, flat irons, and curling irons.


 

Photoprotection misconceptions

At the meeting, Dr. Luke also discussed three misconceptions of photoprotection in skin of color, drawn from an article on the topic published in 2021.

• Myth No. 1: Endogenous melanin provides complete photoprotection for Fitzpatrick skin types IV-V. Many people with skin of color may believe sunscreen is not needed given the melanin already present in their skin, but research has shown that the epidermis of dark skin has an intrinsic sun protection factor (SPF) of 13.4, compared with an SPF of 3.3 in light skin. “That may not provide them with full protection,” Dr. Luke said. “Many dermatologists are not counseling their skin of color patients about photoprotection.”
• Myth No. 2: Individuals with skin of color have negligible risks associated with skin cancer. Skin cancer prevalence in patients with skin of color is significantly lower compared with those with light skin. However, people with skin of color tend to be diagnosed with cancers at a more advanced stage, and cancers associated with a worse prognosis and poorer survival rate. An analysis of ethnic differences among patients with cutaneous melanoma that drew from the Surveillance, Epidemiology, and End Results (SEER) program found that Hispanic individuals (odds ratio [OR], 3.6), Black individuals (OR, 4.2), and Asian individuals (OR, 2.4), were more likely than were White individuals to have stage IV melanoma at the time of presentation. “For melanoma in skin of color, UV radiation does not seem to be a major risk factor, as melanoma tends to occur on palmar/plantar and subungual skin as well as mucous membranes,” Dr. Luke said. “For squamous cell carcinoma in skin of color, lesions are more likely to be present in areas that are not sun exposed. The risk factors for this tend to be chronic wounds, nonhealing ulcers, and people with chronic inflammatory conditions.” For basal cell carcinoma, she added, UV radiation seems to play more of a role and tends to occur in sun-exposed areas in patients with lighter Fitzpatrick skin types. Patients are more likely to present with pigmented BCCs.

• Myth No. 3: Broad-spectrum sunscreens provide photoprotection against all wavelengths of light that cause skin damage. To be labeled “broad-spectrum” the Food and Drug Administration requires that sunscreens have a critical wavelength of 370 nm or below, but Dr. Luke noted that broad-spectrum sunscreens do not necessarily protect against visible light (VL) and UV-A1. Research has demonstrated that VL exposure induces both transient and long-term cutaneous pigmentation in a dose-dependent manner.

“This induces free radicals and reactive oxygen species, leading to a cascade of events including the induction of pro-inflammatory cytokines, matrix metalloproteinases, and melanogenesis,” she said. “More intense and persistent VL-induced pigmentation occurs in subjects with darker skin. However, there is increasing evidence that antioxidants may help to mitigate these negative effects, so we are starting to see the addition of antioxidants into sunscreens.”

Dr. Luke recommends a broad-spectrum sunscreen with an SPF of 30 or higher for skin of color patients. Tinted sunscreens, which contain iron oxide pigments, are recommended for the prevention and treatment of pigmentary disorders in patients with Fitzpatrick skin types IV-VI skin. “What about adding antioxidants to prevent formation of reactive oxygen species?” she asked. “It’s possible but we don’t have a lot of research yet. You also want a sunscreen that’s aesthetically elegant, meaning it doesn’t leave a white cast.”

Dr. Luke reported having no relevant disclosures.

PORTLAND, ORE. – When individuals with skin of color seek help from dermatologists to optimize the treatment and management of scalp and hair disorders, they expect them to understand their concerns, but sometimes their doctors fall short.

“Many times, you may not have race concordant visits with patients of color,” Janiene Luke, MD, said at the annual meeting of the Pacific Dermatologic Association. She referred to a survey of 200 Black women aged 21-83 years, which found that 28% had visited a physician to discuss hair or scalp issues. Of those, 68% felt like their dermatologists did not understand African American hair.

“I recommend trying the best you can to familiarize yourself with various common cultural hair styling methods and practices in patients of color. It’s important to understand what your patients are engaging in and the types of styles they’re using,” said Dr. Luke, associate professor of dermatology at Loma Linda (Calif.) University. “Approach all patients with cultural humility. We know from studies that patients value dermatologists who take time to listen to their concerns, involve them in the decision-making process, and educate them about their conditions,” she added.

National efforts to educate clinicians on treating skin of color have emerged in recent years, including textbooks, CME courses at dermatology conferences, and the American Academy of Dermatology’s Skin of Color Curriculum, which consists of 15-minute modules that can be viewed online.

At the meeting, Dr. Luke, shared her approach to assessing hair and scalp disorders in skin of color. She begins by taking a thorough history, “because not all things that are associated with hair styling will be the reason why your patient comes in,” she said. “Patients of color can have telogen effluvium and seborrheic dermatitis just like anyone else. I ask about the hair styling practices they use. I also ask how often they wash their hair, because sometimes our recommendations for treatment are not realistic based on their current routine.”

Next, she examines the scalp with her hands – which sometimes surprises patients. “I’ve had so many patients come in and say, ‘the dermatologist never touched my scalp,’ or ‘they never even looked at my hair,’ ” said Dr. Luke, who directs the university’s dermatology residency program. She asks patients to remove any hair extensions or weaves prior to the office visit and to remove wigs prior to the exam itself. The lab tests she customarily orders include CBC, TSH, iron, total iron binding capacity, ferritin, vitamin D, and zinc. If there are signs of androgen excess, she may check testosterone, sex hormone binding globulin, and dehydroepiandrosterone sulfate (DHEA-S). She routinely incorporates a dermoscopy-directed biopsy into the evaluation.

Dr. Luke examines the patient from above, the sides, and the back to assess the pattern/distribution of hair loss. A visible scalp at the vertex indicates a 50% reduction in normal hair density. “I’m looking at the hairline, their part width, and the length of their hair,” she said. “I also look at the eyebrows and eyelashes, because these can be involved in alopecia areata, frontal fibrosing alopecia, or congenital hair shaft disorders.”

On closeup examination, she looks for scarring versus non-scarring types of hair loss, and for the presence or absence of follicular ostia. “I also look at hair changes,” she said. “Is the texture of their hair different? Are there signs of breakage or fragility? It’s been noted in studies that breakage can be an early sign of central centrifugal cicatricial alopecia.” (For more tips on examining tightly coiled hair among patients with hair loss in race discordant patient-physician interactions, she recommended a 2021 article in JAMA Dermatology)..

Trichoscopy allows for magnified observation of the hair shafts, hair follicle openings, perifollicular dermis, and blood vessels. Normal trichoscopy findings in skin of color reveal a perifollicular pigment network (honeycomb pattern) and pinpoint white dots that are regularly distributed between follicular units.

Common abnormalities seen on trichoscopy include central centrifugal cicatricial alopecia (CCCA), with one or two hairs emerging together, surrounded by a gray halo; lichen planopilaris/frontal fibrosing alopecia, characterized by hair with peripilar casts and absence of vellus hairs; discoid lupus erythematosus, characterized by keratotic plugs; and traction, characterized by hair casts.

Once a diagnosis is confirmed, Dr. Luke provides other general advice for optimal skin health, including a balanced (whole food) diet to ensure adequate nutrition. “I tend to find a lot of nutrient deficiencies that contribute to and compound their condition,” she said. Other recommendations include avoiding excess tension on the hair, such as hair styles with tight ponytails, buns, braids, and weaves; avoiding or limiting chemical treatments with hair color, relaxers, and permanents; and avoiding or limiting excessive heat styling with blow dryers, flat irons, and curling irons.


 

Photoprotection misconceptions

At the meeting, Dr. Luke also discussed three misconceptions of photoprotection in skin of color, drawn from an article on the topic published in 2021.

• Myth No. 1: Endogenous melanin provides complete photoprotection for Fitzpatrick skin types IV-V. Many people with skin of color may believe sunscreen is not needed given the melanin already present in their skin, but research has shown that the epidermis of dark skin has an intrinsic sun protection factor (SPF) of 13.4, compared with an SPF of 3.3 in light skin. “That may not provide them with full protection,” Dr. Luke said. “Many dermatologists are not counseling their skin of color patients about photoprotection.”
• Myth No. 2: Individuals with skin of color have negligible risks associated with skin cancer. Skin cancer prevalence in patients with skin of color is significantly lower compared with those with light skin. However, people with skin of color tend to be diagnosed with cancers at a more advanced stage, and cancers associated with a worse prognosis and poorer survival rate. An analysis of ethnic differences among patients with cutaneous melanoma that drew from the Surveillance, Epidemiology, and End Results (SEER) program found that Hispanic individuals (odds ratio [OR], 3.6), Black individuals (OR, 4.2), and Asian individuals (OR, 2.4), were more likely than were White individuals to have stage IV melanoma at the time of presentation. “For melanoma in skin of color, UV radiation does not seem to be a major risk factor, as melanoma tends to occur on palmar/plantar and subungual skin as well as mucous membranes,” Dr. Luke said. “For squamous cell carcinoma in skin of color, lesions are more likely to be present in areas that are not sun exposed. The risk factors for this tend to be chronic wounds, nonhealing ulcers, and people with chronic inflammatory conditions.” For basal cell carcinoma, she added, UV radiation seems to play more of a role and tends to occur in sun-exposed areas in patients with lighter Fitzpatrick skin types. Patients are more likely to present with pigmented BCCs.

• Myth No. 3: Broad-spectrum sunscreens provide photoprotection against all wavelengths of light that cause skin damage. To be labeled “broad-spectrum” the Food and Drug Administration requires that sunscreens have a critical wavelength of 370 nm or below, but Dr. Luke noted that broad-spectrum sunscreens do not necessarily protect against visible light (VL) and UV-A1. Research has demonstrated that VL exposure induces both transient and long-term cutaneous pigmentation in a dose-dependent manner.

“This induces free radicals and reactive oxygen species, leading to a cascade of events including the induction of pro-inflammatory cytokines, matrix metalloproteinases, and melanogenesis,” she said. “More intense and persistent VL-induced pigmentation occurs in subjects with darker skin. However, there is increasing evidence that antioxidants may help to mitigate these negative effects, so we are starting to see the addition of antioxidants into sunscreens.”

Dr. Luke recommends a broad-spectrum sunscreen with an SPF of 30 or higher for skin of color patients. Tinted sunscreens, which contain iron oxide pigments, are recommended for the prevention and treatment of pigmentary disorders in patients with Fitzpatrick skin types IV-VI skin. “What about adding antioxidants to prevent formation of reactive oxygen species?” she asked. “It’s possible but we don’t have a lot of research yet. You also want a sunscreen that’s aesthetically elegant, meaning it doesn’t leave a white cast.”

Dr. Luke reported having no relevant disclosures.

To the Editor:

Nail abnormalities associated with SARS-CoV-2 infection that have been reported in the medical literature include nail psoriasis,¹ Beau lines,² onychomadesis,³ heterogeneous red-white discoloration of the nail bed,⁴ transverse orange nail lesions,³ and the red half‐moon nail sign.^3,5 It has been hypothesized that these nail findings may be an indication of microvascular injury to the distal subungual arcade of the digit or may be indicative of a procoagulant state.^5,6 Currently, there is limited knowledge of the effect of COVID-19 vaccines on nail changes. We report a patient who presented with transverse leukonychia (Mees lines) and Beau lines shortly after each dose of the Pfizer-BioNTech COVID-19 messenger RNA vaccine was administered (with a total of 2 doses administered on presentation).

A 64-year-old woman with a history of rheumatoid arthritis presented with peeling of the fingernails and proximal white discoloration of several fingernails of 2 months’ duration. The patient first noticed whitening of the nails 3 weeks after she recevied the first dose of the COVID-19 vaccine. Five days after receiving the second, she presented to the dermatology clinic and exhibited transverse leukonychia in most fingernails (Figure 1).

Six weeks following the second dose of the COVID-19 vaccine, the patient returned to the dermatology clinic with Beau lines on the second and third fingernails on the right hand (Figure 2A). Subtle erythema of the proximal nail folds and distal fingers was observed in both hands. The patient also exhibited mild onychorrhexis of the left thumbnail and mottled red-brown discoloration of the third finger on the left hand (Figure 2B). Splinter hemorrhages and melanonychia of several fingernails also were observed. Our patient denied any known history of infection with SARS-CoV-2, which was confirmed by a negative COVID-19 polymerase chain reaction test result. She also denied fevers, chills, nausea, and vomiting, she and reported feeling generally well in the context of these postvaccination nail changes.

She reported no trauma or worsening of rheumatoid arthritis before or after COVID-19 vaccination. She was seronegative for rheumatoid arthritis and was being treated with hydroxychloroquine for the last year and methotrexate for the last 2 years. After each dose of the vaccine, methotrexate was withheld for 1 week and then resumed.

Subsequent follow-up examinations revealed the migration and resolution of transverse leukonychia and Beau lines. There also was interval improvement of the splinter hemorrhages. At 17 weeks following the second vaccine dose, all transverse leukonychia and Beau lines had resolved (Figure 3). The patient’s melanonychia remained unchanged.

Laboratory evaluations drawn 1 month following the first dose of the COVID-19 vaccine, including comprehensive metabolic panel; erythrocyte sedimentation rate; C-reactive protein; and vitamin B₁₂, ferritin, and iron levels were within reference range. The complete blood cell count only showed a mildly decreased white blood cell count (3.55×10³/µL [reference range, 4.16–9.95×10³/µL]) and mildly elevated mean corpuscular volume (101.9 fL [reference range, 79.3–98.6 fL), both near the patient’s baseline values prior to vaccination.

Documented cutaneous manifestations of SARS‐CoV‐2 infection have included perniolike lesions (known as COVID toes) and vesicular, urticarial, petechial, livedoid, or retiform purpura eruptions. Less frequently, nail findings in patients infected with COVID-19 have been reported, including Beau lines,² onychomadesis,³ transverse leukonychia,^3,7 and the red half‐moon nail sign.^3,5 Single or multiple nails may be affected. Although the pathogenesis of nail manifestations related to COVID-19 remains unclear, complement-mediated microvascular injury and thrombosis as well as the procoagulant state, which have been associated with COVID-19, may offer possible explanations.^5,6 The presence of microvascular abnormalities was observed in a nail fold video capillaroscopy study of the nails of 82 patients with COVID-19, revealing pericapillary edema, capillary ectasia, sludge flow, meandering capillaries and microvascular derangement, and low capillary density.⁸

Our patient exhibited transverse leukonychia of the fingernails, which is thought to result from abnormal keratinization of the nail plate due to systemic disorders that induce a temporary dysfunction of nail growth.⁹ Fernandez-Nieto et al⁷ reported transverse leukonychia in a patient with COVID-19 that was hypothesized to be due to a transitory nail matrix injury.

Beau lines and onychomadesis, which represent nail matrix arrest, commonly are seen with systemic drug treatments such as chemotherapy and in infectious diseases that precipitate systemic illness, such as hand, foot, and mouth disease. Although histologic examination was not performed in our patient due to cosmetic concerns, we believe that inflammation induced by the vaccine response also can trigger nail abnormalities such as transverse leukonychia and Beau lines. Both SARS-CoV-2 infections and the COVID-19 messenger RNA vaccines can induce systemic inflammation largely due a T_H1-dominant response, and they also can trigger other inflammatory conditions. Reports of lichen planus and psoriasis triggered by vaccination—the hepatitis B vaccine,¹⁰ influenza vaccine,¹¹ and even COVID-19 vaccines^1,12—have been reported. Beau lines have been observed to spontaneously resolve in a self-limiting manner in asymptomatic patients with COVID-19.

Interestingly, our patient only showed 2 nails with Beau lines. We hypothesize that the immune response triggered by vaccination was more subdued than that caused by SARS-CoV-2 infection. Additionally, our patient was already being treated with immunosuppressants, which may have been associated with a reduced immune response despite being withheld right before vaccination. One may debate whether the nail abnormalities observed in our patient constituted an isolated finding from COVID-19 vaccination or were caused by reactivation of rheumatoid arthritis. We favor the former, as the rheumatoid arthritis remained stable before and after COVID-19 vaccination. Laboratory evaluations and physical examination revealed no evidence of flares, and our patient was otherwise healthy. Although the splinter hemorrhages also improved, it is difficult to comment as to whether they were caused by the vaccine or had existed prior to vaccination. However, we believe the melanonychia observed in the nails was unrelated to the vaccine and was likely a chronic manifestation due to long-term hydroxychloroquine and/or methotrexate use.

Given accelerated global vaccination efforts to control the COVID-19 pandemic, more cases of adverse nail manifestations associated with COVID-19 vaccines are expected. Dermatologists should be aware of and use the reported nail findings to educate patients and reassure them that ungual abnormalities are potential adverse effects of COVID-19 vaccines, but they should not discourage vaccination because they usually are temporary and self-resolving.

To the Editor:

Nail abnormalities associated with SARS-CoV-2 infection that have been reported in the medical literature include nail psoriasis,¹ Beau lines,² onychomadesis,³ heterogeneous red-white discoloration of the nail bed,⁴ transverse orange nail lesions,³ and the red half‐moon nail sign.^3,5 It has been hypothesized that these nail findings may be an indication of microvascular injury to the distal subungual arcade of the digit or may be indicative of a procoagulant state.^5,6 Currently, there is limited knowledge of the effect of COVID-19 vaccines on nail changes. We report a patient who presented with transverse leukonychia (Mees lines) and Beau lines shortly after each dose of the Pfizer-BioNTech COVID-19 messenger RNA vaccine was administered (with a total of 2 doses administered on presentation).

A 64-year-old woman with a history of rheumatoid arthritis presented with peeling of the fingernails and proximal white discoloration of several fingernails of 2 months’ duration. The patient first noticed whitening of the nails 3 weeks after she recevied the first dose of the COVID-19 vaccine. Five days after receiving the second, she presented to the dermatology clinic and exhibited transverse leukonychia in most fingernails (Figure 1).

Six weeks following the second dose of the COVID-19 vaccine, the patient returned to the dermatology clinic with Beau lines on the second and third fingernails on the right hand (Figure 2A). Subtle erythema of the proximal nail folds and distal fingers was observed in both hands. The patient also exhibited mild onychorrhexis of the left thumbnail and mottled red-brown discoloration of the third finger on the left hand (Figure 2B). Splinter hemorrhages and melanonychia of several fingernails also were observed. Our patient denied any known history of infection with SARS-CoV-2, which was confirmed by a negative COVID-19 polymerase chain reaction test result. She also denied fevers, chills, nausea, and vomiting, she and reported feeling generally well in the context of these postvaccination nail changes.

She reported no trauma or worsening of rheumatoid arthritis before or after COVID-19 vaccination. She was seronegative for rheumatoid arthritis and was being treated with hydroxychloroquine for the last year and methotrexate for the last 2 years. After each dose of the vaccine, methotrexate was withheld for 1 week and then resumed.

Subsequent follow-up examinations revealed the migration and resolution of transverse leukonychia and Beau lines. There also was interval improvement of the splinter hemorrhages. At 17 weeks following the second vaccine dose, all transverse leukonychia and Beau lines had resolved (Figure 3). The patient’s melanonychia remained unchanged.

Laboratory evaluations drawn 1 month following the first dose of the COVID-19 vaccine, including comprehensive metabolic panel; erythrocyte sedimentation rate; C-reactive protein; and vitamin B₁₂, ferritin, and iron levels were within reference range. The complete blood cell count only showed a mildly decreased white blood cell count (3.55×10³/µL [reference range, 4.16–9.95×10³/µL]) and mildly elevated mean corpuscular volume (101.9 fL [reference range, 79.3–98.6 fL), both near the patient’s baseline values prior to vaccination.

Documented cutaneous manifestations of SARS‐CoV‐2 infection have included perniolike lesions (known as COVID toes) and vesicular, urticarial, petechial, livedoid, or retiform purpura eruptions. Less frequently, nail findings in patients infected with COVID-19 have been reported, including Beau lines,² onychomadesis,³ transverse leukonychia,^3,7 and the red half‐moon nail sign.^3,5 Single or multiple nails may be affected. Although the pathogenesis of nail manifestations related to COVID-19 remains unclear, complement-mediated microvascular injury and thrombosis as well as the procoagulant state, which have been associated with COVID-19, may offer possible explanations.^5,6 The presence of microvascular abnormalities was observed in a nail fold video capillaroscopy study of the nails of 82 patients with COVID-19, revealing pericapillary edema, capillary ectasia, sludge flow, meandering capillaries and microvascular derangement, and low capillary density.⁸

Our patient exhibited transverse leukonychia of the fingernails, which is thought to result from abnormal keratinization of the nail plate due to systemic disorders that induce a temporary dysfunction of nail growth.⁹ Fernandez-Nieto et al⁷ reported transverse leukonychia in a patient with COVID-19 that was hypothesized to be due to a transitory nail matrix injury.

Beau lines and onychomadesis, which represent nail matrix arrest, commonly are seen with systemic drug treatments such as chemotherapy and in infectious diseases that precipitate systemic illness, such as hand, foot, and mouth disease. Although histologic examination was not performed in our patient due to cosmetic concerns, we believe that inflammation induced by the vaccine response also can trigger nail abnormalities such as transverse leukonychia and Beau lines. Both SARS-CoV-2 infections and the COVID-19 messenger RNA vaccines can induce systemic inflammation largely due a T_H1-dominant response, and they also can trigger other inflammatory conditions. Reports of lichen planus and psoriasis triggered by vaccination—the hepatitis B vaccine,¹⁰ influenza vaccine,¹¹ and even COVID-19 vaccines^1,12—have been reported. Beau lines have been observed to spontaneously resolve in a self-limiting manner in asymptomatic patients with COVID-19.

Interestingly, our patient only showed 2 nails with Beau lines. We hypothesize that the immune response triggered by vaccination was more subdued than that caused by SARS-CoV-2 infection. Additionally, our patient was already being treated with immunosuppressants, which may have been associated with a reduced immune response despite being withheld right before vaccination. One may debate whether the nail abnormalities observed in our patient constituted an isolated finding from COVID-19 vaccination or were caused by reactivation of rheumatoid arthritis. We favor the former, as the rheumatoid arthritis remained stable before and after COVID-19 vaccination. Laboratory evaluations and physical examination revealed no evidence of flares, and our patient was otherwise healthy. Although the splinter hemorrhages also improved, it is difficult to comment as to whether they were caused by the vaccine or had existed prior to vaccination. However, we believe the melanonychia observed in the nails was unrelated to the vaccine and was likely a chronic manifestation due to long-term hydroxychloroquine and/or methotrexate use.

Given accelerated global vaccination efforts to control the COVID-19 pandemic, more cases of adverse nail manifestations associated with COVID-19 vaccines are expected. Dermatologists should be aware of and use the reported nail findings to educate patients and reassure them that ungual abnormalities are potential adverse effects of COVID-19 vaccines, but they should not discourage vaccination because they usually are temporary and self-resolving.

To the Editor:

Nail abnormalities associated with SARS-CoV-2 infection that have been reported in the medical literature include nail psoriasis,¹ Beau lines,² onychomadesis,³ heterogeneous red-white discoloration of the nail bed,⁴ transverse orange nail lesions,³ and the red half‐moon nail sign.^3,5 It has been hypothesized that these nail findings may be an indication of microvascular injury to the distal subungual arcade of the digit or may be indicative of a procoagulant state.^5,6 Currently, there is limited knowledge of the effect of COVID-19 vaccines on nail changes. We report a patient who presented with transverse leukonychia (Mees lines) and Beau lines shortly after each dose of the Pfizer-BioNTech COVID-19 messenger RNA vaccine was administered (with a total of 2 doses administered on presentation).

A 64-year-old woman with a history of rheumatoid arthritis presented with peeling of the fingernails and proximal white discoloration of several fingernails of 2 months’ duration. The patient first noticed whitening of the nails 3 weeks after she recevied the first dose of the COVID-19 vaccine. Five days after receiving the second, she presented to the dermatology clinic and exhibited transverse leukonychia in most fingernails (Figure 1).

Six weeks following the second dose of the COVID-19 vaccine, the patient returned to the dermatology clinic with Beau lines on the second and third fingernails on the right hand (Figure 2A). Subtle erythema of the proximal nail folds and distal fingers was observed in both hands. The patient also exhibited mild onychorrhexis of the left thumbnail and mottled red-brown discoloration of the third finger on the left hand (Figure 2B). Splinter hemorrhages and melanonychia of several fingernails also were observed. Our patient denied any known history of infection with SARS-CoV-2, which was confirmed by a negative COVID-19 polymerase chain reaction test result. She also denied fevers, chills, nausea, and vomiting, she and reported feeling generally well in the context of these postvaccination nail changes.

She reported no trauma or worsening of rheumatoid arthritis before or after COVID-19 vaccination. She was seronegative for rheumatoid arthritis and was being treated with hydroxychloroquine for the last year and methotrexate for the last 2 years. After each dose of the vaccine, methotrexate was withheld for 1 week and then resumed.

Subsequent follow-up examinations revealed the migration and resolution of transverse leukonychia and Beau lines. There also was interval improvement of the splinter hemorrhages. At 17 weeks following the second vaccine dose, all transverse leukonychia and Beau lines had resolved (Figure 3). The patient’s melanonychia remained unchanged.

Laboratory evaluations drawn 1 month following the first dose of the COVID-19 vaccine, including comprehensive metabolic panel; erythrocyte sedimentation rate; C-reactive protein; and vitamin B₁₂, ferritin, and iron levels were within reference range. The complete blood cell count only showed a mildly decreased white blood cell count (3.55×10³/µL [reference range, 4.16–9.95×10³/µL]) and mildly elevated mean corpuscular volume (101.9 fL [reference range, 79.3–98.6 fL), both near the patient’s baseline values prior to vaccination.

Documented cutaneous manifestations of SARS‐CoV‐2 infection have included perniolike lesions (known as COVID toes) and vesicular, urticarial, petechial, livedoid, or retiform purpura eruptions. Less frequently, nail findings in patients infected with COVID-19 have been reported, including Beau lines,² onychomadesis,³ transverse leukonychia,^3,7 and the red half‐moon nail sign.^3,5 Single or multiple nails may be affected. Although the pathogenesis of nail manifestations related to COVID-19 remains unclear, complement-mediated microvascular injury and thrombosis as well as the procoagulant state, which have been associated with COVID-19, may offer possible explanations.^5,6 The presence of microvascular abnormalities was observed in a nail fold video capillaroscopy study of the nails of 82 patients with COVID-19, revealing pericapillary edema, capillary ectasia, sludge flow, meandering capillaries and microvascular derangement, and low capillary density.⁸

Our patient exhibited transverse leukonychia of the fingernails, which is thought to result from abnormal keratinization of the nail plate due to systemic disorders that induce a temporary dysfunction of nail growth.⁹ Fernandez-Nieto et al⁷ reported transverse leukonychia in a patient with COVID-19 that was hypothesized to be due to a transitory nail matrix injury.

Beau lines and onychomadesis, which represent nail matrix arrest, commonly are seen with systemic drug treatments such as chemotherapy and in infectious diseases that precipitate systemic illness, such as hand, foot, and mouth disease. Although histologic examination was not performed in our patient due to cosmetic concerns, we believe that inflammation induced by the vaccine response also can trigger nail abnormalities such as transverse leukonychia and Beau lines. Both SARS-CoV-2 infections and the COVID-19 messenger RNA vaccines can induce systemic inflammation largely due a T_H1-dominant response, and they also can trigger other inflammatory conditions. Reports of lichen planus and psoriasis triggered by vaccination—the hepatitis B vaccine,¹⁰ influenza vaccine,¹¹ and even COVID-19 vaccines^1,12—have been reported. Beau lines have been observed to spontaneously resolve in a self-limiting manner in asymptomatic patients with COVID-19.

Interestingly, our patient only showed 2 nails with Beau lines. We hypothesize that the immune response triggered by vaccination was more subdued than that caused by SARS-CoV-2 infection. Additionally, our patient was already being treated with immunosuppressants, which may have been associated with a reduced immune response despite being withheld right before vaccination. One may debate whether the nail abnormalities observed in our patient constituted an isolated finding from COVID-19 vaccination or were caused by reactivation of rheumatoid arthritis. We favor the former, as the rheumatoid arthritis remained stable before and after COVID-19 vaccination. Laboratory evaluations and physical examination revealed no evidence of flares, and our patient was otherwise healthy. Although the splinter hemorrhages also improved, it is difficult to comment as to whether they were caused by the vaccine or had existed prior to vaccination. However, we believe the melanonychia observed in the nails was unrelated to the vaccine and was likely a chronic manifestation due to long-term hydroxychloroquine and/or methotrexate use.

Given accelerated global vaccination efforts to control the COVID-19 pandemic, more cases of adverse nail manifestations associated with COVID-19 vaccines are expected. Dermatologists should be aware of and use the reported nail findings to educate patients and reassure them that ungual abnormalities are potential adverse effects of COVID-19 vaccines, but they should not discourage vaccination because they usually are temporary and self-resolving.

One day in 2020, Ronda S. Farah, MD, was spending some downtime from her dermatology practice scrolling through social media. When she opened TikTok, she came across something that piqued her interest: A popular content creator was promoting the supplement biotin as a way to grow hair. Dr. Farah was immediately alarmed, because not only was the evidence that biotin increases hair growth shoddy, but the FDA had also warned that biotin supplements may interfere with lab tests for troponin.

Dr. Farah was moved to action and made a brief TikTok stating that use of biotin does not result in hair growth for most patients, which quickly shot up to over half a million views. She was flooded with messages from influencers and people desperate for an answer to their hair growth questions.

From that point on, Dr. Farah was immersed in the world of hairfluencers, the social media personalities who promote hair care trends, which formed the basis of a review, published in the Journal of Cosmetic Dermatology that she conducted with her colleagues at the University of Minnesota, Minneapolis. .

They reviewed five treatments that represent some of the most frequently discussed hair-growth trends on social media: rosemary, onion juice, rice water, castor oil, and aloe vera. For each, they evaluated recommendations on how the treatments were applied, possible harmful effects to the user, claims that weren’t totally based on scientific evidence, and the theoretical mechanism of action. “Overall,” they concluded, “there is little to no literature supporting these social media trends for hair growth.”

Of the five, rosemary, applied to the scalp or hair, has perhaps the most significant research behind it, according to Dr. Farah and coauthors. Methods of applying rosemary described on social media included use of prepackaged oil, boiling fresh rosemary leaves, adding leaves to oils and spraying it on or massaging it on the scalp, applying it in the hair, or using it as a rinse. Dr. Farah noted that the literature supporting the use of rosemary for hair growth does not represent the most robust science; the studies had small sample sizes and used nonstandardized methods of measuring hair growth.

“It didn’t really meet rigorous, strong study methods that a board-certified dermatologist with their expertise would consider a really solid study,” she said.

For the remaining methods, there was little research to support their use for hair growth. A few, the authors pointed out, can cause scalp burns (aloe vera), damage to hair follicles (rice water), contact dermatitis (aloe vera, onion juice), and, in the case of castor oil, hair felting..

Dr. Farah thinks social media can be a great tool to reach patients, but that people should be wary of what kind of information they’re consuming “and need to be aware of who their hairfluencer is,” she said. And, as she and her coauthors wrote: “We call on dermatologists, as hair and scalp disease experts, to serve as authorities on ‘hairfluencer’ trends and appropriately counsel patients.”

The study was independently supported. Dr. Farah reports no relevant financial relationships.

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

One day in 2020, Ronda S. Farah, MD, was spending some downtime from her dermatology practice scrolling through social media. When she opened TikTok, she came across something that piqued her interest: A popular content creator was promoting the supplement biotin as a way to grow hair. Dr. Farah was immediately alarmed, because not only was the evidence that biotin increases hair growth shoddy, but the FDA had also warned that biotin supplements may interfere with lab tests for troponin.

Dr. Farah was moved to action and made a brief TikTok stating that use of biotin does not result in hair growth for most patients, which quickly shot up to over half a million views. She was flooded with messages from influencers and people desperate for an answer to their hair growth questions.

From that point on, Dr. Farah was immersed in the world of hairfluencers, the social media personalities who promote hair care trends, which formed the basis of a review, published in the Journal of Cosmetic Dermatology that she conducted with her colleagues at the University of Minnesota, Minneapolis. .

They reviewed five treatments that represent some of the most frequently discussed hair-growth trends on social media: rosemary, onion juice, rice water, castor oil, and aloe vera. For each, they evaluated recommendations on how the treatments were applied, possible harmful effects to the user, claims that weren’t totally based on scientific evidence, and the theoretical mechanism of action. “Overall,” they concluded, “there is little to no literature supporting these social media trends for hair growth.”

Of the five, rosemary, applied to the scalp or hair, has perhaps the most significant research behind it, according to Dr. Farah and coauthors. Methods of applying rosemary described on social media included use of prepackaged oil, boiling fresh rosemary leaves, adding leaves to oils and spraying it on or massaging it on the scalp, applying it in the hair, or using it as a rinse. Dr. Farah noted that the literature supporting the use of rosemary for hair growth does not represent the most robust science; the studies had small sample sizes and used nonstandardized methods of measuring hair growth.

“It didn’t really meet rigorous, strong study methods that a board-certified dermatologist with their expertise would consider a really solid study,” she said.

For the remaining methods, there was little research to support their use for hair growth. A few, the authors pointed out, can cause scalp burns (aloe vera), damage to hair follicles (rice water), contact dermatitis (aloe vera, onion juice), and, in the case of castor oil, hair felting..

Dr. Farah thinks social media can be a great tool to reach patients, but that people should be wary of what kind of information they’re consuming “and need to be aware of who their hairfluencer is,” she said. And, as she and her coauthors wrote: “We call on dermatologists, as hair and scalp disease experts, to serve as authorities on ‘hairfluencer’ trends and appropriately counsel patients.”

The study was independently supported. Dr. Farah reports no relevant financial relationships.

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

One day in 2020, Ronda S. Farah, MD, was spending some downtime from her dermatology practice scrolling through social media. When she opened TikTok, she came across something that piqued her interest: A popular content creator was promoting the supplement biotin as a way to grow hair. Dr. Farah was immediately alarmed, because not only was the evidence that biotin increases hair growth shoddy, but the FDA had also warned that biotin supplements may interfere with lab tests for troponin.

Dr. Farah was moved to action and made a brief TikTok stating that use of biotin does not result in hair growth for most patients, which quickly shot up to over half a million views. She was flooded with messages from influencers and people desperate for an answer to their hair growth questions.

From that point on, Dr. Farah was immersed in the world of hairfluencers, the social media personalities who promote hair care trends, which formed the basis of a review, published in the Journal of Cosmetic Dermatology that she conducted with her colleagues at the University of Minnesota, Minneapolis. .

They reviewed five treatments that represent some of the most frequently discussed hair-growth trends on social media: rosemary, onion juice, rice water, castor oil, and aloe vera. For each, they evaluated recommendations on how the treatments were applied, possible harmful effects to the user, claims that weren’t totally based on scientific evidence, and the theoretical mechanism of action. “Overall,” they concluded, “there is little to no literature supporting these social media trends for hair growth.”

Of the five, rosemary, applied to the scalp or hair, has perhaps the most significant research behind it, according to Dr. Farah and coauthors. Methods of applying rosemary described on social media included use of prepackaged oil, boiling fresh rosemary leaves, adding leaves to oils and spraying it on or massaging it on the scalp, applying it in the hair, or using it as a rinse. Dr. Farah noted that the literature supporting the use of rosemary for hair growth does not represent the most robust science; the studies had small sample sizes and used nonstandardized methods of measuring hair growth.

“It didn’t really meet rigorous, strong study methods that a board-certified dermatologist with their expertise would consider a really solid study,” she said.

For the remaining methods, there was little research to support their use for hair growth. A few, the authors pointed out, can cause scalp burns (aloe vera), damage to hair follicles (rice water), contact dermatitis (aloe vera, onion juice), and, in the case of castor oil, hair felting..

Dr. Farah thinks social media can be a great tool to reach patients, but that people should be wary of what kind of information they’re consuming “and need to be aware of who their hairfluencer is,” she said. And, as she and her coauthors wrote: “We call on dermatologists, as hair and scalp disease experts, to serve as authorities on ‘hairfluencer’ trends and appropriately counsel patients.”

The study was independently supported. Dr. Farah reports no relevant financial relationships.

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

Hair loss, reduced sex drive, and erectile dysfunction have joined a list of better-known symptoms linked to long COVID in patients who were not hospitalized, according to findings of a large study.

Anuradhaa Subramanian, PhD, with the Institute of Applied Health Research at the University of Birmingham (England), led the research published online in Nature Medicine.

The team analyzed 486,149 electronic health records from adult patients with confirmed COVID in the United Kingdom, compared with 1.9 million people with no history of COVID, from January 2020 to April 2021. Researchers matched both groups closely in terms of demographic, social, and clinical traits.
 

New symptoms

The team identified 62 symptoms, including the well-known indicators of long COVID, such as fatigue, loss of sense of smell, shortness of breath, and brain fog, but also hair loss, sexual dysfunction, chest pain, fever, loss of control of bowel movements, and limb swelling.

“These differences in symptoms reported between the infected and uninfected groups remained even after we accounted for age, sex, ethnic group, socioeconomic status, body mass index, smoking status, the presence of more than 80 health conditions, and past reporting of the same symptom,” Dr. Subramanian and coresearcher Shamil Haroon, PhD, wrote in a summary of their research in The Conversation.

They pointed out that only 20 of the symptoms they found are included in the World Health Organization’s clinical case definition for long COVID.

They also found that people more likely to have persistent symptoms 3 months after COVID infection were also more likely to be young, female, smokers, to belong to certain minority ethnic groups, and to have lower socioeconomic status. They were also more likely to be obese and have a wide range of health conditions.

Dr. Haroon, an associate clinical professor at the University of Birmingham, said that one reason it appeared that younger people were more likely to get symptoms of long COVID may be that older adults with COVID were more likely to be hospitalized and weren’t included in this study.

“Since we only considered nonhospitalized adults, the older adults we included in our study may have been relatively healthier and thus had a lower symptom burden,” he said.

Dr. Subramania noted that older patients were more likely to report lasting COVID-related symptoms in the study, but when researchers accounted for a wide range of other conditions that patients had before infection (which generally more commonly happen in older adults), they found younger age as a risk factor for long-term COVID-related symptoms.

In the study period, most patients were unvaccinated, and results came before the widespread Delta and Omicron variants.

More than half (56.6%) of the patients infected with the virus that causes COVID had been diagnosed in 2020, and 43.4% in 2021. Less than 5% (4.5%) of the patients infected with the virus and 4.7% of the patients with no recorded evidence of a COVID infection had received at least a single dose of a COVID vaccine before the study started.

Eric Topol, MD, founder and director of the Scripps Research Translational Institute in La Jolla, Calif., and editor-in-chief of Medscape, said more studies need to be done to see whether results would be different with vaccination status and evolving variants.

But he noted that this study has several strengths: “The hair loss, libido loss, and ejaculation difficulty are all new symptoms,” and the study – large and carefully controlled – shows these issues were among those more likely to occur.

A loss of sense of smell – which is not a new observation – was still the most likely risk shown in the study, followed by hair loss, sneezing, ejaculation difficulty, and reduced sex drive; followed by shortness of breath, fatigue, chest pain associated with breathing difficulties, hoarseness, and fever.
 

Three main clusters of symptoms

Given the wide range of symptoms, long COVID likely represents a group of conditions, the authors wrote.

They found three main clusters. The largest, with roughly 80% of people with long COVID in the study, faced a broad spectrum of symptoms, ranging from fatigue to headache and pain. The second-largest group, (15%) mostly had symptoms having to do with mental health and thinking skills, including depression, anxiety, brain fog, and insomnia. The smallest group (5%) had mainly respiratory symptoms such as shortness of breath, coughing, and wheezing.

Putting symptoms in clusters will be important to start understanding what leads to long COVID, said Farha Ikramuddin, MD, a rehabilitation specialist at the University of Minnesota, Minneapolis.

She added that, while the symptoms listed in this paper are new in published research, she has certainly been seeing them over time in her long COVID clinic. (The researchers also used only coded health care data, so they were limited in what symptoms they could discover, she notes.)

Dr. Ikramuddin said a strength of the paper is its large size, but she also cautioned that it’s difficult to determine whether members of the comparison group truly had no COVID infection when the information is taken from their medical records. Often, people test at home or assume they have COVID and don’t test; therefore the information wouldn’t be recorded.

Evaluating nonhospitalized patients is also important, she said, as much of the research on long COVID has come from hospitalized patients, so little has been known about the symptoms of those with milder infections.

“Patients who have been hospitalized and have long COVID look very different from the patients who were not hospitalized,” Dr. Ikramuddin said.

One clear message from the paper, she said, is that listening and asking extensive questions about symptoms are important with patients who have had COVID.

“Counseling has also become very important for our patients in the pandemic,” she said.

It will also be important to do studies on returning to work for patients with long COVID to see how many are able to return and at what capacity, Dr. Ikramuddin said.

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

Hair loss, reduced sex drive, and erectile dysfunction have joined a list of better-known symptoms linked to long COVID in patients who were not hospitalized, according to findings of a large study.

Anuradhaa Subramanian, PhD, with the Institute of Applied Health Research at the University of Birmingham (England), led the research published online in Nature Medicine.

The team analyzed 486,149 electronic health records from adult patients with confirmed COVID in the United Kingdom, compared with 1.9 million people with no history of COVID, from January 2020 to April 2021. Researchers matched both groups closely in terms of demographic, social, and clinical traits.
 

New symptoms

The team identified 62 symptoms, including the well-known indicators of long COVID, such as fatigue, loss of sense of smell, shortness of breath, and brain fog, but also hair loss, sexual dysfunction, chest pain, fever, loss of control of bowel movements, and limb swelling.

“These differences in symptoms reported between the infected and uninfected groups remained even after we accounted for age, sex, ethnic group, socioeconomic status, body mass index, smoking status, the presence of more than 80 health conditions, and past reporting of the same symptom,” Dr. Subramanian and coresearcher Shamil Haroon, PhD, wrote in a summary of their research in The Conversation.

They pointed out that only 20 of the symptoms they found are included in the World Health Organization’s clinical case definition for long COVID.

They also found that people more likely to have persistent symptoms 3 months after COVID infection were also more likely to be young, female, smokers, to belong to certain minority ethnic groups, and to have lower socioeconomic status. They were also more likely to be obese and have a wide range of health conditions.

Dr. Haroon, an associate clinical professor at the University of Birmingham, said that one reason it appeared that younger people were more likely to get symptoms of long COVID may be that older adults with COVID were more likely to be hospitalized and weren’t included in this study.

“Since we only considered nonhospitalized adults, the older adults we included in our study may have been relatively healthier and thus had a lower symptom burden,” he said.

Dr. Subramania noted that older patients were more likely to report lasting COVID-related symptoms in the study, but when researchers accounted for a wide range of other conditions that patients had before infection (which generally more commonly happen in older adults), they found younger age as a risk factor for long-term COVID-related symptoms.

In the study period, most patients were unvaccinated, and results came before the widespread Delta and Omicron variants.

More than half (56.6%) of the patients infected with the virus that causes COVID had been diagnosed in 2020, and 43.4% in 2021. Less than 5% (4.5%) of the patients infected with the virus and 4.7% of the patients with no recorded evidence of a COVID infection had received at least a single dose of a COVID vaccine before the study started.

Eric Topol, MD, founder and director of the Scripps Research Translational Institute in La Jolla, Calif., and editor-in-chief of Medscape, said more studies need to be done to see whether results would be different with vaccination status and evolving variants.

But he noted that this study has several strengths: “The hair loss, libido loss, and ejaculation difficulty are all new symptoms,” and the study – large and carefully controlled – shows these issues were among those more likely to occur.

A loss of sense of smell – which is not a new observation – was still the most likely risk shown in the study, followed by hair loss, sneezing, ejaculation difficulty, and reduced sex drive; followed by shortness of breath, fatigue, chest pain associated with breathing difficulties, hoarseness, and fever.
 

Three main clusters of symptoms

Given the wide range of symptoms, long COVID likely represents a group of conditions, the authors wrote.

They found three main clusters. The largest, with roughly 80% of people with long COVID in the study, faced a broad spectrum of symptoms, ranging from fatigue to headache and pain. The second-largest group, (15%) mostly had symptoms having to do with mental health and thinking skills, including depression, anxiety, brain fog, and insomnia. The smallest group (5%) had mainly respiratory symptoms such as shortness of breath, coughing, and wheezing.

Putting symptoms in clusters will be important to start understanding what leads to long COVID, said Farha Ikramuddin, MD, a rehabilitation specialist at the University of Minnesota, Minneapolis.

She added that, while the symptoms listed in this paper are new in published research, she has certainly been seeing them over time in her long COVID clinic. (The researchers also used only coded health care data, so they were limited in what symptoms they could discover, she notes.)

Dr. Ikramuddin said a strength of the paper is its large size, but she also cautioned that it’s difficult to determine whether members of the comparison group truly had no COVID infection when the information is taken from their medical records. Often, people test at home or assume they have COVID and don’t test; therefore the information wouldn’t be recorded.

Evaluating nonhospitalized patients is also important, she said, as much of the research on long COVID has come from hospitalized patients, so little has been known about the symptoms of those with milder infections.

“Patients who have been hospitalized and have long COVID look very different from the patients who were not hospitalized,” Dr. Ikramuddin said.

One clear message from the paper, she said, is that listening and asking extensive questions about symptoms are important with patients who have had COVID.

“Counseling has also become very important for our patients in the pandemic,” she said.

It will also be important to do studies on returning to work for patients with long COVID to see how many are able to return and at what capacity, Dr. Ikramuddin said.

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

Hair loss, reduced sex drive, and erectile dysfunction have joined a list of better-known symptoms linked to long COVID in patients who were not hospitalized, according to findings of a large study.

Anuradhaa Subramanian, PhD, with the Institute of Applied Health Research at the University of Birmingham (England), led the research published online in Nature Medicine.

The team analyzed 486,149 electronic health records from adult patients with confirmed COVID in the United Kingdom, compared with 1.9 million people with no history of COVID, from January 2020 to April 2021. Researchers matched both groups closely in terms of demographic, social, and clinical traits.
 

New symptoms

The team identified 62 symptoms, including the well-known indicators of long COVID, such as fatigue, loss of sense of smell, shortness of breath, and brain fog, but also hair loss, sexual dysfunction, chest pain, fever, loss of control of bowel movements, and limb swelling.

“These differences in symptoms reported between the infected and uninfected groups remained even after we accounted for age, sex, ethnic group, socioeconomic status, body mass index, smoking status, the presence of more than 80 health conditions, and past reporting of the same symptom,” Dr. Subramanian and coresearcher Shamil Haroon, PhD, wrote in a summary of their research in The Conversation.

They pointed out that only 20 of the symptoms they found are included in the World Health Organization’s clinical case definition for long COVID.

They also found that people more likely to have persistent symptoms 3 months after COVID infection were also more likely to be young, female, smokers, to belong to certain minority ethnic groups, and to have lower socioeconomic status. They were also more likely to be obese and have a wide range of health conditions.

Dr. Haroon, an associate clinical professor at the University of Birmingham, said that one reason it appeared that younger people were more likely to get symptoms of long COVID may be that older adults with COVID were more likely to be hospitalized and weren’t included in this study.

“Since we only considered nonhospitalized adults, the older adults we included in our study may have been relatively healthier and thus had a lower symptom burden,” he said.

Dr. Subramania noted that older patients were more likely to report lasting COVID-related symptoms in the study, but when researchers accounted for a wide range of other conditions that patients had before infection (which generally more commonly happen in older adults), they found younger age as a risk factor for long-term COVID-related symptoms.

In the study period, most patients were unvaccinated, and results came before the widespread Delta and Omicron variants.

More than half (56.6%) of the patients infected with the virus that causes COVID had been diagnosed in 2020, and 43.4% in 2021. Less than 5% (4.5%) of the patients infected with the virus and 4.7% of the patients with no recorded evidence of a COVID infection had received at least a single dose of a COVID vaccine before the study started.

Eric Topol, MD, founder and director of the Scripps Research Translational Institute in La Jolla, Calif., and editor-in-chief of Medscape, said more studies need to be done to see whether results would be different with vaccination status and evolving variants.

But he noted that this study has several strengths: “The hair loss, libido loss, and ejaculation difficulty are all new symptoms,” and the study – large and carefully controlled – shows these issues were among those more likely to occur.

A loss of sense of smell – which is not a new observation – was still the most likely risk shown in the study, followed by hair loss, sneezing, ejaculation difficulty, and reduced sex drive; followed by shortness of breath, fatigue, chest pain associated with breathing difficulties, hoarseness, and fever.
 

Three main clusters of symptoms

Given the wide range of symptoms, long COVID likely represents a group of conditions, the authors wrote.

They found three main clusters. The largest, with roughly 80% of people with long COVID in the study, faced a broad spectrum of symptoms, ranging from fatigue to headache and pain. The second-largest group, (15%) mostly had symptoms having to do with mental health and thinking skills, including depression, anxiety, brain fog, and insomnia. The smallest group (5%) had mainly respiratory symptoms such as shortness of breath, coughing, and wheezing.

Putting symptoms in clusters will be important to start understanding what leads to long COVID, said Farha Ikramuddin, MD, a rehabilitation specialist at the University of Minnesota, Minneapolis.

She added that, while the symptoms listed in this paper are new in published research, she has certainly been seeing them over time in her long COVID clinic. (The researchers also used only coded health care data, so they were limited in what symptoms they could discover, she notes.)

Dr. Ikramuddin said a strength of the paper is its large size, but she also cautioned that it’s difficult to determine whether members of the comparison group truly had no COVID infection when the information is taken from their medical records. Often, people test at home or assume they have COVID and don’t test; therefore the information wouldn’t be recorded.

Evaluating nonhospitalized patients is also important, she said, as much of the research on long COVID has come from hospitalized patients, so little has been known about the symptoms of those with milder infections.

“Patients who have been hospitalized and have long COVID look very different from the patients who were not hospitalized,” Dr. Ikramuddin said.

One clear message from the paper, she said, is that listening and asking extensive questions about symptoms are important with patients who have had COVID.

“Counseling has also become very important for our patients in the pandemic,” she said.

It will also be important to do studies on returning to work for patients with long COVID to see how many are able to return and at what capacity, Dr. Ikramuddin said.

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

A low-level light therapy cap may be a safe, convenient treatment for some patients with central centrifugal cicatricial alopecia, though the treatment effects from a small prospective trial appear to be subtle.

Central centrifugal cicatricial alopecia (CCCA) is a form of scarring hair loss with unknown etiology and no known cure that affects mainly women of African descent.

“The low-level light therapy (LLLT) cap does indeed seem to help with symptoms and mild regrowth in CCCA,” senior study author Amy J. McMichael, MD, told this news organization. “The dual-wavelength cap we used appears to have anti-inflammatory properties, and that makes sense for a primarily inflammatory scarring from of alopecia.

“Quality of life improved with the treatment and there were no reported side effects,” added Dr. McMichael, professor of dermatology at Wake Forest University, Winston-Salem, N.C.

The results of the study were presented in a poster at the annual meeting of the Society for Investigative Dermatology.

The REVIAN RED cap (REVIAN Inc.) used in the study contains 119 light-emitting diodes (LEDs) arrayed on the cap’s interior surface that emit orange (620 nm) and red (660 nm) light.

The hypothesis for how the dual-wavelength lights work is that light is absorbed by the chromophore cytochrome c oxidase in the mitochondrial membrane. This induces the release of nitric oxide and the production of adenosine triphosphate (ATP), which leads to vasodilation, cytokine regulation, and increased transcription and release of growth factors.

LLLT is approved to treat androgenetic alopecia, the authors wrote, but has not been studied as a treatment for CCCA.

To assess the effects of LLLT on CCCA, Dr. McMichael and her colleagues at Wake Forest followed the condition’s progress in five Black women over their 6-month course of treatment. Four participants completed the study.

At baseline, all participants had been on individual stable CCCA treatment regimens for at least 3 months. They continued those treatments along with LLLT therapy throughout the study. The women ranged in age from 38 to 69 years, had had CCCA for an average of 12 years, and their disease severity ranged from stage IIB to IVA.

They were instructed to wear the REVIAN RED cap with the LEDs activated for 10 minutes each day.

At 2, 4, and 6 months, participants self-assessed their symptoms, a clinician evaluated the condition’s severity, and digital photographs were taken.

At 6 months:

• Three patients showed improved Dermatology Life Quality Index (DLQI).
• Three patients showed decreased loss of follicular openings and breakage.
• A dermoscopic image of the scalp of one patient revealed short, regrowing vellus hairs and minimal interfollicular and perifollicular scale.
• No patients reported side effects.

Small study raises big questions

“I hope this study will lead to a larger study that will look at the long-term outcomes of CCCA,” Dr. McMichael said. “This is a nice treatment that does not require application of something to the scalp that may affect hair styling, and it has no systemic side effects.”

Dr. McMichael acknowledges that the small sample size, participants continuing with their individual stable treatments while also undergoing light therapy, and the lack of patients with stage I disease, are weaknesses in the study.

“However, the strength is that none of the patients had side effects or stopped using the treatment due to difficulty with the system,” she added.

Dr. McMichael said she would like to investigate the effects of longer use of the cap and whether the cap can be used to prevent CCCA.

Chesahna Kindred, MD, assistant professor of dermatology at Howard University, Washington, D.C., and founder of Kindred Hair & Skin Center in Columbia, Md., told this news organization that she uses LLLT in her practice.

“I find that LLLT is mildly helpful, or at least does not worsen, androgenetic alopecia,” she said.

“Interestingly, while all four patients had stable disease upon initiating the study, it appears as though two of the four worsened after the use of LLLT, one improved, and one remained relatively stable,” noted Dr. Kindred, who was not involved in the study. “This is important because once there is complete destruction of the follicle, CCCA is difficult to improve.

“Given that there are several options to address inflammation and follicular damage in CCCA, more studies are needed before I would incorporate LLLT into my regular treatment algorithms,” she added.

“Studies like this are important and remind us to not lump all forms of hair loss together,” she said.

REVIAN Inc. provided the caps, but the study received no additional funding. Dr. McMichael and Dr. Kindred report relevant financial relationships with the pharmaceutical industry. Study coauthors have disclosed no relevant financial relationships.
 

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

A low-level light therapy cap may be a safe, convenient treatment for some patients with central centrifugal cicatricial alopecia, though the treatment effects from a small prospective trial appear to be subtle.

Central centrifugal cicatricial alopecia (CCCA) is a form of scarring hair loss with unknown etiology and no known cure that affects mainly women of African descent.

“The low-level light therapy (LLLT) cap does indeed seem to help with symptoms and mild regrowth in CCCA,” senior study author Amy J. McMichael, MD, told this news organization. “The dual-wavelength cap we used appears to have anti-inflammatory properties, and that makes sense for a primarily inflammatory scarring from of alopecia.

“Quality of life improved with the treatment and there were no reported side effects,” added Dr. McMichael, professor of dermatology at Wake Forest University, Winston-Salem, N.C.

The results of the study were presented in a poster at the annual meeting of the Society for Investigative Dermatology.

The REVIAN RED cap (REVIAN Inc.) used in the study contains 119 light-emitting diodes (LEDs) arrayed on the cap’s interior surface that emit orange (620 nm) and red (660 nm) light.

The hypothesis for how the dual-wavelength lights work is that light is absorbed by the chromophore cytochrome c oxidase in the mitochondrial membrane. This induces the release of nitric oxide and the production of adenosine triphosphate (ATP), which leads to vasodilation, cytokine regulation, and increased transcription and release of growth factors.

LLLT is approved to treat androgenetic alopecia, the authors wrote, but has not been studied as a treatment for CCCA.

To assess the effects of LLLT on CCCA, Dr. McMichael and her colleagues at Wake Forest followed the condition’s progress in five Black women over their 6-month course of treatment. Four participants completed the study.

At baseline, all participants had been on individual stable CCCA treatment regimens for at least 3 months. They continued those treatments along with LLLT therapy throughout the study. The women ranged in age from 38 to 69 years, had had CCCA for an average of 12 years, and their disease severity ranged from stage IIB to IVA.

They were instructed to wear the REVIAN RED cap with the LEDs activated for 10 minutes each day.

At 2, 4, and 6 months, participants self-assessed their symptoms, a clinician evaluated the condition’s severity, and digital photographs were taken.

At 6 months:

• Three patients showed improved Dermatology Life Quality Index (DLQI).
• Three patients showed decreased loss of follicular openings and breakage.
• A dermoscopic image of the scalp of one patient revealed short, regrowing vellus hairs and minimal interfollicular and perifollicular scale.
• No patients reported side effects.

Small study raises big questions

“I hope this study will lead to a larger study that will look at the long-term outcomes of CCCA,” Dr. McMichael said. “This is a nice treatment that does not require application of something to the scalp that may affect hair styling, and it has no systemic side effects.”

Dr. McMichael acknowledges that the small sample size, participants continuing with their individual stable treatments while also undergoing light therapy, and the lack of patients with stage I disease, are weaknesses in the study.

“However, the strength is that none of the patients had side effects or stopped using the treatment due to difficulty with the system,” she added.

Dr. McMichael said she would like to investigate the effects of longer use of the cap and whether the cap can be used to prevent CCCA.

Chesahna Kindred, MD, assistant professor of dermatology at Howard University, Washington, D.C., and founder of Kindred Hair & Skin Center in Columbia, Md., told this news organization that she uses LLLT in her practice.

“I find that LLLT is mildly helpful, or at least does not worsen, androgenetic alopecia,” she said.

“Interestingly, while all four patients had stable disease upon initiating the study, it appears as though two of the four worsened after the use of LLLT, one improved, and one remained relatively stable,” noted Dr. Kindred, who was not involved in the study. “This is important because once there is complete destruction of the follicle, CCCA is difficult to improve.

“Given that there are several options to address inflammation and follicular damage in CCCA, more studies are needed before I would incorporate LLLT into my regular treatment algorithms,” she added.

“Studies like this are important and remind us to not lump all forms of hair loss together,” she said.

REVIAN Inc. provided the caps, but the study received no additional funding. Dr. McMichael and Dr. Kindred report relevant financial relationships with the pharmaceutical industry. Study coauthors have disclosed no relevant financial relationships.
 

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

A low-level light therapy cap may be a safe, convenient treatment for some patients with central centrifugal cicatricial alopecia, though the treatment effects from a small prospective trial appear to be subtle.

Central centrifugal cicatricial alopecia (CCCA) is a form of scarring hair loss with unknown etiology and no known cure that affects mainly women of African descent.

“The low-level light therapy (LLLT) cap does indeed seem to help with symptoms and mild regrowth in CCCA,” senior study author Amy J. McMichael, MD, told this news organization. “The dual-wavelength cap we used appears to have anti-inflammatory properties, and that makes sense for a primarily inflammatory scarring from of alopecia.

“Quality of life improved with the treatment and there were no reported side effects,” added Dr. McMichael, professor of dermatology at Wake Forest University, Winston-Salem, N.C.

The results of the study were presented in a poster at the annual meeting of the Society for Investigative Dermatology.

The REVIAN RED cap (REVIAN Inc.) used in the study contains 119 light-emitting diodes (LEDs) arrayed on the cap’s interior surface that emit orange (620 nm) and red (660 nm) light.

The hypothesis for how the dual-wavelength lights work is that light is absorbed by the chromophore cytochrome c oxidase in the mitochondrial membrane. This induces the release of nitric oxide and the production of adenosine triphosphate (ATP), which leads to vasodilation, cytokine regulation, and increased transcription and release of growth factors.

LLLT is approved to treat androgenetic alopecia, the authors wrote, but has not been studied as a treatment for CCCA.

To assess the effects of LLLT on CCCA, Dr. McMichael and her colleagues at Wake Forest followed the condition’s progress in five Black women over their 6-month course of treatment. Four participants completed the study.

At baseline, all participants had been on individual stable CCCA treatment regimens for at least 3 months. They continued those treatments along with LLLT therapy throughout the study. The women ranged in age from 38 to 69 years, had had CCCA for an average of 12 years, and their disease severity ranged from stage IIB to IVA.

They were instructed to wear the REVIAN RED cap with the LEDs activated for 10 minutes each day.

At 2, 4, and 6 months, participants self-assessed their symptoms, a clinician evaluated the condition’s severity, and digital photographs were taken.

At 6 months:

• Three patients showed improved Dermatology Life Quality Index (DLQI).
• Three patients showed decreased loss of follicular openings and breakage.
• A dermoscopic image of the scalp of one patient revealed short, regrowing vellus hairs and minimal interfollicular and perifollicular scale.
• No patients reported side effects.

Small study raises big questions

“I hope this study will lead to a larger study that will look at the long-term outcomes of CCCA,” Dr. McMichael said. “This is a nice treatment that does not require application of something to the scalp that may affect hair styling, and it has no systemic side effects.”

Dr. McMichael acknowledges that the small sample size, participants continuing with their individual stable treatments while also undergoing light therapy, and the lack of patients with stage I disease, are weaknesses in the study.

“However, the strength is that none of the patients had side effects or stopped using the treatment due to difficulty with the system,” she added.

Dr. McMichael said she would like to investigate the effects of longer use of the cap and whether the cap can be used to prevent CCCA.

Chesahna Kindred, MD, assistant professor of dermatology at Howard University, Washington, D.C., and founder of Kindred Hair & Skin Center in Columbia, Md., told this news organization that she uses LLLT in her practice.

“I find that LLLT is mildly helpful, or at least does not worsen, androgenetic alopecia,” she said.

“Interestingly, while all four patients had stable disease upon initiating the study, it appears as though two of the four worsened after the use of LLLT, one improved, and one remained relatively stable,” noted Dr. Kindred, who was not involved in the study. “This is important because once there is complete destruction of the follicle, CCCA is difficult to improve.

“Given that there are several options to address inflammation and follicular damage in CCCA, more studies are needed before I would incorporate LLLT into my regular treatment algorithms,” she added.

“Studies like this are important and remind us to not lump all forms of hair loss together,” she said.

REVIAN Inc. provided the caps, but the study received no additional funding. Dr. McMichael and Dr. Kindred report relevant financial relationships with the pharmaceutical industry. Study coauthors have disclosed no relevant financial relationships.
 

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

Alopecia areata (AA) is an autoimmune disorder characterized by transient hair loss with preservation of the hair follicle (HF). The lifetime incidence risk of AA is approximately 2%,¹ with a mean age of onset of 25 to 36 years and with no clinically relevant significant differences between sex or ethnicity.² Most commonly, it presents as round, well-demarcated patches of alopecia on the scalp and spontaneously resolves in nearly 30% of patients. However, severe disease is associated with younger age of presentation and can progress to a total loss of scalp or body hair—referred to as alopecia totalis and alopecia universalis, respectively—thus severely impacting quality of life.^3,4

First-line treatment options for AA include potent topical steroids^5,6 and intralesional (IL) steroids, most commonly IL triamcinolone acetonide (ILTA). Intralesional steroids have been found to be more effective than topicals in stimulating hair growth at the injection site.^7,8 A recent systemic therapy—the Janus kinase inhibitor baricitinib—was approved by the US Food and Drug Administration for AA.⁹ Other systemic therapies such as oral corticosteroids have been studied in small trials with promising results.¹⁰ However, the risks of systemic therapies may outweigh the benefits.^9,10

Another less common topical therapy is contact immunotherapy, which involves topical application of an unlicensed non–pharmaceutical-grade agent to areas affected with AA. It is reported to have a wide range of response rates (29%–87%).¹¹

We report 2 cases of extensive AA that were treated with a novel combination regimen— 2.5 mg/mL of ILTA diluted with lidocaine 1% and epinephrine 1:100,000 in place of normal saline (NS)— which is a modification to an already widely used first-line treatment.

Case Reports

Patient 1—An 11-year-old girl presented with nonscarring alopecia of the vertex and occipital scalp. Three years prior she was treated with topical and IL corticosteroids by a different provider. Physical examination revealed almost complete alopecia involving the bottom two-thirds of the occipital scalp as well as the medial eyebrows (Figures 1A and 1B). Over the span of 1 year she was treated with betamethasone dipropionate cream 0.05% and several rounds of ILTA 2.5 mg/mL buffered with NS, with minimal improvement. A year after the initial presentation, the decision was made to initiate monthly injections of ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000. Some hair regrowth of the occipital scalp was noted by 3 months, with near-complete regrowth of the scalp hair and eyebrows by 7 months and 5 months, respectively (Figures 1C and 1D). During this period, the patient continued to develop new areas of alopecia of the scalp and eyebrows, which also were injected with this combination. In total, the patient received 8 rounds of IL injections 4 to 6 weeks apart in the scalp and 6 rounds in the eyebrows. The treated areas showed resolution over a follow-up period of 14 months, though there was recurrence at the right medial eyebrow at 5 months. No localized skin atrophy or other adverse effects were noted.

Patient 2—A 34-year-old woman who was otherwise healthy presented with previously untreated AA involving the scalp of 2 months’ duration. Physical examination revealed the following areas of nonscarring alopecia: a 10×10-cm area of the right occipital scalp with some regrowth; a 10×14-cm area of the left parieto-occipital scalp; and a 1-cm area posterior to the vertex (Figure 2A). Given the extensive involvement, the decision was made to initiate ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000 once monthly. Appreciable hair regrowth was noted within 1 month, mostly on the parietal scalp. Substantial improvement was noted after 3 months in all affected areas of the hair-bearing scalp, with near-complete regrowth on the left occipital scalp and greater than 50% regrowth on the right occipital scalp (Figure 2B). No adverse effects were noted. She currently has no alopecia.

Comment

Alopecia Pathogenesis—The most widely adopted theory of AA etiology implicates an aberrant immune response. The HF, which is a dynamic “mini-organ” with its own immune and hormonal microenvironment, is considered an “immune-privileged site”—meaning it is less exposed to immune responses than most other body areas. It is hypothesized that AA results from a breakdown in this immune privilege, with the subsequent attack on the peribulbar part of the follicle by CD8⁺ T lymphocytes. This lymphocytic infiltrate induces apoptosis in the HF keratinocytes, resulting in inhibition of hair shaft production.¹² Other theories suggest a link to the sympathetic-adrenal-medullary system and hypothalamic-pituitary-adrenal axis.¹³

Therapies for Alopecia—Topical and IL corticosteroids are the first-line therapies for localized AA in patients with less than 50% scalp involvement. Triamcinolone acetonide generally is the IL steroid of choice because it is widely available and less atrophogenic than other steroids. Unlike topicals, ILTA bypasses the epidermis when injected, achieving direct access to the HF.¹⁴

High-quality controlled studies regarding the use of ILTA in AA are scarce. A meta-analysis concluded that 5 mg/mL and 10 mg/mL of ILTA diluted in NS were equally effective (80.9% [P<.05] vs 76.4% [P<.005], respectively). Concentrations of less than 5 mg/mL of ILTA resulted in lower rates of hair regrowth (62.3%; P=.04).¹⁵ The role of diluents other than NS has not been studied.

Benefits of Epinephrine in ILTA Therapy—The role of epinephrine 1:100,000 is to decrease the rate of clearance of triamcinolone acetonide from the HF, allowing for a better therapeutic effect. Laser Doppler blood flowmeter studies have shown that epinephrine 1:100,000 injected in the scalp causes vasoconstriction, thereby decreasing the blood flow rate of clearance of other substances in the same solution.¹⁶ Also, a more gradual systemic absorption is achieved, decreasing systemic side effects such as osteoporosis.¹⁷

Another potential benefit of epinephrine has been suggested in animal studies that demonstrate the important role of the sympathetic nervous system in HF growth. In a mouse study, chemical sympathectomy led to diminished norepinephrine levels in the skin, accompanied by a decreased keratinocyte proliferation and hair growth. Conversely, norepinephrine was found to promote HF growth in an organotypic skin culture model.¹⁸ Topically applied isoproterenol, a panadrenergic receptor agonist, accelerated HF growth in an organotypic skin culture. It also has been shown that external light and temperature changes stimulate hair growth via the sympathetic nervous system, promoting anagen HF growth in cultured skin explants, further linking HF activity with sympathetic nerve activity.¹⁹

In our experience, cases of AA that at first failed ILTA 5 mg/mL in NS have been successfully treated with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000. One such case was alopecia totalis, though we do not have high-quality photographs to present for this report. The 2 cases presented here are the ones with the best photographs to demonstrate our outcomes. Both were treated with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000 administered using a 0.5-in long 30-gauge needle, with 0.05 to 0.1 mL per injection approximately 0.51-cm apart. The treatment intervals were 4 weeks, with a maximal dose of 20 mg per session. In addition to the 2 cases reported here, the Table includes 2 other patients in our practice who were successfully treated with this novel regimen.

Prior to adopting this combination regimen, our standard therapy for AA was 5 mg/mL ILTA buffered with NS. Instead of NS, we now use the widely available 1% lidocaine with epinephrine 1:100,000 and dilute the ILTA to 2.5 mg/mL. We postulate that epinephrine 1:100,000 enhances therapeutic efficacy via local vasoconstriction, thus keeping the ILTA in situ longer than NS. This effect allows for a lower concentration of ILTA (2.5 mg/mL) to be effective. Furthermore, epinephrine 1:100,000 may have an independent effect, as suggested in mouse studies.¹⁸

Our first case demonstrated the ophiasis subtype of AA (symmetric bandlike hair loss), which has a poorer prognosis and is less responsive to therapy.²⁰ In this patient, prior treatment with topical corticosteroids and ILTA in NS failed to induce a response. After a series of injections with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000, she entered remission. Our second case is one of alopecia subtotalis, which responded quickly, and the patient entered remission after just 3 months of treatment. These 2 cases are illustrative of the results that we regularly get and have come to expect with this treatment.

Conclusion

Our novel modified regimen of 2.5 mg/mL ILTA diluted with 1% lidocaine and epinephrine 1:100,000 has yielded a series of excellent outcomes in many of our most challenging AA cases without any untoward effects. Two cases are presented here. Higher-powered studies are needed to validate this new yet simple approach. A split-scalp or split-lesion study comparing ILTA with and without epinephrine 1:100,000 would be warranted for further investigation.

Alopecia areata (AA) is an autoimmune disorder characterized by transient hair loss with preservation of the hair follicle (HF). The lifetime incidence risk of AA is approximately 2%,¹ with a mean age of onset of 25 to 36 years and with no clinically relevant significant differences between sex or ethnicity.² Most commonly, it presents as round, well-demarcated patches of alopecia on the scalp and spontaneously resolves in nearly 30% of patients. However, severe disease is associated with younger age of presentation and can progress to a total loss of scalp or body hair—referred to as alopecia totalis and alopecia universalis, respectively—thus severely impacting quality of life.^3,4

First-line treatment options for AA include potent topical steroids^5,6 and intralesional (IL) steroids, most commonly IL triamcinolone acetonide (ILTA). Intralesional steroids have been found to be more effective than topicals in stimulating hair growth at the injection site.^7,8 A recent systemic therapy—the Janus kinase inhibitor baricitinib—was approved by the US Food and Drug Administration for AA.⁹ Other systemic therapies such as oral corticosteroids have been studied in small trials with promising results.¹⁰ However, the risks of systemic therapies may outweigh the benefits.^9,10

Another less common topical therapy is contact immunotherapy, which involves topical application of an unlicensed non–pharmaceutical-grade agent to areas affected with AA. It is reported to have a wide range of response rates (29%–87%).¹¹

We report 2 cases of extensive AA that were treated with a novel combination regimen— 2.5 mg/mL of ILTA diluted with lidocaine 1% and epinephrine 1:100,000 in place of normal saline (NS)— which is a modification to an already widely used first-line treatment.

Case Reports

Patient 1—An 11-year-old girl presented with nonscarring alopecia of the vertex and occipital scalp. Three years prior she was treated with topical and IL corticosteroids by a different provider. Physical examination revealed almost complete alopecia involving the bottom two-thirds of the occipital scalp as well as the medial eyebrows (Figures 1A and 1B). Over the span of 1 year she was treated with betamethasone dipropionate cream 0.05% and several rounds of ILTA 2.5 mg/mL buffered with NS, with minimal improvement. A year after the initial presentation, the decision was made to initiate monthly injections of ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000. Some hair regrowth of the occipital scalp was noted by 3 months, with near-complete regrowth of the scalp hair and eyebrows by 7 months and 5 months, respectively (Figures 1C and 1D). During this period, the patient continued to develop new areas of alopecia of the scalp and eyebrows, which also were injected with this combination. In total, the patient received 8 rounds of IL injections 4 to 6 weeks apart in the scalp and 6 rounds in the eyebrows. The treated areas showed resolution over a follow-up period of 14 months, though there was recurrence at the right medial eyebrow at 5 months. No localized skin atrophy or other adverse effects were noted.

Patient 2—A 34-year-old woman who was otherwise healthy presented with previously untreated AA involving the scalp of 2 months’ duration. Physical examination revealed the following areas of nonscarring alopecia: a 10×10-cm area of the right occipital scalp with some regrowth; a 10×14-cm area of the left parieto-occipital scalp; and a 1-cm area posterior to the vertex (Figure 2A). Given the extensive involvement, the decision was made to initiate ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000 once monthly. Appreciable hair regrowth was noted within 1 month, mostly on the parietal scalp. Substantial improvement was noted after 3 months in all affected areas of the hair-bearing scalp, with near-complete regrowth on the left occipital scalp and greater than 50% regrowth on the right occipital scalp (Figure 2B). No adverse effects were noted. She currently has no alopecia.

Comment

Alopecia Pathogenesis—The most widely adopted theory of AA etiology implicates an aberrant immune response. The HF, which is a dynamic “mini-organ” with its own immune and hormonal microenvironment, is considered an “immune-privileged site”—meaning it is less exposed to immune responses than most other body areas. It is hypothesized that AA results from a breakdown in this immune privilege, with the subsequent attack on the peribulbar part of the follicle by CD8⁺ T lymphocytes. This lymphocytic infiltrate induces apoptosis in the HF keratinocytes, resulting in inhibition of hair shaft production.¹² Other theories suggest a link to the sympathetic-adrenal-medullary system and hypothalamic-pituitary-adrenal axis.¹³

Therapies for Alopecia—Topical and IL corticosteroids are the first-line therapies for localized AA in patients with less than 50% scalp involvement. Triamcinolone acetonide generally is the IL steroid of choice because it is widely available and less atrophogenic than other steroids. Unlike topicals, ILTA bypasses the epidermis when injected, achieving direct access to the HF.¹⁴

High-quality controlled studies regarding the use of ILTA in AA are scarce. A meta-analysis concluded that 5 mg/mL and 10 mg/mL of ILTA diluted in NS were equally effective (80.9% [P<.05] vs 76.4% [P<.005], respectively). Concentrations of less than 5 mg/mL of ILTA resulted in lower rates of hair regrowth (62.3%; P=.04).¹⁵ The role of diluents other than NS has not been studied.

Benefits of Epinephrine in ILTA Therapy—The role of epinephrine 1:100,000 is to decrease the rate of clearance of triamcinolone acetonide from the HF, allowing for a better therapeutic effect. Laser Doppler blood flowmeter studies have shown that epinephrine 1:100,000 injected in the scalp causes vasoconstriction, thereby decreasing the blood flow rate of clearance of other substances in the same solution.¹⁶ Also, a more gradual systemic absorption is achieved, decreasing systemic side effects such as osteoporosis.¹⁷

Another potential benefit of epinephrine has been suggested in animal studies that demonstrate the important role of the sympathetic nervous system in HF growth. In a mouse study, chemical sympathectomy led to diminished norepinephrine levels in the skin, accompanied by a decreased keratinocyte proliferation and hair growth. Conversely, norepinephrine was found to promote HF growth in an organotypic skin culture model.¹⁸ Topically applied isoproterenol, a panadrenergic receptor agonist, accelerated HF growth in an organotypic skin culture. It also has been shown that external light and temperature changes stimulate hair growth via the sympathetic nervous system, promoting anagen HF growth in cultured skin explants, further linking HF activity with sympathetic nerve activity.¹⁹

In our experience, cases of AA that at first failed ILTA 5 mg/mL in NS have been successfully treated with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000. One such case was alopecia totalis, though we do not have high-quality photographs to present for this report. The 2 cases presented here are the ones with the best photographs to demonstrate our outcomes. Both were treated with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000 administered using a 0.5-in long 30-gauge needle, with 0.05 to 0.1 mL per injection approximately 0.51-cm apart. The treatment intervals were 4 weeks, with a maximal dose of 20 mg per session. In addition to the 2 cases reported here, the Table includes 2 other patients in our practice who were successfully treated with this novel regimen.

Prior to adopting this combination regimen, our standard therapy for AA was 5 mg/mL ILTA buffered with NS. Instead of NS, we now use the widely available 1% lidocaine with epinephrine 1:100,000 and dilute the ILTA to 2.5 mg/mL. We postulate that epinephrine 1:100,000 enhances therapeutic efficacy via local vasoconstriction, thus keeping the ILTA in situ longer than NS. This effect allows for a lower concentration of ILTA (2.5 mg/mL) to be effective. Furthermore, epinephrine 1:100,000 may have an independent effect, as suggested in mouse studies.¹⁸

Our first case demonstrated the ophiasis subtype of AA (symmetric bandlike hair loss), which has a poorer prognosis and is less responsive to therapy.²⁰ In this patient, prior treatment with topical corticosteroids and ILTA in NS failed to induce a response. After a series of injections with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000, she entered remission. Our second case is one of alopecia subtotalis, which responded quickly, and the patient entered remission after just 3 months of treatment. These 2 cases are illustrative of the results that we regularly get and have come to expect with this treatment.

Conclusion

Our novel modified regimen of 2.5 mg/mL ILTA diluted with 1% lidocaine and epinephrine 1:100,000 has yielded a series of excellent outcomes in many of our most challenging AA cases without any untoward effects. Two cases are presented here. Higher-powered studies are needed to validate this new yet simple approach. A split-scalp or split-lesion study comparing ILTA with and without epinephrine 1:100,000 would be warranted for further investigation.

Alopecia areata (AA) is an autoimmune disorder characterized by transient hair loss with preservation of the hair follicle (HF). The lifetime incidence risk of AA is approximately 2%,¹ with a mean age of onset of 25 to 36 years and with no clinically relevant significant differences between sex or ethnicity.² Most commonly, it presents as round, well-demarcated patches of alopecia on the scalp and spontaneously resolves in nearly 30% of patients. However, severe disease is associated with younger age of presentation and can progress to a total loss of scalp or body hair—referred to as alopecia totalis and alopecia universalis, respectively—thus severely impacting quality of life.^3,4

First-line treatment options for AA include potent topical steroids^5,6 and intralesional (IL) steroids, most commonly IL triamcinolone acetonide (ILTA). Intralesional steroids have been found to be more effective than topicals in stimulating hair growth at the injection site.^7,8 A recent systemic therapy—the Janus kinase inhibitor baricitinib—was approved by the US Food and Drug Administration for AA.⁹ Other systemic therapies such as oral corticosteroids have been studied in small trials with promising results.¹⁰ However, the risks of systemic therapies may outweigh the benefits.^9,10

Another less common topical therapy is contact immunotherapy, which involves topical application of an unlicensed non–pharmaceutical-grade agent to areas affected with AA. It is reported to have a wide range of response rates (29%–87%).¹¹

We report 2 cases of extensive AA that were treated with a novel combination regimen— 2.5 mg/mL of ILTA diluted with lidocaine 1% and epinephrine 1:100,000 in place of normal saline (NS)— which is a modification to an already widely used first-line treatment.

Case Reports

Patient 1—An 11-year-old girl presented with nonscarring alopecia of the vertex and occipital scalp. Three years prior she was treated with topical and IL corticosteroids by a different provider. Physical examination revealed almost complete alopecia involving the bottom two-thirds of the occipital scalp as well as the medial eyebrows (Figures 1A and 1B). Over the span of 1 year she was treated with betamethasone dipropionate cream 0.05% and several rounds of ILTA 2.5 mg/mL buffered with NS, with minimal improvement. A year after the initial presentation, the decision was made to initiate monthly injections of ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000. Some hair regrowth of the occipital scalp was noted by 3 months, with near-complete regrowth of the scalp hair and eyebrows by 7 months and 5 months, respectively (Figures 1C and 1D). During this period, the patient continued to develop new areas of alopecia of the scalp and eyebrows, which also were injected with this combination. In total, the patient received 8 rounds of IL injections 4 to 6 weeks apart in the scalp and 6 rounds in the eyebrows. The treated areas showed resolution over a follow-up period of 14 months, though there was recurrence at the right medial eyebrow at 5 months. No localized skin atrophy or other adverse effects were noted.

Patient 2—A 34-year-old woman who was otherwise healthy presented with previously untreated AA involving the scalp of 2 months’ duration. Physical examination revealed the following areas of nonscarring alopecia: a 10×10-cm area of the right occipital scalp with some regrowth; a 10×14-cm area of the left parieto-occipital scalp; and a 1-cm area posterior to the vertex (Figure 2A). Given the extensive involvement, the decision was made to initiate ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000 once monthly. Appreciable hair regrowth was noted within 1 month, mostly on the parietal scalp. Substantial improvement was noted after 3 months in all affected areas of the hair-bearing scalp, with near-complete regrowth on the left occipital scalp and greater than 50% regrowth on the right occipital scalp (Figure 2B). No adverse effects were noted. She currently has no alopecia.

Comment

Alopecia Pathogenesis—The most widely adopted theory of AA etiology implicates an aberrant immune response. The HF, which is a dynamic “mini-organ” with its own immune and hormonal microenvironment, is considered an “immune-privileged site”—meaning it is less exposed to immune responses than most other body areas. It is hypothesized that AA results from a breakdown in this immune privilege, with the subsequent attack on the peribulbar part of the follicle by CD8⁺ T lymphocytes. This lymphocytic infiltrate induces apoptosis in the HF keratinocytes, resulting in inhibition of hair shaft production.¹² Other theories suggest a link to the sympathetic-adrenal-medullary system and hypothalamic-pituitary-adrenal axis.¹³

Therapies for Alopecia—Topical and IL corticosteroids are the first-line therapies for localized AA in patients with less than 50% scalp involvement. Triamcinolone acetonide generally is the IL steroid of choice because it is widely available and less atrophogenic than other steroids. Unlike topicals, ILTA bypasses the epidermis when injected, achieving direct access to the HF.¹⁴

High-quality controlled studies regarding the use of ILTA in AA are scarce. A meta-analysis concluded that 5 mg/mL and 10 mg/mL of ILTA diluted in NS were equally effective (80.9% [P<.05] vs 76.4% [P<.005], respectively). Concentrations of less than 5 mg/mL of ILTA resulted in lower rates of hair regrowth (62.3%; P=.04).¹⁵ The role of diluents other than NS has not been studied.

Benefits of Epinephrine in ILTA Therapy—The role of epinephrine 1:100,000 is to decrease the rate of clearance of triamcinolone acetonide from the HF, allowing for a better therapeutic effect. Laser Doppler blood flowmeter studies have shown that epinephrine 1:100,000 injected in the scalp causes vasoconstriction, thereby decreasing the blood flow rate of clearance of other substances in the same solution.¹⁶ Also, a more gradual systemic absorption is achieved, decreasing systemic side effects such as osteoporosis.¹⁷

Another potential benefit of epinephrine has been suggested in animal studies that demonstrate the important role of the sympathetic nervous system in HF growth. In a mouse study, chemical sympathectomy led to diminished norepinephrine levels in the skin, accompanied by a decreased keratinocyte proliferation and hair growth. Conversely, norepinephrine was found to promote HF growth in an organotypic skin culture model.¹⁸ Topically applied isoproterenol, a panadrenergic receptor agonist, accelerated HF growth in an organotypic skin culture. It also has been shown that external light and temperature changes stimulate hair growth via the sympathetic nervous system, promoting anagen HF growth in cultured skin explants, further linking HF activity with sympathetic nerve activity.¹⁹

In our experience, cases of AA that at first failed ILTA 5 mg/mL in NS have been successfully treated with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000. One such case was alopecia totalis, though we do not have high-quality photographs to present for this report. The 2 cases presented here are the ones with the best photographs to demonstrate our outcomes. Both were treated with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000 administered using a 0.5-in long 30-gauge needle, with 0.05 to 0.1 mL per injection approximately 0.51-cm apart. The treatment intervals were 4 weeks, with a maximal dose of 20 mg per session. In addition to the 2 cases reported here, the Table includes 2 other patients in our practice who were successfully treated with this novel regimen.

Prior to adopting this combination regimen, our standard therapy for AA was 5 mg/mL ILTA buffered with NS. Instead of NS, we now use the widely available 1% lidocaine with epinephrine 1:100,000 and dilute the ILTA to 2.5 mg/mL. We postulate that epinephrine 1:100,000 enhances therapeutic efficacy via local vasoconstriction, thus keeping the ILTA in situ longer than NS. This effect allows for a lower concentration of ILTA (2.5 mg/mL) to be effective. Furthermore, epinephrine 1:100,000 may have an independent effect, as suggested in mouse studies.¹⁸

Our first case demonstrated the ophiasis subtype of AA (symmetric bandlike hair loss), which has a poorer prognosis and is less responsive to therapy.²⁰ In this patient, prior treatment with topical corticosteroids and ILTA in NS failed to induce a response. After a series of injections with 2.5 mg/mL ILTA in 1% lidocaine and epinephrine 1:100,000, she entered remission. Our second case is one of alopecia subtotalis, which responded quickly, and the patient entered remission after just 3 months of treatment. These 2 cases are illustrative of the results that we regularly get and have come to expect with this treatment.

Conclusion

Our novel modified regimen of 2.5 mg/mL ILTA diluted with 1% lidocaine and epinephrine 1:100,000 has yielded a series of excellent outcomes in many of our most challenging AA cases without any untoward effects. Two cases are presented here. Higher-powered studies are needed to validate this new yet simple approach. A split-scalp or split-lesion study comparing ILTA with and without epinephrine 1:100,000 would be warranted for further investigation.

The major classifications of thyroid disease include hyperthyroidism, which is seen in Graves disease, and hypothyroidism due to iodine deficiency and Hashimoto thyroiditis, which have potentially devastating health consequences. The prevalence of hyperthyroidism ranges from 0.2% to 1.3% in iodine-sufficient parts of the world, and the prevalence of hypothyroidism in the general population is 5.3% in Europe and 3.7% in the United States.¹ Thyroid hormones physiologically potentiate α- and β-adrenergic receptors by increasing their sensitivity to catecholamines. Excess thyroid hormones manifest as tachycardia, increased cardiac output, increased body temperature, hyperhidrosis, and warm moist skin. Reduced sensitivity of adrenergic receptors to catecholamines from insufficient thyroid hormones results in a lower metabolic rate and decreases response to the sympathetic nervous system.² Nail changes in thyroid patients have not been well studied.³ Our objectives were to characterize nail findings in patients with thyroid disease. Early diagnosis of thyroid disease and prompt referral for treatment may be instrumental in preventing serious morbidities and permanent sequelae.

Methods

PubMed, Scopus, Web of Science, and Google Scholar were searched for the terms nail + thyroid, nail + hyperthyroid, nail + hypothyroid, nail + Graves, and nail + Hashimoto on June 10, 2020, and then updated on November 18, 2020. All English-language articles were included. Non–English-language articles and those that did not describe clinical trials of nail changes in patients with thyroid disease were excluded. One study that utilized survey-based data for nail changes without corroboration with physical examination findings was excluded. Hypothyroidism/hyperthyroidism was defined by all authors as measurement of serum thyroid hormones triiodothyronine, thyroxine, and thyroid-stimulating hormone outside of the normal range. Eight studies were included in the final analysis. Patient demographics, thyroid disease type, physical examination findings, nail clinical findings, age at diagnosis, age at onset of nail changes, treatments/medications, and comorbidities were recorded and analyzed.

Results

Nail changes in patients with thyroid disease were reported in 8 studies (7 cross-sectional, 1 retrospective cohort) and are summarized in the Table.^4-11 The mean age was 41.2 years (range, 5–80 years), with a higher representation of females (range, 70%–94% female). The most common nail changes in thyroid patients were koilonychia, clubbing, and nail brittleness. Other changes included onycholysis, thin nails, dryness, and changes in nail growth rate. Frequent physical findings were xerosis, pruritus, and alopecia.

Both koilonychia and clubbing were reported in patients with hyperthyroidism. In a study of 32 patients with koilonychia, 22 (68.8%) were diagnosed with hyperthyroidism.¹⁰ Nail clubbing affected 7.3% of Graves disease patients (n=150)⁶ and 5.0% of hyperthyroid patients (n=120).⁷ Dermopathy presented more than 1 year after diagnosis of Graves disease in 99 (66%) of 150 patients as a late manifestation of thyrotoxicosis.⁶ Additional physical features in patients with Graves disease (n=150) were pretibial myxedema (100%), ophthalmopathy (99.0%), and proptosis (88.0%). Non–Graves hyperthyroid patients showed physical features of soft hair (83.3%) and soft skin (66.0%).⁷

Nail brittleness was a frequently reported nail change in thyroid patients (4/8 studies, 50%), most often seen in 22% of autoimmune patients, 19.6% of nonautoimmune patients, 13.9% of hypothyroid patients, and 9.2% of hyperthyroid patients.^5,8 For comparison, brittle nails presented in 10.8% of participants in a control group.⁵ Brittle nails in thyroid patients often are accompanied by other nail findings such as thinning, onycholysis, and pitting.

Among hypothyroid patients, nail changes included fragility (70%; n=50), slow growth (48%; n=50), thinning (40%; n=50), onycholysis (38%; n=50),⁷ and brittleness (13.9%; n=173).⁵ Less common nail changes in hypothyroid patients were leukonychia (9.4%; n=32), striped nails (6%; n=50), and pitting (1.2%; n=173).^5,7,11 Among hyperthyroid patients, the most common nail changes were koilonychia (100%; n=22), softening (83%; n=120), onycholysis (29%; n=14), and brittleness (9.2%; n=173).^5,7,9,10 Less common nail changes in hyperthyroid patients were clubbing (5%; n=120), thinning (4.6%; n=173), and leukonychia (3%; n=120).^5,7

Additional cutaneous findings of thyroid disorder included xerosis, alopecia, pruritus, and weight change. Xerosis was most common in hypothyroid disease (57.2%; n=460).⁴ In 2 studies,^8,9 alopecia affected approximately 70% of autoimmune, nonautoimmune, and hyperthyroid patients. Hair loss was reported in 42.6% (n=460)⁴ and 33.0% (n=36)⁹ of hypothyroid patients. Additionally, pruritus affected up to 28% (n=32)¹¹ of hypothyroid and 16.0% (n=120)⁷ of hyperthyroid patients and was more common in autoimmune (41%) vs nonautoimmune (32%) thyroid patients.⁸ Weight gain was seen in 72% of hypothyroid patients (n=32),¹¹ and soft hair and skin were reported in 83.3% and 66% of hyperthyroid patients (n=120), respectively.⁷ Flushing was a less common physical finding in thyroid patients (usually affecting <10%); however, it also was reported in 17.1% of autoimmune and 57.1% of hyperthyroid patients from 2 separate studies.^8,9

 

 

Comment

There are limited data describing nail changes with thyroid disease. Singal and Arora³ reported in their clinical review of nail changes in systemic disease that koilonychia, onycholysis, and melanonychia are associated with thyroid disorders. We similarly found that koilonychia and onycholysis are associated with thyroid disorders without an association with melanonychia.

In his clinical review of thyroid hormone action on the skin, Safer¹² described hypothyroid patients having coarse, dull, thin, and brittle nails, whereas in thyrotoxicosis, patients had shiny, soft, and concave nails with onycholysis; however, the author commented that there were limited data on the clinical findings in thyroid disorders. These nail findings are consistent with our results, but onycholysis was more common in hypothyroid patients than in hyperthyroid patients in our review. Fox¹³ reported on 30 cases of onycholysis, stating that it affected patients with hypothyroidism and improved with thyroid treatment. In a clinical review of 8 commonly seen nail abnormalities, Fowler et al¹⁴ reported that hyperthyroidism was associated with nail findings in 5% of cases and may result in onycholysis of the fourth and fifth nails or all nails. They also reported that onychorrhexis may be seen in patients with hypothyroidism, a finding that differed from our results.¹⁴

The mechanism of nail changes in thyroid disease has not been well studied. A protein/amino acid–deficiency state may contribute to the development of koilonychia. Hyperthyroid patients, who have high metabolic activity, may have hypoalbuminemia, leading to koilonychia.¹⁵ Hypothyroidism causes hypothermia from decreased metabolic rate and secondary compensatory vasoconstriction. Vasoconstriction decreases blood flow of nutrients and oxygen to cutaneous structures and may cause slow-growing, brittle nails. In hyperthyroidism, vasodilation alternatively may contribute to the fast-growing nails. Anti–thyroid-stimulating hormone receptor antibodies in Graves disease may increase the synthesis of hyaluronic acid and glycosaminoglycans from fibroblasts, keratinocytes, adipocytes, or endothelial cells in the dermis and may contribute to development of clubbing.¹⁶

Our review is subject to several limitations. We recorded nail findings as they were described in the original studies; however, we could not confirm the accuracy of these descriptions. In addition, some specific nail changes were not described in sufficient detail. In all but 1 study, dermatologists performed the physical examination. In the study by Al-Dabbagh and Al-Abachi,¹⁰ the physical examinations were performed by general medicine physicians, but they selected only for patients with koilonychia and did not assess for other skin findings. Fragile nails and brittle nails were described in hypothyroid and hyperthyroid patients, but these nail changes were not described in detail. There also were studies describing nail changes in thyroid patients; some studies had small numbers of patients, and many did not have a control group.

Conclusion

Nail changes may be early clinical presenting signs of thyroid disorders and may be the clue to prompt diagnosis of thyroid disease. Dermatologists should be mindful that fragile, slow-growing, thin nails and onycholysis are associated with hypothyroidism and that koilonychia, softening, onycholysis, and brittle nail changes may be seen in hyperthyroidism. Our review aimed to describe nail changes associated with thyroid disease to guide dermatologists on diagnosis and promote future research on dermatologic manifestations of thyroid disease. Future research is necessary to explore the association between koilonychia and hyperthyroidism as well as the association of nail changes with thyroid disease duration and severity.

The major classifications of thyroid disease include hyperthyroidism, which is seen in Graves disease, and hypothyroidism due to iodine deficiency and Hashimoto thyroiditis, which have potentially devastating health consequences. The prevalence of hyperthyroidism ranges from 0.2% to 1.3% in iodine-sufficient parts of the world, and the prevalence of hypothyroidism in the general population is 5.3% in Europe and 3.7% in the United States.¹ Thyroid hormones physiologically potentiate α- and β-adrenergic receptors by increasing their sensitivity to catecholamines. Excess thyroid hormones manifest as tachycardia, increased cardiac output, increased body temperature, hyperhidrosis, and warm moist skin. Reduced sensitivity of adrenergic receptors to catecholamines from insufficient thyroid hormones results in a lower metabolic rate and decreases response to the sympathetic nervous system.² Nail changes in thyroid patients have not been well studied.³ Our objectives were to characterize nail findings in patients with thyroid disease. Early diagnosis of thyroid disease and prompt referral for treatment may be instrumental in preventing serious morbidities and permanent sequelae.

Methods

PubMed, Scopus, Web of Science, and Google Scholar were searched for the terms nail + thyroid, nail + hyperthyroid, nail + hypothyroid, nail + Graves, and nail + Hashimoto on June 10, 2020, and then updated on November 18, 2020. All English-language articles were included. Non–English-language articles and those that did not describe clinical trials of nail changes in patients with thyroid disease were excluded. One study that utilized survey-based data for nail changes without corroboration with physical examination findings was excluded. Hypothyroidism/hyperthyroidism was defined by all authors as measurement of serum thyroid hormones triiodothyronine, thyroxine, and thyroid-stimulating hormone outside of the normal range. Eight studies were included in the final analysis. Patient demographics, thyroid disease type, physical examination findings, nail clinical findings, age at diagnosis, age at onset of nail changes, treatments/medications, and comorbidities were recorded and analyzed.

Results

Nail changes in patients with thyroid disease were reported in 8 studies (7 cross-sectional, 1 retrospective cohort) and are summarized in the Table.^4-11 The mean age was 41.2 years (range, 5–80 years), with a higher representation of females (range, 70%–94% female). The most common nail changes in thyroid patients were koilonychia, clubbing, and nail brittleness. Other changes included onycholysis, thin nails, dryness, and changes in nail growth rate. Frequent physical findings were xerosis, pruritus, and alopecia.

Both koilonychia and clubbing were reported in patients with hyperthyroidism. In a study of 32 patients with koilonychia, 22 (68.8%) were diagnosed with hyperthyroidism.¹⁰ Nail clubbing affected 7.3% of Graves disease patients (n=150)⁶ and 5.0% of hyperthyroid patients (n=120).⁷ Dermopathy presented more than 1 year after diagnosis of Graves disease in 99 (66%) of 150 patients as a late manifestation of thyrotoxicosis.⁶ Additional physical features in patients with Graves disease (n=150) were pretibial myxedema (100%), ophthalmopathy (99.0%), and proptosis (88.0%). Non–Graves hyperthyroid patients showed physical features of soft hair (83.3%) and soft skin (66.0%).⁷

Nail brittleness was a frequently reported nail change in thyroid patients (4/8 studies, 50%), most often seen in 22% of autoimmune patients, 19.6% of nonautoimmune patients, 13.9% of hypothyroid patients, and 9.2% of hyperthyroid patients.^5,8 For comparison, brittle nails presented in 10.8% of participants in a control group.⁵ Brittle nails in thyroid patients often are accompanied by other nail findings such as thinning, onycholysis, and pitting.

Among hypothyroid patients, nail changes included fragility (70%; n=50), slow growth (48%; n=50), thinning (40%; n=50), onycholysis (38%; n=50),⁷ and brittleness (13.9%; n=173).⁵ Less common nail changes in hypothyroid patients were leukonychia (9.4%; n=32), striped nails (6%; n=50), and pitting (1.2%; n=173).^5,7,11 Among hyperthyroid patients, the most common nail changes were koilonychia (100%; n=22), softening (83%; n=120), onycholysis (29%; n=14), and brittleness (9.2%; n=173).^5,7,9,10 Less common nail changes in hyperthyroid patients were clubbing (5%; n=120), thinning (4.6%; n=173), and leukonychia (3%; n=120).^5,7

Additional cutaneous findings of thyroid disorder included xerosis, alopecia, pruritus, and weight change. Xerosis was most common in hypothyroid disease (57.2%; n=460).⁴ In 2 studies,^8,9 alopecia affected approximately 70% of autoimmune, nonautoimmune, and hyperthyroid patients. Hair loss was reported in 42.6% (n=460)⁴ and 33.0% (n=36)⁹ of hypothyroid patients. Additionally, pruritus affected up to 28% (n=32)¹¹ of hypothyroid and 16.0% (n=120)⁷ of hyperthyroid patients and was more common in autoimmune (41%) vs nonautoimmune (32%) thyroid patients.⁸ Weight gain was seen in 72% of hypothyroid patients (n=32),¹¹ and soft hair and skin were reported in 83.3% and 66% of hyperthyroid patients (n=120), respectively.⁷ Flushing was a less common physical finding in thyroid patients (usually affecting <10%); however, it also was reported in 17.1% of autoimmune and 57.1% of hyperthyroid patients from 2 separate studies.^8,9

 

 

Comment

There are limited data describing nail changes with thyroid disease. Singal and Arora³ reported in their clinical review of nail changes in systemic disease that koilonychia, onycholysis, and melanonychia are associated with thyroid disorders. We similarly found that koilonychia and onycholysis are associated with thyroid disorders without an association with melanonychia.

In his clinical review of thyroid hormone action on the skin, Safer¹² described hypothyroid patients having coarse, dull, thin, and brittle nails, whereas in thyrotoxicosis, patients had shiny, soft, and concave nails with onycholysis; however, the author commented that there were limited data on the clinical findings in thyroid disorders. These nail findings are consistent with our results, but onycholysis was more common in hypothyroid patients than in hyperthyroid patients in our review. Fox¹³ reported on 30 cases of onycholysis, stating that it affected patients with hypothyroidism and improved with thyroid treatment. In a clinical review of 8 commonly seen nail abnormalities, Fowler et al¹⁴ reported that hyperthyroidism was associated with nail findings in 5% of cases and may result in onycholysis of the fourth and fifth nails or all nails. They also reported that onychorrhexis may be seen in patients with hypothyroidism, a finding that differed from our results.¹⁴

The mechanism of nail changes in thyroid disease has not been well studied. A protein/amino acid–deficiency state may contribute to the development of koilonychia. Hyperthyroid patients, who have high metabolic activity, may have hypoalbuminemia, leading to koilonychia.¹⁵ Hypothyroidism causes hypothermia from decreased metabolic rate and secondary compensatory vasoconstriction. Vasoconstriction decreases blood flow of nutrients and oxygen to cutaneous structures and may cause slow-growing, brittle nails. In hyperthyroidism, vasodilation alternatively may contribute to the fast-growing nails. Anti–thyroid-stimulating hormone receptor antibodies in Graves disease may increase the synthesis of hyaluronic acid and glycosaminoglycans from fibroblasts, keratinocytes, adipocytes, or endothelial cells in the dermis and may contribute to development of clubbing.¹⁶

Our review is subject to several limitations. We recorded nail findings as they were described in the original studies; however, we could not confirm the accuracy of these descriptions. In addition, some specific nail changes were not described in sufficient detail. In all but 1 study, dermatologists performed the physical examination. In the study by Al-Dabbagh and Al-Abachi,¹⁰ the physical examinations were performed by general medicine physicians, but they selected only for patients with koilonychia and did not assess for other skin findings. Fragile nails and brittle nails were described in hypothyroid and hyperthyroid patients, but these nail changes were not described in detail. There also were studies describing nail changes in thyroid patients; some studies had small numbers of patients, and many did not have a control group.

Conclusion

Nail changes may be early clinical presenting signs of thyroid disorders and may be the clue to prompt diagnosis of thyroid disease. Dermatologists should be mindful that fragile, slow-growing, thin nails and onycholysis are associated with hypothyroidism and that koilonychia, softening, onycholysis, and brittle nail changes may be seen in hyperthyroidism. Our review aimed to describe nail changes associated with thyroid disease to guide dermatologists on diagnosis and promote future research on dermatologic manifestations of thyroid disease. Future research is necessary to explore the association between koilonychia and hyperthyroidism as well as the association of nail changes with thyroid disease duration and severity.

The major classifications of thyroid disease include hyperthyroidism, which is seen in Graves disease, and hypothyroidism due to iodine deficiency and Hashimoto thyroiditis, which have potentially devastating health consequences. The prevalence of hyperthyroidism ranges from 0.2% to 1.3% in iodine-sufficient parts of the world, and the prevalence of hypothyroidism in the general population is 5.3% in Europe and 3.7% in the United States.¹ Thyroid hormones physiologically potentiate α- and β-adrenergic receptors by increasing their sensitivity to catecholamines. Excess thyroid hormones manifest as tachycardia, increased cardiac output, increased body temperature, hyperhidrosis, and warm moist skin. Reduced sensitivity of adrenergic receptors to catecholamines from insufficient thyroid hormones results in a lower metabolic rate and decreases response to the sympathetic nervous system.² Nail changes in thyroid patients have not been well studied.³ Our objectives were to characterize nail findings in patients with thyroid disease. Early diagnosis of thyroid disease and prompt referral for treatment may be instrumental in preventing serious morbidities and permanent sequelae.

Methods

PubMed, Scopus, Web of Science, and Google Scholar were searched for the terms nail + thyroid, nail + hyperthyroid, nail + hypothyroid, nail + Graves, and nail + Hashimoto on June 10, 2020, and then updated on November 18, 2020. All English-language articles were included. Non–English-language articles and those that did not describe clinical trials of nail changes in patients with thyroid disease were excluded. One study that utilized survey-based data for nail changes without corroboration with physical examination findings was excluded. Hypothyroidism/hyperthyroidism was defined by all authors as measurement of serum thyroid hormones triiodothyronine, thyroxine, and thyroid-stimulating hormone outside of the normal range. Eight studies were included in the final analysis. Patient demographics, thyroid disease type, physical examination findings, nail clinical findings, age at diagnosis, age at onset of nail changes, treatments/medications, and comorbidities were recorded and analyzed.

Results

Nail changes in patients with thyroid disease were reported in 8 studies (7 cross-sectional, 1 retrospective cohort) and are summarized in the Table.^4-11 The mean age was 41.2 years (range, 5–80 years), with a higher representation of females (range, 70%–94% female). The most common nail changes in thyroid patients were koilonychia, clubbing, and nail brittleness. Other changes included onycholysis, thin nails, dryness, and changes in nail growth rate. Frequent physical findings were xerosis, pruritus, and alopecia.

Both koilonychia and clubbing were reported in patients with hyperthyroidism. In a study of 32 patients with koilonychia, 22 (68.8%) were diagnosed with hyperthyroidism.¹⁰ Nail clubbing affected 7.3% of Graves disease patients (n=150)⁶ and 5.0% of hyperthyroid patients (n=120).⁷ Dermopathy presented more than 1 year after diagnosis of Graves disease in 99 (66%) of 150 patients as a late manifestation of thyrotoxicosis.⁶ Additional physical features in patients with Graves disease (n=150) were pretibial myxedema (100%), ophthalmopathy (99.0%), and proptosis (88.0%). Non–Graves hyperthyroid patients showed physical features of soft hair (83.3%) and soft skin (66.0%).⁷

Nail brittleness was a frequently reported nail change in thyroid patients (4/8 studies, 50%), most often seen in 22% of autoimmune patients, 19.6% of nonautoimmune patients, 13.9% of hypothyroid patients, and 9.2% of hyperthyroid patients.^5,8 For comparison, brittle nails presented in 10.8% of participants in a control group.⁵ Brittle nails in thyroid patients often are accompanied by other nail findings such as thinning, onycholysis, and pitting.

Among hypothyroid patients, nail changes included fragility (70%; n=50), slow growth (48%; n=50), thinning (40%; n=50), onycholysis (38%; n=50),⁷ and brittleness (13.9%; n=173).⁵ Less common nail changes in hypothyroid patients were leukonychia (9.4%; n=32), striped nails (6%; n=50), and pitting (1.2%; n=173).^5,7,11 Among hyperthyroid patients, the most common nail changes were koilonychia (100%; n=22), softening (83%; n=120), onycholysis (29%; n=14), and brittleness (9.2%; n=173).^5,7,9,10 Less common nail changes in hyperthyroid patients were clubbing (5%; n=120), thinning (4.6%; n=173), and leukonychia (3%; n=120).^5,7

Additional cutaneous findings of thyroid disorder included xerosis, alopecia, pruritus, and weight change. Xerosis was most common in hypothyroid disease (57.2%; n=460).⁴ In 2 studies,^8,9 alopecia affected approximately 70% of autoimmune, nonautoimmune, and hyperthyroid patients. Hair loss was reported in 42.6% (n=460)⁴ and 33.0% (n=36)⁹ of hypothyroid patients. Additionally, pruritus affected up to 28% (n=32)¹¹ of hypothyroid and 16.0% (n=120)⁷ of hyperthyroid patients and was more common in autoimmune (41%) vs nonautoimmune (32%) thyroid patients.⁸ Weight gain was seen in 72% of hypothyroid patients (n=32),¹¹ and soft hair and skin were reported in 83.3% and 66% of hyperthyroid patients (n=120), respectively.⁷ Flushing was a less common physical finding in thyroid patients (usually affecting <10%); however, it also was reported in 17.1% of autoimmune and 57.1% of hyperthyroid patients from 2 separate studies.^8,9

 

 

Comment

There are limited data describing nail changes with thyroid disease. Singal and Arora³ reported in their clinical review of nail changes in systemic disease that koilonychia, onycholysis, and melanonychia are associated with thyroid disorders. We similarly found that koilonychia and onycholysis are associated with thyroid disorders without an association with melanonychia.

In his clinical review of thyroid hormone action on the skin, Safer¹² described hypothyroid patients having coarse, dull, thin, and brittle nails, whereas in thyrotoxicosis, patients had shiny, soft, and concave nails with onycholysis; however, the author commented that there were limited data on the clinical findings in thyroid disorders. These nail findings are consistent with our results, but onycholysis was more common in hypothyroid patients than in hyperthyroid patients in our review. Fox¹³ reported on 30 cases of onycholysis, stating that it affected patients with hypothyroidism and improved with thyroid treatment. In a clinical review of 8 commonly seen nail abnormalities, Fowler et al¹⁴ reported that hyperthyroidism was associated with nail findings in 5% of cases and may result in onycholysis of the fourth and fifth nails or all nails. They also reported that onychorrhexis may be seen in patients with hypothyroidism, a finding that differed from our results.¹⁴

The mechanism of nail changes in thyroid disease has not been well studied. A protein/amino acid–deficiency state may contribute to the development of koilonychia. Hyperthyroid patients, who have high metabolic activity, may have hypoalbuminemia, leading to koilonychia.¹⁵ Hypothyroidism causes hypothermia from decreased metabolic rate and secondary compensatory vasoconstriction. Vasoconstriction decreases blood flow of nutrients and oxygen to cutaneous structures and may cause slow-growing, brittle nails. In hyperthyroidism, vasodilation alternatively may contribute to the fast-growing nails. Anti–thyroid-stimulating hormone receptor antibodies in Graves disease may increase the synthesis of hyaluronic acid and glycosaminoglycans from fibroblasts, keratinocytes, adipocytes, or endothelial cells in the dermis and may contribute to development of clubbing.¹⁶

Our review is subject to several limitations. We recorded nail findings as they were described in the original studies; however, we could not confirm the accuracy of these descriptions. In addition, some specific nail changes were not described in sufficient detail. In all but 1 study, dermatologists performed the physical examination. In the study by Al-Dabbagh and Al-Abachi,¹⁰ the physical examinations were performed by general medicine physicians, but they selected only for patients with koilonychia and did not assess for other skin findings. Fragile nails and brittle nails were described in hypothyroid and hyperthyroid patients, but these nail changes were not described in detail. There also were studies describing nail changes in thyroid patients; some studies had small numbers of patients, and many did not have a control group.

Conclusion

Nail changes may be early clinical presenting signs of thyroid disorders and may be the clue to prompt diagnosis of thyroid disease. Dermatologists should be mindful that fragile, slow-growing, thin nails and onycholysis are associated with hypothyroidism and that koilonychia, softening, onycholysis, and brittle nail changes may be seen in hyperthyroidism. Our review aimed to describe nail changes associated with thyroid disease to guide dermatologists on diagnosis and promote future research on dermatologic manifestations of thyroid disease. Future research is necessary to explore the association between koilonychia and hyperthyroidism as well as the association of nail changes with thyroid disease duration and severity.

As residents, it is important to understand the steps of the manicuring process and be able to inform patients on how to maintain optimal nail health while continuing to go to nail salons. Most patients are not aware of the possible allergic, traumatic, and/or infectious complications of manicuring their nails. There are practical steps that can be taken to prevent nail issues, such as avoiding cutting one’s cuticles or using allergen-free nail polishes. These simple fixes can make a big difference in long-term nail health in our patients.

Nail Polish Application Process

The nails are first soaked in a warm soapy solution to soften the nail plate and cuticles.¹ Then the nail tips and plates are filed and occasionally are smoothed with a drill. The cuticles are cut with a cuticle cutter. Nail polish—base coat, color enamel, and top coat—is then applied to the nail. Acrylic or sculptured nails and gel and dip manicures are composed of chemical monomers and polymers that harden either at room temperature or through UV or light-emitting diode (LED) exposure. The chemicals in these products can damage nails and cause allergic reactions.

Contact Dermatitis

Approximately 2% of individuals have been found to have allergic or irritant contact dermatitis to nail care products. The top 5 allergens implicated in nail products are (1) 2-hydroxyethyl methacrylate, (2) methyl methacrylate, (3) ethyl acrylate, (4) ethyl-2-cyanoacrylate, and (5) tosylamide.² Methyl methacrylate was banned in 1974 by the US Food and Drug Administration due to reports of severe contact dermatitis, paronychia, and nail dystrophy.³ Due to their potent sensitizing effects, acrylates were named the contact allergen of the year in 2012 by the American Contact Dermatitis Society.³

Acrylates are plastic products formed by polymerization of acrylic or methacrylic acid.⁴ Artificial sculptured nails are created by mixing powdered polymethyl methacrylate polymers and liquid ethyl or isobutyl methacrylate monomers and then applying this mixture to the nail plate.⁵ Gel and powder nails employ a mixture that is similar to acrylic powders, which require UV or LED radiation to polymerize and harden on the nail plate.

Tosylamide, or tosylamide formaldehyde resin, is another potent allergen that promotes adhesion of the enamel to the nail.⁶ It is important to note that sensitization may develop months to years after using artificial nails.

Clinical features of contact allergy secondary to nail polish can vary. Some patients experience severe periungual dermatitis. Others can present with facial or eyelid dermatitis due to exposure to airborne particles of acrylates or from contact with fingertips bearing acrylic nails.^6,7 If inhaled, acrylates also can cause wheezing asthma or allergic rhinoconjunctivitis.

Common Onychodystrophies

Damage to the natural nail plate is inevitable with continued wear of sculptured nails. With 2 to 4 months of consecutive wear, the natural nails turn yellow, brittle, and weak.⁵ One study noted that the thickness of an individual’s left thumb nail plate thinned from 0.059 cm to 0.03 cm after a gel manicure was removed from the nail.⁸ Nail injuries due to manicuring include keratin granulations, onycholysis, pincer nail deformities, pseudopsoriatic nails, lamellar onychoschizia, transverse leukonychia, and ingrown nails.⁶ One interesting nail dystrophy reported secondary to gel manicures is pterygium inversum unguis or a ventral pterygium that causes an abnormal painful adherence of the hyponychium to the ventral surface of the nail plate. Patients prone to developing pterygium inversum unguis can experience sensitivity, pain, or burning sensations during LED or UVA light exposure.⁹

Infections

In addition to contact allergies and nail dystrophies, each step of the manicuring process, such as cutting cuticles, presents opportunities for infectious agents to enter the nail fold. Acute or chronic paronychia, or inflammation of the nail fold, most commonly is caused by bacterial infections with Staphylococcus aureus. Green nail syndrome caused by Pseudomonas aeruginosa also is common.¹ Onychomycosis due to Trichophyton rubrum is one of the most frequent fungal infections contracted at nail salons. Mycobacteria such as Mycobacterium fortuitum also have been implicated in infections from salons, as they can be found in the jets of pedicure spas, which are not sanitized regularly.¹⁰

Final Thoughts

Nail cosmetics are an integral part of many patients’ lives. Being able to educate yourself and your patients on the hazards of nail salons can help them avoid painful infections, contact allergies, and acute to chronic nail deformities. It is important for residents to be aware of the different dermatoses that can arise in men and women who frequent nail salons as the popularity of the nail beauty industry continues to rise.

As residents, it is important to understand the steps of the manicuring process and be able to inform patients on how to maintain optimal nail health while continuing to go to nail salons. Most patients are not aware of the possible allergic, traumatic, and/or infectious complications of manicuring their nails. There are practical steps that can be taken to prevent nail issues, such as avoiding cutting one’s cuticles or using allergen-free nail polishes. These simple fixes can make a big difference in long-term nail health in our patients.

Nail Polish Application Process

The nails are first soaked in a warm soapy solution to soften the nail plate and cuticles.¹ Then the nail tips and plates are filed and occasionally are smoothed with a drill. The cuticles are cut with a cuticle cutter. Nail polish—base coat, color enamel, and top coat—is then applied to the nail. Acrylic or sculptured nails and gel and dip manicures are composed of chemical monomers and polymers that harden either at room temperature or through UV or light-emitting diode (LED) exposure. The chemicals in these products can damage nails and cause allergic reactions.

Contact Dermatitis

Approximately 2% of individuals have been found to have allergic or irritant contact dermatitis to nail care products. The top 5 allergens implicated in nail products are (1) 2-hydroxyethyl methacrylate, (2) methyl methacrylate, (3) ethyl acrylate, (4) ethyl-2-cyanoacrylate, and (5) tosylamide.² Methyl methacrylate was banned in 1974 by the US Food and Drug Administration due to reports of severe contact dermatitis, paronychia, and nail dystrophy.³ Due to their potent sensitizing effects, acrylates were named the contact allergen of the year in 2012 by the American Contact Dermatitis Society.³

Acrylates are plastic products formed by polymerization of acrylic or methacrylic acid.⁴ Artificial sculptured nails are created by mixing powdered polymethyl methacrylate polymers and liquid ethyl or isobutyl methacrylate monomers and then applying this mixture to the nail plate.⁵ Gel and powder nails employ a mixture that is similar to acrylic powders, which require UV or LED radiation to polymerize and harden on the nail plate.

Tosylamide, or tosylamide formaldehyde resin, is another potent allergen that promotes adhesion of the enamel to the nail.⁶ It is important to note that sensitization may develop months to years after using artificial nails.

Clinical features of contact allergy secondary to nail polish can vary. Some patients experience severe periungual dermatitis. Others can present with facial or eyelid dermatitis due to exposure to airborne particles of acrylates or from contact with fingertips bearing acrylic nails.^6,7 If inhaled, acrylates also can cause wheezing asthma or allergic rhinoconjunctivitis.

Common Onychodystrophies

Damage to the natural nail plate is inevitable with continued wear of sculptured nails. With 2 to 4 months of consecutive wear, the natural nails turn yellow, brittle, and weak.⁵ One study noted that the thickness of an individual’s left thumb nail plate thinned from 0.059 cm to 0.03 cm after a gel manicure was removed from the nail.⁸ Nail injuries due to manicuring include keratin granulations, onycholysis, pincer nail deformities, pseudopsoriatic nails, lamellar onychoschizia, transverse leukonychia, and ingrown nails.⁶ One interesting nail dystrophy reported secondary to gel manicures is pterygium inversum unguis or a ventral pterygium that causes an abnormal painful adherence of the hyponychium to the ventral surface of the nail plate. Patients prone to developing pterygium inversum unguis can experience sensitivity, pain, or burning sensations during LED or UVA light exposure.⁹

Infections

In addition to contact allergies and nail dystrophies, each step of the manicuring process, such as cutting cuticles, presents opportunities for infectious agents to enter the nail fold. Acute or chronic paronychia, or inflammation of the nail fold, most commonly is caused by bacterial infections with Staphylococcus aureus. Green nail syndrome caused by Pseudomonas aeruginosa also is common.¹ Onychomycosis due to Trichophyton rubrum is one of the most frequent fungal infections contracted at nail salons. Mycobacteria such as Mycobacterium fortuitum also have been implicated in infections from salons, as they can be found in the jets of pedicure spas, which are not sanitized regularly.¹⁰

Final Thoughts

Nail cosmetics are an integral part of many patients’ lives. Being able to educate yourself and your patients on the hazards of nail salons can help them avoid painful infections, contact allergies, and acute to chronic nail deformities. It is important for residents to be aware of the different dermatoses that can arise in men and women who frequent nail salons as the popularity of the nail beauty industry continues to rise.

As residents, it is important to understand the steps of the manicuring process and be able to inform patients on how to maintain optimal nail health while continuing to go to nail salons. Most patients are not aware of the possible allergic, traumatic, and/or infectious complications of manicuring their nails. There are practical steps that can be taken to prevent nail issues, such as avoiding cutting one’s cuticles or using allergen-free nail polishes. These simple fixes can make a big difference in long-term nail health in our patients.

Nail Polish Application Process

The nails are first soaked in a warm soapy solution to soften the nail plate and cuticles.¹ Then the nail tips and plates are filed and occasionally are smoothed with a drill. The cuticles are cut with a cuticle cutter. Nail polish—base coat, color enamel, and top coat—is then applied to the nail. Acrylic or sculptured nails and gel and dip manicures are composed of chemical monomers and polymers that harden either at room temperature or through UV or light-emitting diode (LED) exposure. The chemicals in these products can damage nails and cause allergic reactions.

Contact Dermatitis

Approximately 2% of individuals have been found to have allergic or irritant contact dermatitis to nail care products. The top 5 allergens implicated in nail products are (1) 2-hydroxyethyl methacrylate, (2) methyl methacrylate, (3) ethyl acrylate, (4) ethyl-2-cyanoacrylate, and (5) tosylamide.² Methyl methacrylate was banned in 1974 by the US Food and Drug Administration due to reports of severe contact dermatitis, paronychia, and nail dystrophy.³ Due to their potent sensitizing effects, acrylates were named the contact allergen of the year in 2012 by the American Contact Dermatitis Society.³

Acrylates are plastic products formed by polymerization of acrylic or methacrylic acid.⁴ Artificial sculptured nails are created by mixing powdered polymethyl methacrylate polymers and liquid ethyl or isobutyl methacrylate monomers and then applying this mixture to the nail plate.⁵ Gel and powder nails employ a mixture that is similar to acrylic powders, which require UV or LED radiation to polymerize and harden on the nail plate.

Tosylamide, or tosylamide formaldehyde resin, is another potent allergen that promotes adhesion of the enamel to the nail.⁶ It is important to note that sensitization may develop months to years after using artificial nails.

Clinical features of contact allergy secondary to nail polish can vary. Some patients experience severe periungual dermatitis. Others can present with facial or eyelid dermatitis due to exposure to airborne particles of acrylates or from contact with fingertips bearing acrylic nails.^6,7 If inhaled, acrylates also can cause wheezing asthma or allergic rhinoconjunctivitis.

Common Onychodystrophies

Damage to the natural nail plate is inevitable with continued wear of sculptured nails. With 2 to 4 months of consecutive wear, the natural nails turn yellow, brittle, and weak.⁵ One study noted that the thickness of an individual’s left thumb nail plate thinned from 0.059 cm to 0.03 cm after a gel manicure was removed from the nail.⁸ Nail injuries due to manicuring include keratin granulations, onycholysis, pincer nail deformities, pseudopsoriatic nails, lamellar onychoschizia, transverse leukonychia, and ingrown nails.⁶ One interesting nail dystrophy reported secondary to gel manicures is pterygium inversum unguis or a ventral pterygium that causes an abnormal painful adherence of the hyponychium to the ventral surface of the nail plate. Patients prone to developing pterygium inversum unguis can experience sensitivity, pain, or burning sensations during LED or UVA light exposure.⁹

Infections

In addition to contact allergies and nail dystrophies, each step of the manicuring process, such as cutting cuticles, presents opportunities for infectious agents to enter the nail fold. Acute or chronic paronychia, or inflammation of the nail fold, most commonly is caused by bacterial infections with Staphylococcus aureus. Green nail syndrome caused by Pseudomonas aeruginosa also is common.¹ Onychomycosis due to Trichophyton rubrum is one of the most frequent fungal infections contracted at nail salons. Mycobacteria such as Mycobacterium fortuitum also have been implicated in infections from salons, as they can be found in the jets of pedicure spas, which are not sanitized regularly.¹⁰

Final Thoughts

Nail cosmetics are an integral part of many patients’ lives. Being able to educate yourself and your patients on the hazards of nail salons can help them avoid painful infections, contact allergies, and acute to chronic nail deformities. It is important for residents to be aware of the different dermatoses that can arise in men and women who frequent nail salons as the popularity of the nail beauty industry continues to rise.

INDIANAPOLIS – Despite the common prevalence of skin-picking disorder and trichotillomania (hair pulling), no Food and Drug Administration–approved treatments exist for either condition.

And while both body-focused repetitive behavior disorders affect a greater proportion of females than males, “we have no current information that is useful about what hormonal influences may or may not play in terms of picking and pulling behaviors,” Jon E. Grant, MD, JD, MPH, professor of psychiatry and behavioral neuroscience at the University of Chicago, said at the annual meeting of the Society for Pediatric Dermatology. “On a cognitive level, affected children and adolescents often have impaired inhibitory control but they are often 1-2 standard deviations above average IQ. They have Type A personalities [and are] very driven young kids. They also do not tolerate any down time or boredom. They need to be doing something all the time.”

According to the DSM-5, the diagnostic criteria for skin picking includes recurrent skin picking that results in skin lesions and is not attributable to another medical condition or substance. It also involves repeated attempts to decrease or stop the behavior and causes clinically significant distress or impairment.

“The other medical condition that we are interested in is the misuse of or dependence upon amphetamines or other prescription-based or illicit stimulants,” Dr. Grant said. “I saw a young man who was using about 600 mg of Ritalin a day, and he was picking all over the place. He did not have a primary skin disorder.”

The lifetime prevalence of skin picking disorder ranges between 1.4% and 5.4% of the general population. However, about 63% of people in a community sample endorsed some form of skin picking, and in a study of 105 college students, almost 40% said they picked their skin and had noticeable tissue damage as a result.

“Skin picking is not the same as self-injury,” Dr. Grant said. “It is also not simply an anxiety disorder. Anxiety will make people who pick worse, so people will say that they pick when they’re under stress. I can give them benzodiazepines and they’re still going to pick.”

Animal and human studies demonstrate that skin picking and hair pulling primarily affect females. “You will encounter young boys that pick and pull, but it largely affects females, and it tends to start around puberty,” he said. “Picking can have an onset after the age of 30, which is quite uncommon.”

From a cognitive standpoint, pathological skin pickers demonstrate impaired inhibitory control, impaired stop signal reaction time, increased rates of negative urgency (a tendency to act impulsively in response to negative emotions), and increased rates of positive urgency (a tendency to act impulsively in response to exciting or pleasurable emotions).

Trichotillomania

The lifetime prevalence of trichotillomania ranges between 0.6% and 3.9%. The onset is typically from ages 10-13 years, and the mean duration of illness is 22 years.

The DSM-5 criteria for trichotillomania are similar to that of skin-picking disorder, “although we don’t really worry about the substance use issue with people who pull their hair,” Dr. Grant said. “It doesn’t seem to have a correlation.” In addition, sometimes, children “will worsen pulling or picking when they have co-occurring ADHD and they’ve been started on a stimulant, even at a typical dose. For kids who have those issues, we prefer to try nonstimulant options for their ADHD such as bupropion or atomoxetine.”

Individuals with trichotillomania also tend to have low self-esteem and increased social anxiety, he added, and about one-third report low or very low quality of life. “When you notice alopecia, particularly in young girls who often have longer hair, up to 20% will eat their hair,” Dr. Grant said. “We don’t know why. It’s not related to vitamin deficiencies; it’s not a pica type of iron deficiency. There seems to be a shame piece about eating one’s own hair, but it’s important to assess that. Ask about constipation or overflow incontinence because they can get a bezoar, which can rupture” and can be fatal.

Skin-picking disorder and trichotillomania co-occur in up to 20% of cases. “When they do it tends to be a more difficult problem,” he said. These patients often come for mental health care because of depression, and most, he added, say “I don’t think I would be depressed if I wasn’t covered with excoriations or missing most of my hair.”
 

Treatment for both conditions

According to Dr. Grant, the treatment of choice for skin-picking disorder and trichotillomania is a specific psychotherapy known as “habit reversal therapy,” which involves helping the patient gain better self-control. The drawback is that it’s difficult to find someone trained in habit reversal therapy, “who know anything about skin picking and hair pulling,” he said. “That has been a huge challenge in the field.”

In his experience, the medical treatment of choice for skin-picking disorder and trichotillomania is N-acetylcysteine, an over-the-counter amino acid and antioxidant, which has been shown to be helpful at a dose of 2,400 mg per day. “Patients report to me that some of the excoriations clear up a little quicker as they’re taking it,” Dr. Grant said.

There may also be a role for antipsychotic therapy, he said, “but because of the associated weight gain with most antipsychotics we prefer not to use them.”

The opioid antagonist naltrexone has been shown to be effective in the subset of patients with skin-picking or hair-pulling disorders whose parents have a substance use disorder, Dr. Grant said. “The thought is that there’s something addictive about this behavior in some kids. These kids will look forward to picking and find it rewarding and exciting.”

Dr. Grant reported having no relevant financial disclosures.

INDIANAPOLIS – Despite the common prevalence of skin-picking disorder and trichotillomania (hair pulling), no Food and Drug Administration–approved treatments exist for either condition.

And while both body-focused repetitive behavior disorders affect a greater proportion of females than males, “we have no current information that is useful about what hormonal influences may or may not play in terms of picking and pulling behaviors,” Jon E. Grant, MD, JD, MPH, professor of psychiatry and behavioral neuroscience at the University of Chicago, said at the annual meeting of the Society for Pediatric Dermatology. “On a cognitive level, affected children and adolescents often have impaired inhibitory control but they are often 1-2 standard deviations above average IQ. They have Type A personalities [and are] very driven young kids. They also do not tolerate any down time or boredom. They need to be doing something all the time.”

According to the DSM-5, the diagnostic criteria for skin picking includes recurrent skin picking that results in skin lesions and is not attributable to another medical condition or substance. It also involves repeated attempts to decrease or stop the behavior and causes clinically significant distress or impairment.

“The other medical condition that we are interested in is the misuse of or dependence upon amphetamines or other prescription-based or illicit stimulants,” Dr. Grant said. “I saw a young man who was using about 600 mg of Ritalin a day, and he was picking all over the place. He did not have a primary skin disorder.”

The lifetime prevalence of skin picking disorder ranges between 1.4% and 5.4% of the general population. However, about 63% of people in a community sample endorsed some form of skin picking, and in a study of 105 college students, almost 40% said they picked their skin and had noticeable tissue damage as a result.

“Skin picking is not the same as self-injury,” Dr. Grant said. “It is also not simply an anxiety disorder. Anxiety will make people who pick worse, so people will say that they pick when they’re under stress. I can give them benzodiazepines and they’re still going to pick.”

Animal and human studies demonstrate that skin picking and hair pulling primarily affect females. “You will encounter young boys that pick and pull, but it largely affects females, and it tends to start around puberty,” he said. “Picking can have an onset after the age of 30, which is quite uncommon.”

From a cognitive standpoint, pathological skin pickers demonstrate impaired inhibitory control, impaired stop signal reaction time, increased rates of negative urgency (a tendency to act impulsively in response to negative emotions), and increased rates of positive urgency (a tendency to act impulsively in response to exciting or pleasurable emotions).

Trichotillomania

The lifetime prevalence of trichotillomania ranges between 0.6% and 3.9%. The onset is typically from ages 10-13 years, and the mean duration of illness is 22 years.

The DSM-5 criteria for trichotillomania are similar to that of skin-picking disorder, “although we don’t really worry about the substance use issue with people who pull their hair,” Dr. Grant said. “It doesn’t seem to have a correlation.” In addition, sometimes, children “will worsen pulling or picking when they have co-occurring ADHD and they’ve been started on a stimulant, even at a typical dose. For kids who have those issues, we prefer to try nonstimulant options for their ADHD such as bupropion or atomoxetine.”

Individuals with trichotillomania also tend to have low self-esteem and increased social anxiety, he added, and about one-third report low or very low quality of life. “When you notice alopecia, particularly in young girls who often have longer hair, up to 20% will eat their hair,” Dr. Grant said. “We don’t know why. It’s not related to vitamin deficiencies; it’s not a pica type of iron deficiency. There seems to be a shame piece about eating one’s own hair, but it’s important to assess that. Ask about constipation or overflow incontinence because they can get a bezoar, which can rupture” and can be fatal.

Skin-picking disorder and trichotillomania co-occur in up to 20% of cases. “When they do it tends to be a more difficult problem,” he said. These patients often come for mental health care because of depression, and most, he added, say “I don’t think I would be depressed if I wasn’t covered with excoriations or missing most of my hair.”
 

Treatment for both conditions

According to Dr. Grant, the treatment of choice for skin-picking disorder and trichotillomania is a specific psychotherapy known as “habit reversal therapy,” which involves helping the patient gain better self-control. The drawback is that it’s difficult to find someone trained in habit reversal therapy, “who know anything about skin picking and hair pulling,” he said. “That has been a huge challenge in the field.”

In his experience, the medical treatment of choice for skin-picking disorder and trichotillomania is N-acetylcysteine, an over-the-counter amino acid and antioxidant, which has been shown to be helpful at a dose of 2,400 mg per day. “Patients report to me that some of the excoriations clear up a little quicker as they’re taking it,” Dr. Grant said.

There may also be a role for antipsychotic therapy, he said, “but because of the associated weight gain with most antipsychotics we prefer not to use them.”

The opioid antagonist naltrexone has been shown to be effective in the subset of patients with skin-picking or hair-pulling disorders whose parents have a substance use disorder, Dr. Grant said. “The thought is that there’s something addictive about this behavior in some kids. These kids will look forward to picking and find it rewarding and exciting.”

Dr. Grant reported having no relevant financial disclosures.

INDIANAPOLIS – Despite the common prevalence of skin-picking disorder and trichotillomania (hair pulling), no Food and Drug Administration–approved treatments exist for either condition.

And while both body-focused repetitive behavior disorders affect a greater proportion of females than males, “we have no current information that is useful about what hormonal influences may or may not play in terms of picking and pulling behaviors,” Jon E. Grant, MD, JD, MPH, professor of psychiatry and behavioral neuroscience at the University of Chicago, said at the annual meeting of the Society for Pediatric Dermatology. “On a cognitive level, affected children and adolescents often have impaired inhibitory control but they are often 1-2 standard deviations above average IQ. They have Type A personalities [and are] very driven young kids. They also do not tolerate any down time or boredom. They need to be doing something all the time.”

According to the DSM-5, the diagnostic criteria for skin picking includes recurrent skin picking that results in skin lesions and is not attributable to another medical condition or substance. It also involves repeated attempts to decrease or stop the behavior and causes clinically significant distress or impairment.

“The other medical condition that we are interested in is the misuse of or dependence upon amphetamines or other prescription-based or illicit stimulants,” Dr. Grant said. “I saw a young man who was using about 600 mg of Ritalin a day, and he was picking all over the place. He did not have a primary skin disorder.”

The lifetime prevalence of skin picking disorder ranges between 1.4% and 5.4% of the general population. However, about 63% of people in a community sample endorsed some form of skin picking, and in a study of 105 college students, almost 40% said they picked their skin and had noticeable tissue damage as a result.

“Skin picking is not the same as self-injury,” Dr. Grant said. “It is also not simply an anxiety disorder. Anxiety will make people who pick worse, so people will say that they pick when they’re under stress. I can give them benzodiazepines and they’re still going to pick.”

Animal and human studies demonstrate that skin picking and hair pulling primarily affect females. “You will encounter young boys that pick and pull, but it largely affects females, and it tends to start around puberty,” he said. “Picking can have an onset after the age of 30, which is quite uncommon.”

From a cognitive standpoint, pathological skin pickers demonstrate impaired inhibitory control, impaired stop signal reaction time, increased rates of negative urgency (a tendency to act impulsively in response to negative emotions), and increased rates of positive urgency (a tendency to act impulsively in response to exciting or pleasurable emotions).

Trichotillomania

The lifetime prevalence of trichotillomania ranges between 0.6% and 3.9%. The onset is typically from ages 10-13 years, and the mean duration of illness is 22 years.

The DSM-5 criteria for trichotillomania are similar to that of skin-picking disorder, “although we don’t really worry about the substance use issue with people who pull their hair,” Dr. Grant said. “It doesn’t seem to have a correlation.” In addition, sometimes, children “will worsen pulling or picking when they have co-occurring ADHD and they’ve been started on a stimulant, even at a typical dose. For kids who have those issues, we prefer to try nonstimulant options for their ADHD such as bupropion or atomoxetine.”

Individuals with trichotillomania also tend to have low self-esteem and increased social anxiety, he added, and about one-third report low or very low quality of life. “When you notice alopecia, particularly in young girls who often have longer hair, up to 20% will eat their hair,” Dr. Grant said. “We don’t know why. It’s not related to vitamin deficiencies; it’s not a pica type of iron deficiency. There seems to be a shame piece about eating one’s own hair, but it’s important to assess that. Ask about constipation or overflow incontinence because they can get a bezoar, which can rupture” and can be fatal.

Skin-picking disorder and trichotillomania co-occur in up to 20% of cases. “When they do it tends to be a more difficult problem,” he said. These patients often come for mental health care because of depression, and most, he added, say “I don’t think I would be depressed if I wasn’t covered with excoriations or missing most of my hair.”
 

Treatment for both conditions

According to Dr. Grant, the treatment of choice for skin-picking disorder and trichotillomania is a specific psychotherapy known as “habit reversal therapy,” which involves helping the patient gain better self-control. The drawback is that it’s difficult to find someone trained in habit reversal therapy, “who know anything about skin picking and hair pulling,” he said. “That has been a huge challenge in the field.”

In his experience, the medical treatment of choice for skin-picking disorder and trichotillomania is N-acetylcysteine, an over-the-counter amino acid and antioxidant, which has been shown to be helpful at a dose of 2,400 mg per day. “Patients report to me that some of the excoriations clear up a little quicker as they’re taking it,” Dr. Grant said.

There may also be a role for antipsychotic therapy, he said, “but because of the associated weight gain with most antipsychotics we prefer not to use them.”

The opioid antagonist naltrexone has been shown to be effective in the subset of patients with skin-picking or hair-pulling disorders whose parents have a substance use disorder, Dr. Grant said. “The thought is that there’s something addictive about this behavior in some kids. These kids will look forward to picking and find it rewarding and exciting.”

Dr. Grant reported having no relevant financial disclosures.