Hair & Nails

TOPLINE:

Women with daily exposure to spironolactone for dermatologic conditions showed no higher risk of developing breast or gynecologic cancer than that of unexposed women.

METHODOLOGY:

• Spironolactone, used off-label for several skin conditions in women, carries a warning about an increased tumor risk associated with high doses in rat models, and its antiandrogen properties have prompted hypotheses about a possible increased risk for breast or gynecologic cancers.
• The researchers reviewed data on 420 women with a history of spironolactone use for acne, hair loss, and hirsutism and 3272 women with no spironolactone use at the authors› institution. Their mean age ranged from 42 to 63 years; the majority were White, and 38% were non-White.
• Median spironolactone doses ranged from 25 mg to 225 mg; chart reviews included 5-year follow-up data from the first spironolactone exposure to allow time for tumor development.

TAKEAWAY:

• A total of 37 of the 420 women exposed to spironolactone developed any tumors, as did 546 of the 3272 with no spironolactone exposure.
• After the researchers controlled for age and race, women exposed to spironolactone were no more likely to develop a malignant tumor than a benign tumor, compared with unexposed women (odds ratio [OR], 0.48, P = .2).
• The risk for breast or uterine cancer was not significantly different in the spironolactone and non-spironolactone groups (OR, 0.95, P > .9).

IN PRACTICE:

“Women taking spironolactone for acne, hair loss, and hirsutism and who are at low risk of breast or gynecologic cancers may be counseled to have regular gynecology follow-up, but no more frequently than the general population,” but more studies are needed to evaluate risk over longer periods of time, the researchers wrote.

SOURCE:

The lead author of the study was Rachel C. Hill, BS, a student at Weill Cornell Medical College, New York City, and Shari R. Lipner, MD, PhD, of the department of dermatology at Weill Cornell Medical College, was the corresponding author. The study was published online in The Journal of the American Academy of Dermatology.

LIMITATIONS:

The findings were limited by the retrospective design, as well as the small number of spironolactone patients analyzed, the short follow-up period, the lack of information about spironolactone courses, and the inability to control for family history of malignancy.

DISCLOSURES:

The study was supported by the National Center for Advancing Translational Sciences and a grant from the Clinical and Translational Science Center at Weill Cornell Medical College awarded to Ms. Hill. None of the authors had relevant disclosures; Dr. Lipner disclosed serving as a consultant for Ortho-Dermatologics, Eli Lilly, Moberg Pharmaceuticals, and BelleTorus Corporation.

A version of this article appeared on Medscape.com.

TOPLINE:

Women with daily exposure to spironolactone for dermatologic conditions showed no higher risk of developing breast or gynecologic cancer than that of unexposed women.

METHODOLOGY:

• Spironolactone, used off-label for several skin conditions in women, carries a warning about an increased tumor risk associated with high doses in rat models, and its antiandrogen properties have prompted hypotheses about a possible increased risk for breast or gynecologic cancers.
• The researchers reviewed data on 420 women with a history of spironolactone use for acne, hair loss, and hirsutism and 3272 women with no spironolactone use at the authors› institution. Their mean age ranged from 42 to 63 years; the majority were White, and 38% were non-White.
• Median spironolactone doses ranged from 25 mg to 225 mg; chart reviews included 5-year follow-up data from the first spironolactone exposure to allow time for tumor development.

TAKEAWAY:

• A total of 37 of the 420 women exposed to spironolactone developed any tumors, as did 546 of the 3272 with no spironolactone exposure.
• After the researchers controlled for age and race, women exposed to spironolactone were no more likely to develop a malignant tumor than a benign tumor, compared with unexposed women (odds ratio [OR], 0.48, P = .2).
• The risk for breast or uterine cancer was not significantly different in the spironolactone and non-spironolactone groups (OR, 0.95, P > .9).

IN PRACTICE:

“Women taking spironolactone for acne, hair loss, and hirsutism and who are at low risk of breast or gynecologic cancers may be counseled to have regular gynecology follow-up, but no more frequently than the general population,” but more studies are needed to evaluate risk over longer periods of time, the researchers wrote.

SOURCE:

The lead author of the study was Rachel C. Hill, BS, a student at Weill Cornell Medical College, New York City, and Shari R. Lipner, MD, PhD, of the department of dermatology at Weill Cornell Medical College, was the corresponding author. The study was published online in The Journal of the American Academy of Dermatology.

LIMITATIONS:

The findings were limited by the retrospective design, as well as the small number of spironolactone patients analyzed, the short follow-up period, the lack of information about spironolactone courses, and the inability to control for family history of malignancy.

DISCLOSURES:

The study was supported by the National Center for Advancing Translational Sciences and a grant from the Clinical and Translational Science Center at Weill Cornell Medical College awarded to Ms. Hill. None of the authors had relevant disclosures; Dr. Lipner disclosed serving as a consultant for Ortho-Dermatologics, Eli Lilly, Moberg Pharmaceuticals, and BelleTorus Corporation.

A version of this article appeared on Medscape.com.

TOPLINE:

Women with daily exposure to spironolactone for dermatologic conditions showed no higher risk of developing breast or gynecologic cancer than that of unexposed women.

METHODOLOGY:

• Spironolactone, used off-label for several skin conditions in women, carries a warning about an increased tumor risk associated with high doses in rat models, and its antiandrogen properties have prompted hypotheses about a possible increased risk for breast or gynecologic cancers.
• The researchers reviewed data on 420 women with a history of spironolactone use for acne, hair loss, and hirsutism and 3272 women with no spironolactone use at the authors› institution. Their mean age ranged from 42 to 63 years; the majority were White, and 38% were non-White.
• Median spironolactone doses ranged from 25 mg to 225 mg; chart reviews included 5-year follow-up data from the first spironolactone exposure to allow time for tumor development.

TAKEAWAY:

• A total of 37 of the 420 women exposed to spironolactone developed any tumors, as did 546 of the 3272 with no spironolactone exposure.
• After the researchers controlled for age and race, women exposed to spironolactone were no more likely to develop a malignant tumor than a benign tumor, compared with unexposed women (odds ratio [OR], 0.48, P = .2).
• The risk for breast or uterine cancer was not significantly different in the spironolactone and non-spironolactone groups (OR, 0.95, P > .9).

IN PRACTICE:

“Women taking spironolactone for acne, hair loss, and hirsutism and who are at low risk of breast or gynecologic cancers may be counseled to have regular gynecology follow-up, but no more frequently than the general population,” but more studies are needed to evaluate risk over longer periods of time, the researchers wrote.

SOURCE:

The lead author of the study was Rachel C. Hill, BS, a student at Weill Cornell Medical College, New York City, and Shari R. Lipner, MD, PhD, of the department of dermatology at Weill Cornell Medical College, was the corresponding author. The study was published online in The Journal of the American Academy of Dermatology.

LIMITATIONS:

The findings were limited by the retrospective design, as well as the small number of spironolactone patients analyzed, the short follow-up period, the lack of information about spironolactone courses, and the inability to control for family history of malignancy.

DISCLOSURES:

The study was supported by the National Center for Advancing Translational Sciences and a grant from the Clinical and Translational Science Center at Weill Cornell Medical College awarded to Ms. Hill. None of the authors had relevant disclosures; Dr. Lipner disclosed serving as a consultant for Ortho-Dermatologics, Eli Lilly, Moberg Pharmaceuticals, and BelleTorus Corporation.

A version of this article appeared on Medscape.com.

Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Melanoma in situ manifesting as longitudinal melanonychia (LM) in a single digit in a Black man. Dermoscopy showed irregular dark bands of brown pigmentation and micro-Hutchinson sign on the cuticle (inset).

B Melanoma manifesting as LM with a prominent Hutchinson sign in a Hispanic man, with variable shades of brown covering more than 50% of the nail width.

C Longitudinal melanonychia of at least 2 nails with a pseudo-Hutchinson sign (pigment on the nail folds in a benign case of LM) in a young Black man demonstrating ethnic/racial melanosis. The longitudinal bands, which were caused by benign melanocytic activation, are more gray than brown and are less than 3 mm wide.

Longitudinal melanonychia (LM) is a pigmented linear band—brown, black, or gray—spanning the length of the nail plate due to the presence of excess melanin, which may be attributed to a benign or malignant process and may warrant further investigation.^1,2 The majority of patients who present with LM are diagnosed with melanocytic activation of the nail matrix due to their inherent darker skin tone or various triggers including trauma, infection, and medications. Longitudinal melanonychia secondary to melanocytic activation often occurs spontaneously in patients with skin of color.³ Less commonly, LM is caused by a nail matrix nevus or lentigo; however, LM may arise secondary to subungual melanoma, a more dangerous cause.

A thorough clinical history including duration, recent changes in LM manifestation, nail trauma, or infection is helpful in evaluating patients with LM; however, a history of nail trauma can be misleading, as nail changes attributed to the trauma may in fact be melanoma. Irregularly spaced vertical lines of pigmentation ranging from brown to black with variations in spacing and width are characteristic of subungual melanoma.⁴ Nail dystrophy, granular hyperpigmentation, and Hutchinson sign (extension of pigmentation to the nail folds) also are worrisome features.⁵ In recent years, dermoscopy has become an important tool in the clinical examination of LM, with the development of criteria based on color and pattern recognition.^5,6 Dermoscopy can be useful in screening potential candidates for biopsy. Although clinical examination and dermoscopy are essential to evaluating LM, the gold-standard diagnostic test when malignancy is suspected is a nail matrix biopsy.^1,2,6,7

Epidemiology

It is not unusual for patients with darker skin tones to develop LM due to melanocytic activation of multiple nails with age. This finding can be seen in approximately 80% of African American individuals, 30% of Japanese individuals, and 50% of Hispanic individuals.² It has even been reported that approximately 100% of Black patients older than 50 years will have evidence of LM.³

In a retrospective analysis, children presenting with LM tend to have a higher prevalence of nail matrix nevi compared to adults (56.1% [60/106] vs 34.3% [23/66]; P=.005).⁸ Involvement of a single digit in children is most likely indicative of a nevus; however, when an adult presents with LM in a single digit, suspicion for subungual melanoma should be raised.^2,3,9

Two separate single-center retrospective studies showed the prevalence of subungual melanoma in patients presenting with melanonychia in Asia. Jin et al10 reported subungual melanoma in 6.2% (17/275) of Korean patients presenting with melanonychia at a general dermatology clinic from 2002 to 2014. Lyu et al⁸ studied LM in 172 Chinese patients in a dermatology clinic from 2018 to 2021 and reported 9% (6/66) of adults (aged ≥18 years) with subungual melanoma, with no reported cases in childhood (aged <18 years).

Although the prevalence of subungual melanoma in patients with LM is low, it is an important diagnosis that should not be missed. In confirmed cases of subungual melanoma, two-thirds of lesions manifested as LM.^3,10,11 Thus, LM arising in an adult in a single digit is more concerning for malignancy.^2,3,7,9

Individuals of African and Asian descent as well as American Indian individuals are at highest risk for subungual melanoma with a poor prognosis compared to other types of melanoma, largely due to diagnosis at an advanced stage of disease.^3,9 In a retrospective study of 25 patients with surgically treated subungual melanoma, the mean recurrence-free survival was 33.6 months. The recurrence-free survival was 66% at 1 year and 40% at 3 years, and the overall survival rate was 37% at 3 years.¹²

Key clinical features in individuals with darker skin tones

• In patients with darker skin tones, LM tends to occur on multiple nails as a result of melanocytic activation.^2,13
• Several longitudinal bands may be noted on the same nail and the pigmentation of the bands may vary. With age, these longitudinal bands typically increase in number and width.¹³
• Pseudo-Hutchinson sign may be present due to ethnic melanosis of the proximal nail fold.^13,14
• Dermoscopic findings of LM in patients with skin of color include wider bands (P=.0125), lower band brightness (P<.032), and higher frequency of changing appearance of bands (P=.0071).¹⁵

Worth noting

When patients present with LM, thorough examination of the nail plate, periungual skin, and distal pulp of all digits on all extremities with adequate lighting is important.² Dermoscopy is useful, and a gel interface helps for examining the nail plates.⁷

Clinicians should be encouraged to biopsy or immediately refer patients with concerning nail unit lesions. Cases of LM most likely are benign, but if some doubt exists, the lesions should be biopsied or tracked closely with clinical and dermoscopic images, with a biopsy if changes occur.¹⁶ In conjunction with evaluation by a qualified clinician, patients also should be encouraged to take photographs, as the evolution of nail changes is a critical part of clinical decision-making on the need for a biopsy or referral.

Health disparity highlight

Despite the disproportionately high mortality rates from subungual melanoma in Black and Hispanic populations,^3,9 studies often do not adequately represent these populations. Although subungual melanoma is rare, a delay in the diagnosis contributes to high morbidity and mortality rates.

Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Melanoma in situ manifesting as longitudinal melanonychia (LM) in a single digit in a Black man. Dermoscopy showed irregular dark bands of brown pigmentation and micro-Hutchinson sign on the cuticle (inset).

B Melanoma manifesting as LM with a prominent Hutchinson sign in a Hispanic man, with variable shades of brown covering more than 50% of the nail width.

C Longitudinal melanonychia of at least 2 nails with a pseudo-Hutchinson sign (pigment on the nail folds in a benign case of LM) in a young Black man demonstrating ethnic/racial melanosis. The longitudinal bands, which were caused by benign melanocytic activation, are more gray than brown and are less than 3 mm wide.

Longitudinal melanonychia (LM) is a pigmented linear band—brown, black, or gray—spanning the length of the nail plate due to the presence of excess melanin, which may be attributed to a benign or malignant process and may warrant further investigation.^1,2 The majority of patients who present with LM are diagnosed with melanocytic activation of the nail matrix due to their inherent darker skin tone or various triggers including trauma, infection, and medications. Longitudinal melanonychia secondary to melanocytic activation often occurs spontaneously in patients with skin of color.³ Less commonly, LM is caused by a nail matrix nevus or lentigo; however, LM may arise secondary to subungual melanoma, a more dangerous cause.

A thorough clinical history including duration, recent changes in LM manifestation, nail trauma, or infection is helpful in evaluating patients with LM; however, a history of nail trauma can be misleading, as nail changes attributed to the trauma may in fact be melanoma. Irregularly spaced vertical lines of pigmentation ranging from brown to black with variations in spacing and width are characteristic of subungual melanoma.⁴ Nail dystrophy, granular hyperpigmentation, and Hutchinson sign (extension of pigmentation to the nail folds) also are worrisome features.⁵ In recent years, dermoscopy has become an important tool in the clinical examination of LM, with the development of criteria based on color and pattern recognition.^5,6 Dermoscopy can be useful in screening potential candidates for biopsy. Although clinical examination and dermoscopy are essential to evaluating LM, the gold-standard diagnostic test when malignancy is suspected is a nail matrix biopsy.^1,2,6,7

Epidemiology

It is not unusual for patients with darker skin tones to develop LM due to melanocytic activation of multiple nails with age. This finding can be seen in approximately 80% of African American individuals, 30% of Japanese individuals, and 50% of Hispanic individuals.² It has even been reported that approximately 100% of Black patients older than 50 years will have evidence of LM.³

In a retrospective analysis, children presenting with LM tend to have a higher prevalence of nail matrix nevi compared to adults (56.1% [60/106] vs 34.3% [23/66]; P=.005).⁸ Involvement of a single digit in children is most likely indicative of a nevus; however, when an adult presents with LM in a single digit, suspicion for subungual melanoma should be raised.^2,3,9

Two separate single-center retrospective studies showed the prevalence of subungual melanoma in patients presenting with melanonychia in Asia. Jin et al10 reported subungual melanoma in 6.2% (17/275) of Korean patients presenting with melanonychia at a general dermatology clinic from 2002 to 2014. Lyu et al⁸ studied LM in 172 Chinese patients in a dermatology clinic from 2018 to 2021 and reported 9% (6/66) of adults (aged ≥18 years) with subungual melanoma, with no reported cases in childhood (aged <18 years).

Although the prevalence of subungual melanoma in patients with LM is low, it is an important diagnosis that should not be missed. In confirmed cases of subungual melanoma, two-thirds of lesions manifested as LM.^3,10,11 Thus, LM arising in an adult in a single digit is more concerning for malignancy.^2,3,7,9

Individuals of African and Asian descent as well as American Indian individuals are at highest risk for subungual melanoma with a poor prognosis compared to other types of melanoma, largely due to diagnosis at an advanced stage of disease.^3,9 In a retrospective study of 25 patients with surgically treated subungual melanoma, the mean recurrence-free survival was 33.6 months. The recurrence-free survival was 66% at 1 year and 40% at 3 years, and the overall survival rate was 37% at 3 years.¹²

Key clinical features in individuals with darker skin tones

• In patients with darker skin tones, LM tends to occur on multiple nails as a result of melanocytic activation.^2,13
• Several longitudinal bands may be noted on the same nail and the pigmentation of the bands may vary. With age, these longitudinal bands typically increase in number and width.¹³
• Pseudo-Hutchinson sign may be present due to ethnic melanosis of the proximal nail fold.^13,14
• Dermoscopic findings of LM in patients with skin of color include wider bands (P=.0125), lower band brightness (P<.032), and higher frequency of changing appearance of bands (P=.0071).¹⁵

Worth noting

When patients present with LM, thorough examination of the nail plate, periungual skin, and distal pulp of all digits on all extremities with adequate lighting is important.² Dermoscopy is useful, and a gel interface helps for examining the nail plates.⁷

Clinicians should be encouraged to biopsy or immediately refer patients with concerning nail unit lesions. Cases of LM most likely are benign, but if some doubt exists, the lesions should be biopsied or tracked closely with clinical and dermoscopic images, with a biopsy if changes occur.¹⁶ In conjunction with evaluation by a qualified clinician, patients also should be encouraged to take photographs, as the evolution of nail changes is a critical part of clinical decision-making on the need for a biopsy or referral.

Health disparity highlight

Despite the disproportionately high mortality rates from subungual melanoma in Black and Hispanic populations,^3,9 studies often do not adequately represent these populations. Although subungual melanoma is rare, a delay in the diagnosis contributes to high morbidity and mortality rates.

Photographs courtesy of Richard P. Usatine, MD.

THE COMPARISON

A Melanoma in situ manifesting as longitudinal melanonychia (LM) in a single digit in a Black man. Dermoscopy showed irregular dark bands of brown pigmentation and micro-Hutchinson sign on the cuticle (inset).

B Melanoma manifesting as LM with a prominent Hutchinson sign in a Hispanic man, with variable shades of brown covering more than 50% of the nail width.

C Longitudinal melanonychia of at least 2 nails with a pseudo-Hutchinson sign (pigment on the nail folds in a benign case of LM) in a young Black man demonstrating ethnic/racial melanosis. The longitudinal bands, which were caused by benign melanocytic activation, are more gray than brown and are less than 3 mm wide.

Longitudinal melanonychia (LM) is a pigmented linear band—brown, black, or gray—spanning the length of the nail plate due to the presence of excess melanin, which may be attributed to a benign or malignant process and may warrant further investigation.^1,2 The majority of patients who present with LM are diagnosed with melanocytic activation of the nail matrix due to their inherent darker skin tone or various triggers including trauma, infection, and medications. Longitudinal melanonychia secondary to melanocytic activation often occurs spontaneously in patients with skin of color.³ Less commonly, LM is caused by a nail matrix nevus or lentigo; however, LM may arise secondary to subungual melanoma, a more dangerous cause.

A thorough clinical history including duration, recent changes in LM manifestation, nail trauma, or infection is helpful in evaluating patients with LM; however, a history of nail trauma can be misleading, as nail changes attributed to the trauma may in fact be melanoma. Irregularly spaced vertical lines of pigmentation ranging from brown to black with variations in spacing and width are characteristic of subungual melanoma.⁴ Nail dystrophy, granular hyperpigmentation, and Hutchinson sign (extension of pigmentation to the nail folds) also are worrisome features.⁵ In recent years, dermoscopy has become an important tool in the clinical examination of LM, with the development of criteria based on color and pattern recognition.^5,6 Dermoscopy can be useful in screening potential candidates for biopsy. Although clinical examination and dermoscopy are essential to evaluating LM, the gold-standard diagnostic test when malignancy is suspected is a nail matrix biopsy.^1,2,6,7

Epidemiology

It is not unusual for patients with darker skin tones to develop LM due to melanocytic activation of multiple nails with age. This finding can be seen in approximately 80% of African American individuals, 30% of Japanese individuals, and 50% of Hispanic individuals.² It has even been reported that approximately 100% of Black patients older than 50 years will have evidence of LM.³

In a retrospective analysis, children presenting with LM tend to have a higher prevalence of nail matrix nevi compared to adults (56.1% [60/106] vs 34.3% [23/66]; P=.005).⁸ Involvement of a single digit in children is most likely indicative of a nevus; however, when an adult presents with LM in a single digit, suspicion for subungual melanoma should be raised.^2,3,9

Two separate single-center retrospective studies showed the prevalence of subungual melanoma in patients presenting with melanonychia in Asia. Jin et al10 reported subungual melanoma in 6.2% (17/275) of Korean patients presenting with melanonychia at a general dermatology clinic from 2002 to 2014. Lyu et al⁸ studied LM in 172 Chinese patients in a dermatology clinic from 2018 to 2021 and reported 9% (6/66) of adults (aged ≥18 years) with subungual melanoma, with no reported cases in childhood (aged <18 years).

Although the prevalence of subungual melanoma in patients with LM is low, it is an important diagnosis that should not be missed. In confirmed cases of subungual melanoma, two-thirds of lesions manifested as LM.^3,10,11 Thus, LM arising in an adult in a single digit is more concerning for malignancy.^2,3,7,9

Individuals of African and Asian descent as well as American Indian individuals are at highest risk for subungual melanoma with a poor prognosis compared to other types of melanoma, largely due to diagnosis at an advanced stage of disease.^3,9 In a retrospective study of 25 patients with surgically treated subungual melanoma, the mean recurrence-free survival was 33.6 months. The recurrence-free survival was 66% at 1 year and 40% at 3 years, and the overall survival rate was 37% at 3 years.¹²

Key clinical features in individuals with darker skin tones

• In patients with darker skin tones, LM tends to occur on multiple nails as a result of melanocytic activation.^2,13
• Several longitudinal bands may be noted on the same nail and the pigmentation of the bands may vary. With age, these longitudinal bands typically increase in number and width.¹³
• Pseudo-Hutchinson sign may be present due to ethnic melanosis of the proximal nail fold.^13,14
• Dermoscopic findings of LM in patients with skin of color include wider bands (P=.0125), lower band brightness (P<.032), and higher frequency of changing appearance of bands (P=.0071).¹⁵

Worth noting

When patients present with LM, thorough examination of the nail plate, periungual skin, and distal pulp of all digits on all extremities with adequate lighting is important.² Dermoscopy is useful, and a gel interface helps for examining the nail plates.⁷

Clinicians should be encouraged to biopsy or immediately refer patients with concerning nail unit lesions. Cases of LM most likely are benign, but if some doubt exists, the lesions should be biopsied or tracked closely with clinical and dermoscopic images, with a biopsy if changes occur.¹⁶ In conjunction with evaluation by a qualified clinician, patients also should be encouraged to take photographs, as the evolution of nail changes is a critical part of clinical decision-making on the need for a biopsy or referral.

Health disparity highlight

Despite the disproportionately high mortality rates from subungual melanoma in Black and Hispanic populations,^3,9 studies often do not adequately represent these populations. Although subungual melanoma is rare, a delay in the diagnosis contributes to high morbidity and mortality rates.

Frontal fibrosing alopecia (FFA) is an increasingly common diagnosis, especially in middle-aged women, and was first described by Kossard¹ in 1994. It is a variant of lichen planopilaris (LPP), a progressive scarring cicatricial alopecia that affects the frontotemporal area of the scalp, eyebrows, and sometimes even body hair.¹ Although its etiology remains unclear, genetic causes, drugs, hormones, and environmental exposures—including certain chemicals found in sunscreens—have been implicated in its pathogenesis.^2,3 An association between contact allergy to ingredients in personal care products and FFA diagnosis has been suggested; however, there is no evidence of causality to date. In this article, we highlight the potential relationship between contact allergy and FFA as well as clinical considerations for management.

Clinical Features and Diagnosis

Frontal fibrosing alopecia typically manifests with gradual symmetric recession of the frontal hairline leading to bandlike hair loss along the forehead, sometimes extending to the temporal region.⁴ Some patients may experience symptoms of scalp itching, burning, or tenderness that may precede or accompany the hair loss. Perifollicular erythema may be visible during the early stages and can be visualized on trichoscopy. The affected skin may appear pale and shiny and may have a smooth texture with a distinct lack of follicular openings. Aside from scalp involvement, other manifestations may include lichen planus pigmentosus, facial papules, body hair involvement, hypochromic lesions, diffuse redness on the face and neck, and prominent frontal veins.⁵ Although most FFA cases have characteristic clinical features and trichoscopic findings, biopsy for histopathologic examination is still recommended to confirm the diagnosis and ensure appropriate treatment.⁴ Classic histopathologic features include perifollicular lymphocytic inflammation, follicular destruction, and scarring.

Pathophysiology of FFA

The pathogenesis of FFA is thought to involve a variety of triggers, including immune-mediated inflammation, stress, genetics, hormones, and possibly environmental factors.⁶ Frontal fibrosing alopecia demonstrates considerable upregulation in cytotoxic helper T cells (T_H1) and IFN-γ activity resulting in epithelial hair follicle stem cell apoptosis and replacement of normal epithelial tissue with fibrous tissue.⁷ There is some suspicion of genetic susceptibility in the onset of FFA as suggested by familial reports and genome-wide association studies.^8-10 Hormonal and autoimmune factors also have been linked to FFA, including an increased risk for thyroid disease and the postmenopausal rise of androgen levels.⁶

Allergic Contact Dermatitis and FFA

Although they are 2 distinct conditions with differing etiologies, allergic contact dermatitis (ACD) and FFA may share environmental triggers, especially in susceptible individuals. This may support the coexistence and potential association between ACD and FFA.

In one case report, a woman who developed facial eczema followed by FFA showed positive patch tests to the UV filters drometrizole trisiloxane and ethylhexyl salicylate, which were listed as ingredients in her sunscreens. Avoidance of these allergens reportedly led to notable improvement of the symptoms.¹¹ Case-control studies have found an association between the use of facial sunscreen and risk for FFA.¹² A 2016 questionnaire that assessed a wide range of lifestyle, social, and medical factors related to FFA found that the use of sunscreens was significantly higher in patients with FFA than controls (P<.001), pointing to sunscreens as a potential contributing factor, but further research has been inconclusive. A higher frequency of positive patch tests to hydroperoxides of linalool and balsam of Peru (BoP) in patients with FFA have been documented; however, a direct cause cannot be established.²

In a 2020 prospective study conducted at multiple international centers, 65% (13/20) of FFA patients and 37.5% (9/24) of the control group had a positive patch test reaction to one or more allergens (P=.003). The most common allergens that were identified included cobalt chloride (positive in 35% [7/20] of patients with FFA), nickel sulfate (25% [5/20]), and potassium dichromate (15% [3/20]).¹³ In a recent 2-year cohort study of 42 patients with FFA who were referred for patch testing, the most common allergens included gallates, hydroperoxides of linalool, and other fragrances.¹⁴ After a 3-month period of allergen avoidance, 70% (29/42) of patients had decreased scalp erythema on examination, indicating that avoiding relevant allergens may reduce local inflammation. Furthermore, 76.2% (32/42) of patients with FFA showed delayed-type hypersensitivity to allergens found in daily personal care products such as shampoos, sunscreens, and moisturizers, among others.¹⁴ Notably, the study lacked a control group. A case-control study of 36 Hispanic women conducted in Mexico also resulted in 83.3% (15/18) of patients with FFA and 55.5% (10/18) of controls having at least 1 positive patch test; in the FFA group, these included iodopropynyl butylcarbamate (16.7% [3/18]) and propolis (16.7% [3/18]).¹⁵

Most recently, a retrospective study conducted by Shtaynberger et al¹⁶ included 12 patients with LPP or FFA diagnosed via clinical findings or biopsy. It also included an age- and temporally matched control group tested with identical allergens. Among the 12 patients who had FFA/LPP, all had at least 1 allergen identified on patch testing. The most common allergens identified were propolis (positive in 50% [6/12] of patients with FFA/LPP), fragrance mix I (16%), and methylisothiazolinone (16% [2/12]). Follow-up data were available for 9 of these patients, of whom 6 (66.7%) experienced symptom improvement after 6 months of allergen avoidance. Four (44.4%) patients experienced decreased follicular redness or scaling, 2 (22.2%) patients experienced improved scalp pain/itch, 2 (22.2%) patients had stable/improved hair density, and 1 (1.1%) patient had decreased hair shedding. Although this suggests an environmental trigger for FFA/LPP, the authors stated that changes in patient treatment plans could have contributed to their improvement. The study also was limited by its small size and its overall generalizability.¹⁶

These studies have underscored the significance of patch testing in individuals diagnosed with FFA and have identified common allergens prevalent in this patient population. They have suggested that patients with FFA are more likely to have positive patch tests, and in some cases patients could experience improvements in scalp pruritus and erythema with allergen avoidance; however, we emphasize that a causal association between contact allergy and FFA remains unproven to date.

Most Common Allergens Pertinent to FFA

Preservatives—In some studies, patients with FFA have had positive patch tests to preservatives such as gallates and methylchloroisothiazolinone/methylisothiazolinone (MCI/MI).¹⁴ Gallates are antioxidants that are used in food preservation, pharmaceuticals, and cosmetics due to their ability to inhibit oxidation and rancidity of fats and oils.¹⁷ The most common gallates include propyl gallate, octyl gallate, and dodecyl gallate. Propyl gallate is utilized in some waxy or oily cosmetics and personal care items including sunscreens, shampoos, conditioners, bar soaps, facial cleansers, and moisturizers.¹⁸ Typically, if patients have a positive patch test to one gallate, they should be advised to avoid all gallate compounds, as they can cross-react.

Similarly, MCI/MI can prevent product degradation through their antibacterial and antifungal properties. This combination of MCI and MI is used as an effective method of prolonging the shelf life of cosmetic products and commonly is found in sunscreens, facial moisturizing creams, shampoos, and conditioners¹⁹; it is banned from use in leave-on products in the European Union and Canada due to increased rates of contact allergy.²⁰ In patients with FFA who commonly use facial sunscreen, preservatives can be a potential allergen exposure to consider.

Iodopropynyl butylcarbamate also is a preservative used in cosmetic formulations. Similar to MCI/MI, it is a potent fungicide and bactericide. This allergen can be found in hair care products, bodywashes, and other personal products.²¹

UV Light–Absorbing Agents—A systematic review and meta-analysis conducted in 2022 showed a significant (P<.001) association between sunscreen use and FFA.²² A majority of allergens identified on patch testing included UVA- and UVB-absorbing agents found in sunscreens and other products including cosmetics,^11,12 such as drometrizole trisiloxane, ethylhexyl salicylate, avobenzone, and benzophenone-4. Drometrizole trisiloxane is a photostabilizer and a broad-spectrum UV filter that is not approved for use in sunscreens in the United States.²³ It also is effective in stabilizing and preventing the degradation of avobenzone, a commonly used UVA filter.²⁴

Fragrances—Fragrances are present in nearly every personal and cosmetic product, sometimes even in those advertised as being “fragrance free.” Hydroperoxides of linalool, BoP, and fragrance mix are common allergens that are found in a variety of personal care products including perfumes, cosmetics, and even household cleaning supplies.²⁵ Simultaneous positive patch tests to BoP and fragrance mix are common due to shared components. Linalool can be found in various plants such as lavender, rose, bergamot, and jasmine.²⁶ Upon air exposure, linalool auto-oxidizes to form allergenic hydroperoxides of linalool. Among patients with FFA, positive patch test reactions to fragrance chemicals are common and could be attributed to the use of fragranced hair products and facial cosmetics.

Hair Dyes and Bleaches—Allergic reactions to hair dyes and bleaches can result in severe ACD of the head/neck and, in rare cases, scarring alopecia.²⁷ Chemicals found in these products include paraphenylenediamine (PPD) and ammonium persulfate. The most common hair dye allergen, PPD also is used in some rubbers and plastics. Ammonium persulfate is a chemical used in hair bleaches and to deodorize oils. One case study reported a patient with FFA who developed chemically induced vitiligo immediately after the use of a hair color product that contained PPD.²⁸ However, without patch testing to confirm the presence of contact allergy, other patient-specific and environmental risk factors could have contributed to FFA in this case.

In this endeavor to untangle the truth, it should be remembered that at the time of writing, the purported association between FFA and ACD remains debatable. Contact dermatitis specialists have voiced that the association between FFA and ACD, especially with regard to sunscreen, cannot be supported due to the lack of sufficient evidence.²⁹ A large majority of the research conducted on FFA and ACD is based on case reports and studies limited to a small sample size, and most of these patch test studies lack a control group. Felmingham et al³⁰ noted that the recent epidemiology of FFA aligns with increased sunscreen use. They also highlighted the limitations of the aforementioned studies, which include misclassification of exposures in the control group² and recall bias in questionnaire participants.^2,12 The most pressing limitation that permeates through most of these studies is the temporal ambiguity associated with sunscreen use. A study by Dhana et al³¹ failed to specify whether increased sunscreen use preceded the diagnosis of FFA or if it stems from the need to protect more exposed skin as a consequence of disease. Broad sunscreen avoidance due to concern for a possible association with hair loss could have detrimental health implications by increasing the risk for photodamage and skin cancer.

FFA Patch Testing

The avoidance of pertinent allergens could be effective in reducing local inflammation, pruritus, and erythema in FFA.^9,14,32 At our institution, we selectively patch test patients with FFA when there is a suspected contact allergy. Clinical features that may allude to a potential contact allergy include an erythematous or eczematous dermatitis or symptoms of pruritus along the scalp or eyebrows. If patients recall hair loss or symptoms after using a hair or facial product, then a potential contact allergy to these products could be considered. Patch testing in patients with FFA includes the North American 80 Comprehensive Series and the cosmetic and hairdresser supplemental series, as well as an additional customized panel of 8 allergens as determined by patch testing experts at the University of Massachusetts, Brigham and Women’s Hospital, and Massachusetts General Hospital (private email communication, November 2017). Patch test readings are performed at 48 and 96 or 120 hours. Using the American Contact Dermatitis Society’s Contact Allergen Management Program, patients are provided personalized safe product lists and avoidance strategies are discussed.

Final Interpretation

In a world where cosmetic products are ubiquitous, it is hard to define the potential role of contact allergens in the entangled pathogenesis of FFA and ACD. As evidenced by emerging literature that correlates the 2 conditions and their exacerbating factors, it is important for physicians to have a comprehensive diagnostic approach and heightened awareness for potential allergens at play in FFA (Table). The identification of certain chemicals and preservatives as potential triggers for FFA should emphasize the importance of patch testing in these patients; however, whether the positive reactions are relevant to the pathogenesis or disease course of FFA still is unknown. While these findings begin to unravel the intertwined causes of FFA and ACD, further research encompassing larger cohorts and prospective studies is imperative to solidify these associations, define concrete guidelines, and improve patient outcomes.

Frontal fibrosing alopecia (FFA) is an increasingly common diagnosis, especially in middle-aged women, and was first described by Kossard¹ in 1994. It is a variant of lichen planopilaris (LPP), a progressive scarring cicatricial alopecia that affects the frontotemporal area of the scalp, eyebrows, and sometimes even body hair.¹ Although its etiology remains unclear, genetic causes, drugs, hormones, and environmental exposures—including certain chemicals found in sunscreens—have been implicated in its pathogenesis.^2,3 An association between contact allergy to ingredients in personal care products and FFA diagnosis has been suggested; however, there is no evidence of causality to date. In this article, we highlight the potential relationship between contact allergy and FFA as well as clinical considerations for management.

Clinical Features and Diagnosis

Frontal fibrosing alopecia typically manifests with gradual symmetric recession of the frontal hairline leading to bandlike hair loss along the forehead, sometimes extending to the temporal region.⁴ Some patients may experience symptoms of scalp itching, burning, or tenderness that may precede or accompany the hair loss. Perifollicular erythema may be visible during the early stages and can be visualized on trichoscopy. The affected skin may appear pale and shiny and may have a smooth texture with a distinct lack of follicular openings. Aside from scalp involvement, other manifestations may include lichen planus pigmentosus, facial papules, body hair involvement, hypochromic lesions, diffuse redness on the face and neck, and prominent frontal veins.⁵ Although most FFA cases have characteristic clinical features and trichoscopic findings, biopsy for histopathologic examination is still recommended to confirm the diagnosis and ensure appropriate treatment.⁴ Classic histopathologic features include perifollicular lymphocytic inflammation, follicular destruction, and scarring.

Pathophysiology of FFA

The pathogenesis of FFA is thought to involve a variety of triggers, including immune-mediated inflammation, stress, genetics, hormones, and possibly environmental factors.⁶ Frontal fibrosing alopecia demonstrates considerable upregulation in cytotoxic helper T cells (T_H1) and IFN-γ activity resulting in epithelial hair follicle stem cell apoptosis and replacement of normal epithelial tissue with fibrous tissue.⁷ There is some suspicion of genetic susceptibility in the onset of FFA as suggested by familial reports and genome-wide association studies.^8-10 Hormonal and autoimmune factors also have been linked to FFA, including an increased risk for thyroid disease and the postmenopausal rise of androgen levels.⁶

Allergic Contact Dermatitis and FFA

Although they are 2 distinct conditions with differing etiologies, allergic contact dermatitis (ACD) and FFA may share environmental triggers, especially in susceptible individuals. This may support the coexistence and potential association between ACD and FFA.

In one case report, a woman who developed facial eczema followed by FFA showed positive patch tests to the UV filters drometrizole trisiloxane and ethylhexyl salicylate, which were listed as ingredients in her sunscreens. Avoidance of these allergens reportedly led to notable improvement of the symptoms.¹¹ Case-control studies have found an association between the use of facial sunscreen and risk for FFA.¹² A 2016 questionnaire that assessed a wide range of lifestyle, social, and medical factors related to FFA found that the use of sunscreens was significantly higher in patients with FFA than controls (P<.001), pointing to sunscreens as a potential contributing factor, but further research has been inconclusive. A higher frequency of positive patch tests to hydroperoxides of linalool and balsam of Peru (BoP) in patients with FFA have been documented; however, a direct cause cannot be established.²

In a 2020 prospective study conducted at multiple international centers, 65% (13/20) of FFA patients and 37.5% (9/24) of the control group had a positive patch test reaction to one or more allergens (P=.003). The most common allergens that were identified included cobalt chloride (positive in 35% [7/20] of patients with FFA), nickel sulfate (25% [5/20]), and potassium dichromate (15% [3/20]).¹³ In a recent 2-year cohort study of 42 patients with FFA who were referred for patch testing, the most common allergens included gallates, hydroperoxides of linalool, and other fragrances.¹⁴ After a 3-month period of allergen avoidance, 70% (29/42) of patients had decreased scalp erythema on examination, indicating that avoiding relevant allergens may reduce local inflammation. Furthermore, 76.2% (32/42) of patients with FFA showed delayed-type hypersensitivity to allergens found in daily personal care products such as shampoos, sunscreens, and moisturizers, among others.¹⁴ Notably, the study lacked a control group. A case-control study of 36 Hispanic women conducted in Mexico also resulted in 83.3% (15/18) of patients with FFA and 55.5% (10/18) of controls having at least 1 positive patch test; in the FFA group, these included iodopropynyl butylcarbamate (16.7% [3/18]) and propolis (16.7% [3/18]).¹⁵

Most recently, a retrospective study conducted by Shtaynberger et al¹⁶ included 12 patients with LPP or FFA diagnosed via clinical findings or biopsy. It also included an age- and temporally matched control group tested with identical allergens. Among the 12 patients who had FFA/LPP, all had at least 1 allergen identified on patch testing. The most common allergens identified were propolis (positive in 50% [6/12] of patients with FFA/LPP), fragrance mix I (16%), and methylisothiazolinone (16% [2/12]). Follow-up data were available for 9 of these patients, of whom 6 (66.7%) experienced symptom improvement after 6 months of allergen avoidance. Four (44.4%) patients experienced decreased follicular redness or scaling, 2 (22.2%) patients experienced improved scalp pain/itch, 2 (22.2%) patients had stable/improved hair density, and 1 (1.1%) patient had decreased hair shedding. Although this suggests an environmental trigger for FFA/LPP, the authors stated that changes in patient treatment plans could have contributed to their improvement. The study also was limited by its small size and its overall generalizability.¹⁶

These studies have underscored the significance of patch testing in individuals diagnosed with FFA and have identified common allergens prevalent in this patient population. They have suggested that patients with FFA are more likely to have positive patch tests, and in some cases patients could experience improvements in scalp pruritus and erythema with allergen avoidance; however, we emphasize that a causal association between contact allergy and FFA remains unproven to date.

Most Common Allergens Pertinent to FFA

Preservatives—In some studies, patients with FFA have had positive patch tests to preservatives such as gallates and methylchloroisothiazolinone/methylisothiazolinone (MCI/MI).¹⁴ Gallates are antioxidants that are used in food preservation, pharmaceuticals, and cosmetics due to their ability to inhibit oxidation and rancidity of fats and oils.¹⁷ The most common gallates include propyl gallate, octyl gallate, and dodecyl gallate. Propyl gallate is utilized in some waxy or oily cosmetics and personal care items including sunscreens, shampoos, conditioners, bar soaps, facial cleansers, and moisturizers.¹⁸ Typically, if patients have a positive patch test to one gallate, they should be advised to avoid all gallate compounds, as they can cross-react.

Similarly, MCI/MI can prevent product degradation through their antibacterial and antifungal properties. This combination of MCI and MI is used as an effective method of prolonging the shelf life of cosmetic products and commonly is found in sunscreens, facial moisturizing creams, shampoos, and conditioners¹⁹; it is banned from use in leave-on products in the European Union and Canada due to increased rates of contact allergy.²⁰ In patients with FFA who commonly use facial sunscreen, preservatives can be a potential allergen exposure to consider.

Iodopropynyl butylcarbamate also is a preservative used in cosmetic formulations. Similar to MCI/MI, it is a potent fungicide and bactericide. This allergen can be found in hair care products, bodywashes, and other personal products.²¹

UV Light–Absorbing Agents—A systematic review and meta-analysis conducted in 2022 showed a significant (P<.001) association between sunscreen use and FFA.²² A majority of allergens identified on patch testing included UVA- and UVB-absorbing agents found in sunscreens and other products including cosmetics,^11,12 such as drometrizole trisiloxane, ethylhexyl salicylate, avobenzone, and benzophenone-4. Drometrizole trisiloxane is a photostabilizer and a broad-spectrum UV filter that is not approved for use in sunscreens in the United States.²³ It also is effective in stabilizing and preventing the degradation of avobenzone, a commonly used UVA filter.²⁴

Fragrances—Fragrances are present in nearly every personal and cosmetic product, sometimes even in those advertised as being “fragrance free.” Hydroperoxides of linalool, BoP, and fragrance mix are common allergens that are found in a variety of personal care products including perfumes, cosmetics, and even household cleaning supplies.²⁵ Simultaneous positive patch tests to BoP and fragrance mix are common due to shared components. Linalool can be found in various plants such as lavender, rose, bergamot, and jasmine.²⁶ Upon air exposure, linalool auto-oxidizes to form allergenic hydroperoxides of linalool. Among patients with FFA, positive patch test reactions to fragrance chemicals are common and could be attributed to the use of fragranced hair products and facial cosmetics.

Hair Dyes and Bleaches—Allergic reactions to hair dyes and bleaches can result in severe ACD of the head/neck and, in rare cases, scarring alopecia.²⁷ Chemicals found in these products include paraphenylenediamine (PPD) and ammonium persulfate. The most common hair dye allergen, PPD also is used in some rubbers and plastics. Ammonium persulfate is a chemical used in hair bleaches and to deodorize oils. One case study reported a patient with FFA who developed chemically induced vitiligo immediately after the use of a hair color product that contained PPD.²⁸ However, without patch testing to confirm the presence of contact allergy, other patient-specific and environmental risk factors could have contributed to FFA in this case.

In this endeavor to untangle the truth, it should be remembered that at the time of writing, the purported association between FFA and ACD remains debatable. Contact dermatitis specialists have voiced that the association between FFA and ACD, especially with regard to sunscreen, cannot be supported due to the lack of sufficient evidence.²⁹ A large majority of the research conducted on FFA and ACD is based on case reports and studies limited to a small sample size, and most of these patch test studies lack a control group. Felmingham et al³⁰ noted that the recent epidemiology of FFA aligns with increased sunscreen use. They also highlighted the limitations of the aforementioned studies, which include misclassification of exposures in the control group² and recall bias in questionnaire participants.^2,12 The most pressing limitation that permeates through most of these studies is the temporal ambiguity associated with sunscreen use. A study by Dhana et al³¹ failed to specify whether increased sunscreen use preceded the diagnosis of FFA or if it stems from the need to protect more exposed skin as a consequence of disease. Broad sunscreen avoidance due to concern for a possible association with hair loss could have detrimental health implications by increasing the risk for photodamage and skin cancer.

FFA Patch Testing

The avoidance of pertinent allergens could be effective in reducing local inflammation, pruritus, and erythema in FFA.^9,14,32 At our institution, we selectively patch test patients with FFA when there is a suspected contact allergy. Clinical features that may allude to a potential contact allergy include an erythematous or eczematous dermatitis or symptoms of pruritus along the scalp or eyebrows. If patients recall hair loss or symptoms after using a hair or facial product, then a potential contact allergy to these products could be considered. Patch testing in patients with FFA includes the North American 80 Comprehensive Series and the cosmetic and hairdresser supplemental series, as well as an additional customized panel of 8 allergens as determined by patch testing experts at the University of Massachusetts, Brigham and Women’s Hospital, and Massachusetts General Hospital (private email communication, November 2017). Patch test readings are performed at 48 and 96 or 120 hours. Using the American Contact Dermatitis Society’s Contact Allergen Management Program, patients are provided personalized safe product lists and avoidance strategies are discussed.

Final Interpretation

In a world where cosmetic products are ubiquitous, it is hard to define the potential role of contact allergens in the entangled pathogenesis of FFA and ACD. As evidenced by emerging literature that correlates the 2 conditions and their exacerbating factors, it is important for physicians to have a comprehensive diagnostic approach and heightened awareness for potential allergens at play in FFA (Table). The identification of certain chemicals and preservatives as potential triggers for FFA should emphasize the importance of patch testing in these patients; however, whether the positive reactions are relevant to the pathogenesis or disease course of FFA still is unknown. While these findings begin to unravel the intertwined causes of FFA and ACD, further research encompassing larger cohorts and prospective studies is imperative to solidify these associations, define concrete guidelines, and improve patient outcomes.

Frontal fibrosing alopecia (FFA) is an increasingly common diagnosis, especially in middle-aged women, and was first described by Kossard¹ in 1994. It is a variant of lichen planopilaris (LPP), a progressive scarring cicatricial alopecia that affects the frontotemporal area of the scalp, eyebrows, and sometimes even body hair.¹ Although its etiology remains unclear, genetic causes, drugs, hormones, and environmental exposures—including certain chemicals found in sunscreens—have been implicated in its pathogenesis.^2,3 An association between contact allergy to ingredients in personal care products and FFA diagnosis has been suggested; however, there is no evidence of causality to date. In this article, we highlight the potential relationship between contact allergy and FFA as well as clinical considerations for management.

Clinical Features and Diagnosis

Frontal fibrosing alopecia typically manifests with gradual symmetric recession of the frontal hairline leading to bandlike hair loss along the forehead, sometimes extending to the temporal region.⁴ Some patients may experience symptoms of scalp itching, burning, or tenderness that may precede or accompany the hair loss. Perifollicular erythema may be visible during the early stages and can be visualized on trichoscopy. The affected skin may appear pale and shiny and may have a smooth texture with a distinct lack of follicular openings. Aside from scalp involvement, other manifestations may include lichen planus pigmentosus, facial papules, body hair involvement, hypochromic lesions, diffuse redness on the face and neck, and prominent frontal veins.⁵ Although most FFA cases have characteristic clinical features and trichoscopic findings, biopsy for histopathologic examination is still recommended to confirm the diagnosis and ensure appropriate treatment.⁴ Classic histopathologic features include perifollicular lymphocytic inflammation, follicular destruction, and scarring.

Pathophysiology of FFA

The pathogenesis of FFA is thought to involve a variety of triggers, including immune-mediated inflammation, stress, genetics, hormones, and possibly environmental factors.⁶ Frontal fibrosing alopecia demonstrates considerable upregulation in cytotoxic helper T cells (T_H1) and IFN-γ activity resulting in epithelial hair follicle stem cell apoptosis and replacement of normal epithelial tissue with fibrous tissue.⁷ There is some suspicion of genetic susceptibility in the onset of FFA as suggested by familial reports and genome-wide association studies.^8-10 Hormonal and autoimmune factors also have been linked to FFA, including an increased risk for thyroid disease and the postmenopausal rise of androgen levels.⁶

Allergic Contact Dermatitis and FFA

Although they are 2 distinct conditions with differing etiologies, allergic contact dermatitis (ACD) and FFA may share environmental triggers, especially in susceptible individuals. This may support the coexistence and potential association between ACD and FFA.

In one case report, a woman who developed facial eczema followed by FFA showed positive patch tests to the UV filters drometrizole trisiloxane and ethylhexyl salicylate, which were listed as ingredients in her sunscreens. Avoidance of these allergens reportedly led to notable improvement of the symptoms.¹¹ Case-control studies have found an association between the use of facial sunscreen and risk for FFA.¹² A 2016 questionnaire that assessed a wide range of lifestyle, social, and medical factors related to FFA found that the use of sunscreens was significantly higher in patients with FFA than controls (P<.001), pointing to sunscreens as a potential contributing factor, but further research has been inconclusive. A higher frequency of positive patch tests to hydroperoxides of linalool and balsam of Peru (BoP) in patients with FFA have been documented; however, a direct cause cannot be established.²

In a 2020 prospective study conducted at multiple international centers, 65% (13/20) of FFA patients and 37.5% (9/24) of the control group had a positive patch test reaction to one or more allergens (P=.003). The most common allergens that were identified included cobalt chloride (positive in 35% [7/20] of patients with FFA), nickel sulfate (25% [5/20]), and potassium dichromate (15% [3/20]).¹³ In a recent 2-year cohort study of 42 patients with FFA who were referred for patch testing, the most common allergens included gallates, hydroperoxides of linalool, and other fragrances.¹⁴ After a 3-month period of allergen avoidance, 70% (29/42) of patients had decreased scalp erythema on examination, indicating that avoiding relevant allergens may reduce local inflammation. Furthermore, 76.2% (32/42) of patients with FFA showed delayed-type hypersensitivity to allergens found in daily personal care products such as shampoos, sunscreens, and moisturizers, among others.¹⁴ Notably, the study lacked a control group. A case-control study of 36 Hispanic women conducted in Mexico also resulted in 83.3% (15/18) of patients with FFA and 55.5% (10/18) of controls having at least 1 positive patch test; in the FFA group, these included iodopropynyl butylcarbamate (16.7% [3/18]) and propolis (16.7% [3/18]).¹⁵

Most recently, a retrospective study conducted by Shtaynberger et al¹⁶ included 12 patients with LPP or FFA diagnosed via clinical findings or biopsy. It also included an age- and temporally matched control group tested with identical allergens. Among the 12 patients who had FFA/LPP, all had at least 1 allergen identified on patch testing. The most common allergens identified were propolis (positive in 50% [6/12] of patients with FFA/LPP), fragrance mix I (16%), and methylisothiazolinone (16% [2/12]). Follow-up data were available for 9 of these patients, of whom 6 (66.7%) experienced symptom improvement after 6 months of allergen avoidance. Four (44.4%) patients experienced decreased follicular redness or scaling, 2 (22.2%) patients experienced improved scalp pain/itch, 2 (22.2%) patients had stable/improved hair density, and 1 (1.1%) patient had decreased hair shedding. Although this suggests an environmental trigger for FFA/LPP, the authors stated that changes in patient treatment plans could have contributed to their improvement. The study also was limited by its small size and its overall generalizability.¹⁶

These studies have underscored the significance of patch testing in individuals diagnosed with FFA and have identified common allergens prevalent in this patient population. They have suggested that patients with FFA are more likely to have positive patch tests, and in some cases patients could experience improvements in scalp pruritus and erythema with allergen avoidance; however, we emphasize that a causal association between contact allergy and FFA remains unproven to date.

Most Common Allergens Pertinent to FFA

Preservatives—In some studies, patients with FFA have had positive patch tests to preservatives such as gallates and methylchloroisothiazolinone/methylisothiazolinone (MCI/MI).¹⁴ Gallates are antioxidants that are used in food preservation, pharmaceuticals, and cosmetics due to their ability to inhibit oxidation and rancidity of fats and oils.¹⁷ The most common gallates include propyl gallate, octyl gallate, and dodecyl gallate. Propyl gallate is utilized in some waxy or oily cosmetics and personal care items including sunscreens, shampoos, conditioners, bar soaps, facial cleansers, and moisturizers.¹⁸ Typically, if patients have a positive patch test to one gallate, they should be advised to avoid all gallate compounds, as they can cross-react.

Similarly, MCI/MI can prevent product degradation through their antibacterial and antifungal properties. This combination of MCI and MI is used as an effective method of prolonging the shelf life of cosmetic products and commonly is found in sunscreens, facial moisturizing creams, shampoos, and conditioners¹⁹; it is banned from use in leave-on products in the European Union and Canada due to increased rates of contact allergy.²⁰ In patients with FFA who commonly use facial sunscreen, preservatives can be a potential allergen exposure to consider.

Iodopropynyl butylcarbamate also is a preservative used in cosmetic formulations. Similar to MCI/MI, it is a potent fungicide and bactericide. This allergen can be found in hair care products, bodywashes, and other personal products.²¹

UV Light–Absorbing Agents—A systematic review and meta-analysis conducted in 2022 showed a significant (P<.001) association between sunscreen use and FFA.²² A majority of allergens identified on patch testing included UVA- and UVB-absorbing agents found in sunscreens and other products including cosmetics,^11,12 such as drometrizole trisiloxane, ethylhexyl salicylate, avobenzone, and benzophenone-4. Drometrizole trisiloxane is a photostabilizer and a broad-spectrum UV filter that is not approved for use in sunscreens in the United States.²³ It also is effective in stabilizing and preventing the degradation of avobenzone, a commonly used UVA filter.²⁴

Fragrances—Fragrances are present in nearly every personal and cosmetic product, sometimes even in those advertised as being “fragrance free.” Hydroperoxides of linalool, BoP, and fragrance mix are common allergens that are found in a variety of personal care products including perfumes, cosmetics, and even household cleaning supplies.²⁵ Simultaneous positive patch tests to BoP and fragrance mix are common due to shared components. Linalool can be found in various plants such as lavender, rose, bergamot, and jasmine.²⁶ Upon air exposure, linalool auto-oxidizes to form allergenic hydroperoxides of linalool. Among patients with FFA, positive patch test reactions to fragrance chemicals are common and could be attributed to the use of fragranced hair products and facial cosmetics.

Hair Dyes and Bleaches—Allergic reactions to hair dyes and bleaches can result in severe ACD of the head/neck and, in rare cases, scarring alopecia.²⁷ Chemicals found in these products include paraphenylenediamine (PPD) and ammonium persulfate. The most common hair dye allergen, PPD also is used in some rubbers and plastics. Ammonium persulfate is a chemical used in hair bleaches and to deodorize oils. One case study reported a patient with FFA who developed chemically induced vitiligo immediately after the use of a hair color product that contained PPD.²⁸ However, without patch testing to confirm the presence of contact allergy, other patient-specific and environmental risk factors could have contributed to FFA in this case.

In this endeavor to untangle the truth, it should be remembered that at the time of writing, the purported association between FFA and ACD remains debatable. Contact dermatitis specialists have voiced that the association between FFA and ACD, especially with regard to sunscreen, cannot be supported due to the lack of sufficient evidence.²⁹ A large majority of the research conducted on FFA and ACD is based on case reports and studies limited to a small sample size, and most of these patch test studies lack a control group. Felmingham et al³⁰ noted that the recent epidemiology of FFA aligns with increased sunscreen use. They also highlighted the limitations of the aforementioned studies, which include misclassification of exposures in the control group² and recall bias in questionnaire participants.^2,12 The most pressing limitation that permeates through most of these studies is the temporal ambiguity associated with sunscreen use. A study by Dhana et al³¹ failed to specify whether increased sunscreen use preceded the diagnosis of FFA or if it stems from the need to protect more exposed skin as a consequence of disease. Broad sunscreen avoidance due to concern for a possible association with hair loss could have detrimental health implications by increasing the risk for photodamage and skin cancer.

FFA Patch Testing

The avoidance of pertinent allergens could be effective in reducing local inflammation, pruritus, and erythema in FFA.^9,14,32 At our institution, we selectively patch test patients with FFA when there is a suspected contact allergy. Clinical features that may allude to a potential contact allergy include an erythematous or eczematous dermatitis or symptoms of pruritus along the scalp or eyebrows. If patients recall hair loss or symptoms after using a hair or facial product, then a potential contact allergy to these products could be considered. Patch testing in patients with FFA includes the North American 80 Comprehensive Series and the cosmetic and hairdresser supplemental series, as well as an additional customized panel of 8 allergens as determined by patch testing experts at the University of Massachusetts, Brigham and Women’s Hospital, and Massachusetts General Hospital (private email communication, November 2017). Patch test readings are performed at 48 and 96 or 120 hours. Using the American Contact Dermatitis Society’s Contact Allergen Management Program, patients are provided personalized safe product lists and avoidance strategies are discussed.

Final Interpretation

In a world where cosmetic products are ubiquitous, it is hard to define the potential role of contact allergens in the entangled pathogenesis of FFA and ACD. As evidenced by emerging literature that correlates the 2 conditions and their exacerbating factors, it is important for physicians to have a comprehensive diagnostic approach and heightened awareness for potential allergens at play in FFA (Table). The identification of certain chemicals and preservatives as potential triggers for FFA should emphasize the importance of patch testing in these patients; however, whether the positive reactions are relevant to the pathogenesis or disease course of FFA still is unknown. While these findings begin to unravel the intertwined causes of FFA and ACD, further research encompassing larger cohorts and prospective studies is imperative to solidify these associations, define concrete guidelines, and improve patient outcomes.

To the Editor:

Female pattern hair loss (FPHL), or androgenetic alopecia (AGA), is the most common form of alopecia worldwide and is characterized by a reduction of hair follicles spent in the anagen phase of growth as well as progressive terminal hair loss.¹ It is caused by an excessive response to androgens and leads to the characteristic distribution of hair loss in both sexes. Studies have shown a notable association between AGA and markers of metabolic syndrome such as dyslipidemia, insulin resistance, and obesity in age- and sex-matched controls.^2,3 However, research describing the relationship between AGA severity and these markers is scarce.

To understand the relationship between FPHL severity and abnormal cholesterol levels, we performed a retrospective chart review of patients diagnosed with FPHL at a specialty alopecia clinic from June 2022 to December 2022. Patient age and age at onset of FPHL were collected. The severity of FPHL was measured using the Sinclair scale (score range, 1–5) and unidentifiable patient photographs. Laboratory values were collected; abnormal cholesterol was defined by the American Heart Association as having a low-density lipoprotein cholesterol (LDL-C) level of 100 mg/dL or higher.⁴ Finally, data on medication use were noted to understand patient treatment status (Table).

We identified 54 female patients with FPHL with an average age of 59 years (range, 34–80 years). Thirty-three females (61.11%) had a normal LDL-C level and 21 (38.89%) had an abnormal level. The mean (SD) LDL-C level was 66.02 (15.20) mg/dL (range, 29–92 mg/dL) in the group with normal levels and 138.81 (29.90) mg/dL (range, 100–193 mg/dL) in the group with abnormal levels. Patients with abnormal LDL-C had significantly higher Sinclair scale scores compared to those with normal levels (2.43 vs 1.91; P=.01). There were no significant differences in patient age (58.71 vs 59.70 years; P=.39), age at onset of AGA (47.75 vs 47.65 years; P=.49), history of polycystic ovary syndrome (9.52% vs 6.06%; P=.64), or statin use (38.09% vs 36.36%; P=.89) between patients with abnormal and normal LDL-C levels, respectively. There also were no significant differences in ferritin (96.42 vs 91.54 ng/mL; P=.40), vitamin D (42.35 vs 48.96 ng/mL; P=.09), or hemoglobin A_1c levels (5.60 ng/mL vs 5.38 ng/mL; P=.06)—variables that could have confounded this relationship. Triglycerides were within reference range in both groups (121.36 vs 116.16 mg/dL; P=.32), while total cholesterol was mildly elevated in both groups but not significantly different (213.19 vs 201.21 mg/dL; P=.13). Use of hair loss treatments such as topical minoxidil (14.29% vs 21.21%; P=.53), oral low-dose minoxidil (57.14% vs 66.67%; P=.48), oral spironolactone (47.62% vs 57.58%; P=.47), and platelet-rich plasma injections (47.62% vs 27.27%; P=.90) were not significantly different across both groups.

The data suggest a significant (P<.05) association between abnormal LDL-C and hair loss severity in FPHL patients. Our study was limited by its small sample size and lack of causality; however, it coincides with and reiterates the findings established in the literature. The mechanism of the association between hyperlipidemia and AGA is not well understood but is thought to stem from the homology between cholesterol and androgens. Increased cholesterol release from dermal adipocytes and subsequent absorption into hair follicle cell populations may increase hair follicle steroidogenesis, thereby accelerating the anagen-catagen transition and inducing AGA. Alternatively, impaired cholesterol homeostasis may disrupt normal hair follicle cycling by interrupting signaling pathways in follicle proliferation and differentiation.⁵ Adequate control and monitoring of LDL-C levels may be important, particularly in patients with more severe FPHL.

To the Editor:

Female pattern hair loss (FPHL), or androgenetic alopecia (AGA), is the most common form of alopecia worldwide and is characterized by a reduction of hair follicles spent in the anagen phase of growth as well as progressive terminal hair loss.¹ It is caused by an excessive response to androgens and leads to the characteristic distribution of hair loss in both sexes. Studies have shown a notable association between AGA and markers of metabolic syndrome such as dyslipidemia, insulin resistance, and obesity in age- and sex-matched controls.^2,3 However, research describing the relationship between AGA severity and these markers is scarce.

To understand the relationship between FPHL severity and abnormal cholesterol levels, we performed a retrospective chart review of patients diagnosed with FPHL at a specialty alopecia clinic from June 2022 to December 2022. Patient age and age at onset of FPHL were collected. The severity of FPHL was measured using the Sinclair scale (score range, 1–5) and unidentifiable patient photographs. Laboratory values were collected; abnormal cholesterol was defined by the American Heart Association as having a low-density lipoprotein cholesterol (LDL-C) level of 100 mg/dL or higher.⁴ Finally, data on medication use were noted to understand patient treatment status (Table).

We identified 54 female patients with FPHL with an average age of 59 years (range, 34–80 years). Thirty-three females (61.11%) had a normal LDL-C level and 21 (38.89%) had an abnormal level. The mean (SD) LDL-C level was 66.02 (15.20) mg/dL (range, 29–92 mg/dL) in the group with normal levels and 138.81 (29.90) mg/dL (range, 100–193 mg/dL) in the group with abnormal levels. Patients with abnormal LDL-C had significantly higher Sinclair scale scores compared to those with normal levels (2.43 vs 1.91; P=.01). There were no significant differences in patient age (58.71 vs 59.70 years; P=.39), age at onset of AGA (47.75 vs 47.65 years; P=.49), history of polycystic ovary syndrome (9.52% vs 6.06%; P=.64), or statin use (38.09% vs 36.36%; P=.89) between patients with abnormal and normal LDL-C levels, respectively. There also were no significant differences in ferritin (96.42 vs 91.54 ng/mL; P=.40), vitamin D (42.35 vs 48.96 ng/mL; P=.09), or hemoglobin A_1c levels (5.60 ng/mL vs 5.38 ng/mL; P=.06)—variables that could have confounded this relationship. Triglycerides were within reference range in both groups (121.36 vs 116.16 mg/dL; P=.32), while total cholesterol was mildly elevated in both groups but not significantly different (213.19 vs 201.21 mg/dL; P=.13). Use of hair loss treatments such as topical minoxidil (14.29% vs 21.21%; P=.53), oral low-dose minoxidil (57.14% vs 66.67%; P=.48), oral spironolactone (47.62% vs 57.58%; P=.47), and platelet-rich plasma injections (47.62% vs 27.27%; P=.90) were not significantly different across both groups.

The data suggest a significant (P<.05) association between abnormal LDL-C and hair loss severity in FPHL patients. Our study was limited by its small sample size and lack of causality; however, it coincides with and reiterates the findings established in the literature. The mechanism of the association between hyperlipidemia and AGA is not well understood but is thought to stem from the homology between cholesterol and androgens. Increased cholesterol release from dermal adipocytes and subsequent absorption into hair follicle cell populations may increase hair follicle steroidogenesis, thereby accelerating the anagen-catagen transition and inducing AGA. Alternatively, impaired cholesterol homeostasis may disrupt normal hair follicle cycling by interrupting signaling pathways in follicle proliferation and differentiation.⁵ Adequate control and monitoring of LDL-C levels may be important, particularly in patients with more severe FPHL.

To the Editor:

Female pattern hair loss (FPHL), or androgenetic alopecia (AGA), is the most common form of alopecia worldwide and is characterized by a reduction of hair follicles spent in the anagen phase of growth as well as progressive terminal hair loss.¹ It is caused by an excessive response to androgens and leads to the characteristic distribution of hair loss in both sexes. Studies have shown a notable association between AGA and markers of metabolic syndrome such as dyslipidemia, insulin resistance, and obesity in age- and sex-matched controls.^2,3 However, research describing the relationship between AGA severity and these markers is scarce.

To understand the relationship between FPHL severity and abnormal cholesterol levels, we performed a retrospective chart review of patients diagnosed with FPHL at a specialty alopecia clinic from June 2022 to December 2022. Patient age and age at onset of FPHL were collected. The severity of FPHL was measured using the Sinclair scale (score range, 1–5) and unidentifiable patient photographs. Laboratory values were collected; abnormal cholesterol was defined by the American Heart Association as having a low-density lipoprotein cholesterol (LDL-C) level of 100 mg/dL or higher.⁴ Finally, data on medication use were noted to understand patient treatment status (Table).

We identified 54 female patients with FPHL with an average age of 59 years (range, 34–80 years). Thirty-three females (61.11%) had a normal LDL-C level and 21 (38.89%) had an abnormal level. The mean (SD) LDL-C level was 66.02 (15.20) mg/dL (range, 29–92 mg/dL) in the group with normal levels and 138.81 (29.90) mg/dL (range, 100–193 mg/dL) in the group with abnormal levels. Patients with abnormal LDL-C had significantly higher Sinclair scale scores compared to those with normal levels (2.43 vs 1.91; P=.01). There were no significant differences in patient age (58.71 vs 59.70 years; P=.39), age at onset of AGA (47.75 vs 47.65 years; P=.49), history of polycystic ovary syndrome (9.52% vs 6.06%; P=.64), or statin use (38.09% vs 36.36%; P=.89) between patients with abnormal and normal LDL-C levels, respectively. There also were no significant differences in ferritin (96.42 vs 91.54 ng/mL; P=.40), vitamin D (42.35 vs 48.96 ng/mL; P=.09), or hemoglobin A_1c levels (5.60 ng/mL vs 5.38 ng/mL; P=.06)—variables that could have confounded this relationship. Triglycerides were within reference range in both groups (121.36 vs 116.16 mg/dL; P=.32), while total cholesterol was mildly elevated in both groups but not significantly different (213.19 vs 201.21 mg/dL; P=.13). Use of hair loss treatments such as topical minoxidil (14.29% vs 21.21%; P=.53), oral low-dose minoxidil (57.14% vs 66.67%; P=.48), oral spironolactone (47.62% vs 57.58%; P=.47), and platelet-rich plasma injections (47.62% vs 27.27%; P=.90) were not significantly different across both groups.

The data suggest a significant (P<.05) association between abnormal LDL-C and hair loss severity in FPHL patients. Our study was limited by its small sample size and lack of causality; however, it coincides with and reiterates the findings established in the literature. The mechanism of the association between hyperlipidemia and AGA is not well understood but is thought to stem from the homology between cholesterol and androgens. Increased cholesterol release from dermal adipocytes and subsequent absorption into hair follicle cell populations may increase hair follicle steroidogenesis, thereby accelerating the anagen-catagen transition and inducing AGA. Alternatively, impaired cholesterol homeostasis may disrupt normal hair follicle cycling by interrupting signaling pathways in follicle proliferation and differentiation.⁵ Adequate control and monitoring of LDL-C levels may be important, particularly in patients with more severe FPHL.

To the Editor:

Partial or total nail plate excisions commonly are used for the treatment of onychocryptosis and nail spicules. Procedures involving the nail unit require advanced technical skills to achieve optimal functional and aesthetic outcomes, avoid complications, and minimize health care costs. Data on the frequency of nail plate excisions performed by dermatologists and their relative frequency compared to other medical providers are limited. The objective of our study was to analyze trends in nail excision practice patterns among medical providers in the United States.

A retrospective analysis on nail excisions using the Current Procedural Terminology (CPT) code 11750 (excision of nail and nail matrix, partial or complete [eg, ingrown or deformed nail] for permanent removal), which is distinct from code 11755 (biopsy of nail unit [eg, plate, bed, matrix, hyponychium, proximal and lateral nail folds][separate procedure]), was performed using data from the Medicare Provider Utilization and Payment Database 2012-2017.^1,2 This file also is used by Peck et al³ in an article submitted to the Journal of the American Podiatric Medical Association and currently under consideration for publication. Procedures were recorded by year and provider type—dermatologist, podiatrist, physician assistant (PA)/nurse practitioner (NP), nondermatologist physician—and subcategorized by provider specialty (Table). Practice locations subcategorized by provider type were mapped using Tableau Software (Salesforce)(Figure). Descriptive statistics including number of providers, mean and median excisions per provider, and minimum/maximum nail excisions were calculated (Table). Practice types of PAs/NPs and specialization of nondermatologist physicians were determined using provider name, identification number, and practice address. This study did not require institutional review board review, as only publicly available data were utilized in our analysis.

A total of 6936 podiatrists, 58 nondermatologist physicians, 25 PAs/NPs, and 4 dermatologists performed 10 or more nail excisions annually under CPT code 11750 from January 2012 to December 2017 with annual means of 31, 31, 25, and 34, respectively (Table). No PAs/NPs included in the dataset worked in dermatology practices during the study period. Physician assistants and NPs most often practiced in podiatry and family medicine (FM) settings (both 40% [10/25]). Nondermatologist physicians most often specialized in FM (40% [23/58])(Table). The greatest number of providers practiced in 3 of the 4 most-populous states: California, Texas, and Florida; the fewest number practiced in 3 of the 10 least-populous states: Alaska, Hawaii, and Vermont. Vermont, Wyoming, and North Dakota—3 of the 5 least-populous states—had the fewest practitioners among the contiguous United States (Figure).

Figure generated using Tableau, which integrates with Mapbox. © Mapbox (https://www.mapbox.com/about/maps/), © OpenStreetMap (http://www.openstreetmap.org/copyright).

Our study showed that from January 2012 to December 2017, fewer dermatologists performed nail excisions than any other provider type (0.06%, 4 dermatologists of 7023 total providers), and dermatologists performed 1734-fold fewer nail excisions than podiatrists (99%, 6936 podiatrists of 7023 total providers). Only dermatologists practicing in California, Georgia, Indiana, and Oklahoma performed nail excisions. Conversely, podiatrists were more geographically distributed across the United States and other territories, with representation in all 50 states as well as the District of Columbia, Puerto Rico, and Guam.

Reasons for these large discrepancies in practice between dermatologists and other providers likely are multifactorial, encompassing a lack of emphasis on nail procedures in dermatology training, patient perception of the scope of dermatologic practice, and nail excision reimbursement patterns. Most dermatologists likely lack experience in performing nail procedures. The Accreditation Council for Graduate Medical Education requirements mandate that dermatology residents observe or perform 3 nail procedures over 3 years of residency, including 1 that may be performed on a human cadaver.⁴ In contrast, podiatry trainees must gain competency in toenail avulsion (both partial and complete), participate in anesthesia workshops, and become proficient in administering lower extremity blocks by the end of their training.⁵ Therefore, incorporating aspects of podiatric surgical training into dermatology residency requirements may increase the competency and comfort of dermatologists in performing nail excisions and practicing as nail experts as attending physicians.

It is likely that US patients do not perceive dermatologists as nail specialists and instead primarily consult podiatrists or FM and/or internal medicine physicians for treatment; for example, nail disease was one of the least common reasons for consulting a dermatologist (5%) in a German nationwide survey-based study (N=1015).⁶ Therefore, increased efforts are needed to educate the general public about the expertise of dermatologists in the diagnosis and management of nail conditions.

Reimbursement also may be a barrier to dermatologists performing nail procedures as part of their scope of practice; for example, in a retrospective study of nail biopsies using the Medicare Provider Utilization and Payment Database, there was no statistically significant difference in reimbursements for nail biopsies vs skin biopsies from 2012 to 2017 (P=0.69).⁷ Similar to nail biopsies, nail excisions typically are much more time consuming and technically demanding than skin biopsies, which may discourage dermatologists from routinely performing nail excision procedures.

Our study is subject to a number of limitations. The data reflected only US-based practice patterns and may not be applicable to nail procedures globally. There also is the potential for miscoding of procedures in the Medicare database. The data included only Part B Medicare fee-for-service and excludes non-Medicare insured, uninsured, and self-pay patients, as well as aggregated records from 10 or fewer Medicare beneficiaries.

Dermatologists rarely perform nail excisions and perform fewer nail excisions than any other provider type in the United States. There currently is an unmet need for comprehensive nail surgery education in US-based dermatology residency programs. We hope that our study fosters interdisciplinary collegiality and training between podiatrists and dermatologists and promotes expanded access to care across the United States to serve patients with nail disorders.

To the Editor:

Partial or total nail plate excisions commonly are used for the treatment of onychocryptosis and nail spicules. Procedures involving the nail unit require advanced technical skills to achieve optimal functional and aesthetic outcomes, avoid complications, and minimize health care costs. Data on the frequency of nail plate excisions performed by dermatologists and their relative frequency compared to other medical providers are limited. The objective of our study was to analyze trends in nail excision practice patterns among medical providers in the United States.

A retrospective analysis on nail excisions using the Current Procedural Terminology (CPT) code 11750 (excision of nail and nail matrix, partial or complete [eg, ingrown or deformed nail] for permanent removal), which is distinct from code 11755 (biopsy of nail unit [eg, plate, bed, matrix, hyponychium, proximal and lateral nail folds][separate procedure]), was performed using data from the Medicare Provider Utilization and Payment Database 2012-2017.^1,2 This file also is used by Peck et al³ in an article submitted to the Journal of the American Podiatric Medical Association and currently under consideration for publication. Procedures were recorded by year and provider type—dermatologist, podiatrist, physician assistant (PA)/nurse practitioner (NP), nondermatologist physician—and subcategorized by provider specialty (Table). Practice locations subcategorized by provider type were mapped using Tableau Software (Salesforce)(Figure). Descriptive statistics including number of providers, mean and median excisions per provider, and minimum/maximum nail excisions were calculated (Table). Practice types of PAs/NPs and specialization of nondermatologist physicians were determined using provider name, identification number, and practice address. This study did not require institutional review board review, as only publicly available data were utilized in our analysis.

A total of 6936 podiatrists, 58 nondermatologist physicians, 25 PAs/NPs, and 4 dermatologists performed 10 or more nail excisions annually under CPT code 11750 from January 2012 to December 2017 with annual means of 31, 31, 25, and 34, respectively (Table). No PAs/NPs included in the dataset worked in dermatology practices during the study period. Physician assistants and NPs most often practiced in podiatry and family medicine (FM) settings (both 40% [10/25]). Nondermatologist physicians most often specialized in FM (40% [23/58])(Table). The greatest number of providers practiced in 3 of the 4 most-populous states: California, Texas, and Florida; the fewest number practiced in 3 of the 10 least-populous states: Alaska, Hawaii, and Vermont. Vermont, Wyoming, and North Dakota—3 of the 5 least-populous states—had the fewest practitioners among the contiguous United States (Figure).

Figure generated using Tableau, which integrates with Mapbox. © Mapbox (https://www.mapbox.com/about/maps/), © OpenStreetMap (http://www.openstreetmap.org/copyright).

Our study showed that from January 2012 to December 2017, fewer dermatologists performed nail excisions than any other provider type (0.06%, 4 dermatologists of 7023 total providers), and dermatologists performed 1734-fold fewer nail excisions than podiatrists (99%, 6936 podiatrists of 7023 total providers). Only dermatologists practicing in California, Georgia, Indiana, and Oklahoma performed nail excisions. Conversely, podiatrists were more geographically distributed across the United States and other territories, with representation in all 50 states as well as the District of Columbia, Puerto Rico, and Guam.

Reasons for these large discrepancies in practice between dermatologists and other providers likely are multifactorial, encompassing a lack of emphasis on nail procedures in dermatology training, patient perception of the scope of dermatologic practice, and nail excision reimbursement patterns. Most dermatologists likely lack experience in performing nail procedures. The Accreditation Council for Graduate Medical Education requirements mandate that dermatology residents observe or perform 3 nail procedures over 3 years of residency, including 1 that may be performed on a human cadaver.⁴ In contrast, podiatry trainees must gain competency in toenail avulsion (both partial and complete), participate in anesthesia workshops, and become proficient in administering lower extremity blocks by the end of their training.⁵ Therefore, incorporating aspects of podiatric surgical training into dermatology residency requirements may increase the competency and comfort of dermatologists in performing nail excisions and practicing as nail experts as attending physicians.

It is likely that US patients do not perceive dermatologists as nail specialists and instead primarily consult podiatrists or FM and/or internal medicine physicians for treatment; for example, nail disease was one of the least common reasons for consulting a dermatologist (5%) in a German nationwide survey-based study (N=1015).⁶ Therefore, increased efforts are needed to educate the general public about the expertise of dermatologists in the diagnosis and management of nail conditions.

Reimbursement also may be a barrier to dermatologists performing nail procedures as part of their scope of practice; for example, in a retrospective study of nail biopsies using the Medicare Provider Utilization and Payment Database, there was no statistically significant difference in reimbursements for nail biopsies vs skin biopsies from 2012 to 2017 (P=0.69).⁷ Similar to nail biopsies, nail excisions typically are much more time consuming and technically demanding than skin biopsies, which may discourage dermatologists from routinely performing nail excision procedures.

Our study is subject to a number of limitations. The data reflected only US-based practice patterns and may not be applicable to nail procedures globally. There also is the potential for miscoding of procedures in the Medicare database. The data included only Part B Medicare fee-for-service and excludes non-Medicare insured, uninsured, and self-pay patients, as well as aggregated records from 10 or fewer Medicare beneficiaries.

Dermatologists rarely perform nail excisions and perform fewer nail excisions than any other provider type in the United States. There currently is an unmet need for comprehensive nail surgery education in US-based dermatology residency programs. We hope that our study fosters interdisciplinary collegiality and training between podiatrists and dermatologists and promotes expanded access to care across the United States to serve patients with nail disorders.

To the Editor:

Partial or total nail plate excisions commonly are used for the treatment of onychocryptosis and nail spicules. Procedures involving the nail unit require advanced technical skills to achieve optimal functional and aesthetic outcomes, avoid complications, and minimize health care costs. Data on the frequency of nail plate excisions performed by dermatologists and their relative frequency compared to other medical providers are limited. The objective of our study was to analyze trends in nail excision practice patterns among medical providers in the United States.

A retrospective analysis on nail excisions using the Current Procedural Terminology (CPT) code 11750 (excision of nail and nail matrix, partial or complete [eg, ingrown or deformed nail] for permanent removal), which is distinct from code 11755 (biopsy of nail unit [eg, plate, bed, matrix, hyponychium, proximal and lateral nail folds][separate procedure]), was performed using data from the Medicare Provider Utilization and Payment Database 2012-2017.^1,2 This file also is used by Peck et al³ in an article submitted to the Journal of the American Podiatric Medical Association and currently under consideration for publication. Procedures were recorded by year and provider type—dermatologist, podiatrist, physician assistant (PA)/nurse practitioner (NP), nondermatologist physician—and subcategorized by provider specialty (Table). Practice locations subcategorized by provider type were mapped using Tableau Software (Salesforce)(Figure). Descriptive statistics including number of providers, mean and median excisions per provider, and minimum/maximum nail excisions were calculated (Table). Practice types of PAs/NPs and specialization of nondermatologist physicians were determined using provider name, identification number, and practice address. This study did not require institutional review board review, as only publicly available data were utilized in our analysis.

A total of 6936 podiatrists, 58 nondermatologist physicians, 25 PAs/NPs, and 4 dermatologists performed 10 or more nail excisions annually under CPT code 11750 from January 2012 to December 2017 with annual means of 31, 31, 25, and 34, respectively (Table). No PAs/NPs included in the dataset worked in dermatology practices during the study period. Physician assistants and NPs most often practiced in podiatry and family medicine (FM) settings (both 40% [10/25]). Nondermatologist physicians most often specialized in FM (40% [23/58])(Table). The greatest number of providers practiced in 3 of the 4 most-populous states: California, Texas, and Florida; the fewest number practiced in 3 of the 10 least-populous states: Alaska, Hawaii, and Vermont. Vermont, Wyoming, and North Dakota—3 of the 5 least-populous states—had the fewest practitioners among the contiguous United States (Figure).

Figure generated using Tableau, which integrates with Mapbox. © Mapbox (https://www.mapbox.com/about/maps/), © OpenStreetMap (http://www.openstreetmap.org/copyright).

Our study showed that from January 2012 to December 2017, fewer dermatologists performed nail excisions than any other provider type (0.06%, 4 dermatologists of 7023 total providers), and dermatologists performed 1734-fold fewer nail excisions than podiatrists (99%, 6936 podiatrists of 7023 total providers). Only dermatologists practicing in California, Georgia, Indiana, and Oklahoma performed nail excisions. Conversely, podiatrists were more geographically distributed across the United States and other territories, with representation in all 50 states as well as the District of Columbia, Puerto Rico, and Guam.

Reasons for these large discrepancies in practice between dermatologists and other providers likely are multifactorial, encompassing a lack of emphasis on nail procedures in dermatology training, patient perception of the scope of dermatologic practice, and nail excision reimbursement patterns. Most dermatologists likely lack experience in performing nail procedures. The Accreditation Council for Graduate Medical Education requirements mandate that dermatology residents observe or perform 3 nail procedures over 3 years of residency, including 1 that may be performed on a human cadaver.⁴ In contrast, podiatry trainees must gain competency in toenail avulsion (both partial and complete), participate in anesthesia workshops, and become proficient in administering lower extremity blocks by the end of their training.⁵ Therefore, incorporating aspects of podiatric surgical training into dermatology residency requirements may increase the competency and comfort of dermatologists in performing nail excisions and practicing as nail experts as attending physicians.

It is likely that US patients do not perceive dermatologists as nail specialists and instead primarily consult podiatrists or FM and/or internal medicine physicians for treatment; for example, nail disease was one of the least common reasons for consulting a dermatologist (5%) in a German nationwide survey-based study (N=1015).⁶ Therefore, increased efforts are needed to educate the general public about the expertise of dermatologists in the diagnosis and management of nail conditions.

Reimbursement also may be a barrier to dermatologists performing nail procedures as part of their scope of practice; for example, in a retrospective study of nail biopsies using the Medicare Provider Utilization and Payment Database, there was no statistically significant difference in reimbursements for nail biopsies vs skin biopsies from 2012 to 2017 (P=0.69).⁷ Similar to nail biopsies, nail excisions typically are much more time consuming and technically demanding than skin biopsies, which may discourage dermatologists from routinely performing nail excision procedures.

Our study is subject to a number of limitations. The data reflected only US-based practice patterns and may not be applicable to nail procedures globally. There also is the potential for miscoding of procedures in the Medicare database. The data included only Part B Medicare fee-for-service and excludes non-Medicare insured, uninsured, and self-pay patients, as well as aggregated records from 10 or fewer Medicare beneficiaries.

Dermatologists rarely perform nail excisions and perform fewer nail excisions than any other provider type in the United States. There currently is an unmet need for comprehensive nail surgery education in US-based dermatology residency programs. We hope that our study fosters interdisciplinary collegiality and training between podiatrists and dermatologists and promotes expanded access to care across the United States to serve patients with nail disorders.

The Diagnosis: Argyria-Induced Azure Lunulae

Argyria is an acquired condition resulting from excessive exogenous exposure to silver with subsequent gastrointestinal absorption and pigmentary tissue deposition. Upon further questioning, our patient disclosed a lifetime history of colloidal silver use, both as a topical antiseptic agent and intraorally for aphthous ulcers. Silver has a predilection for granular deposition in stromal tissues and basement membranes with sparing of the epidermis, manifesting as progressive, permanent, blue to slate gray discoloration of sunexposed skin, mucous membranes, and nail beds.¹ The patient was advised to discontinue use of colloidal silver to avoid development of further pigmentary changes. The appearance of his nails remained unchanged in the months following initial presentation, as expected, since argyria pigmentation is not anticipated to reverse upon colloidal silver cessation.

Nail involvement may be an early presentation of generalized argyria or may be found in isolation, as seen in our patient. Early recognition and patient education are essential to minimize cumulative silver deposition. Although dyspigmentation may impact psychosocial well-being secondary to aesthetic concerns, there is limited research supporting adverse systemic effects of argyria confined to the nail beds. Similarly, the majority of generalized cases are not associated with systemic complications; however, potential toxicities, as described in isolated case reports without conclusive causal relationships, include nyctalopia, renal or hepatic toxicity, pulmonary fibrosis, and neuropsychiatric events.^1-6 Successful treatment of cutaneous argyria has been reported with the 1064-nm Q-switched Nd:YAG laser; however, there have been no reported treatments for nail bed involvement.⁷ Due to the absence of systemic symptoms, additional mucocutaneous dyspigmentation, or cosmetic concerns regarding nail bed lunulae discoloration in our patient, no further intervention was pursued, except for continued colloidal silver cessation.

The differential diagnosis of blue-gray nail bed dyspigmentation is broad and includes cyanosis secondary to cardiopulmonary disease, drug-induced dyspigmentation, Wilson disease, argyria, chrysiasis, hereditary acrolabial telangiectasia, and pseudomonal infection or chloronychia.^1,8,9 Etiologic insight may be provided from a thorough review of prescription and over-the-counter medications as well as careful attention to the distribution of dyspigmentation. Medications commonly associated with bluish nail bed dyspigmentation include antimalarials, amiodarone, minocycline, clofazimine, chlorpromazine/phenothiazines, and various chemotherapeutic drugs; our patient was not taking any of these.^1,9

Cyanotic nail bed dyspigmentation secondary to cardiopulmonary disease likely manifests with more diffuse nail bed dyspigmentation and is not confined solely to the lunulae. Only drug-induced dyspigmentation, classically due to phenolphthalein-containing laxatives; Wilson disease; and argyria have a tendency to spare the distal nail bed, which is a presentation termed azure lunulae.⁸ The toenails typically are spared in argyria, while toenail involvement is variable in Wilson disease, and additional systemic symptoms—including hepatic, ophthalmologic, and neuropsychiatric—as well as potential family history would be expected.⁸ Phenolphthalein is no longer available in over-the-counter laxatives, as it was formally banned by the US Food and Drug Administration in 1999 due to concerns of carcinogenicity.¹⁰

Hereditary acrolabial telangiectasia is a familial condition with autosomal-dominant inheritance that can manifest similarly to argyria with blue-gray discoloration of the proximal nail bed; however, this condition also would demonstrate involvement of the vermilion border and nipple areolae, often with associated telangiectasia and migraine headaches.¹¹

Chloronychia (also known as green nail syndrome) is an infection of the nail bed with Pseudomonas aeruginosa that more commonly presents with greenblack discoloration with variable involvement of the fingernails and toenails. Chloronychia, often with associated onycholysis, typically is found in individuals with repeated exposure to water, soaps, and detergents.¹² Our patient’s long-standing and unwavering nail bed appearance, involvement of all fingernail lunulae, lack of additional symptoms, and disclosed use of over-the-counter colloidal silver supported a clinical diagnosis of argyriainduced azure lunulae.

Argyria-induced azure lunulae secondary to colloidal silver exposure is an uncommon yet clinically significant cause of nail bed dyspigmentation. Prompt identification and cessation of the offending agent can prevent progression of mucocutaneous dyspigmentation and avoid potential long-term sequelae from systemic deposition.

The Diagnosis: Argyria-Induced Azure Lunulae

Argyria is an acquired condition resulting from excessive exogenous exposure to silver with subsequent gastrointestinal absorption and pigmentary tissue deposition. Upon further questioning, our patient disclosed a lifetime history of colloidal silver use, both as a topical antiseptic agent and intraorally for aphthous ulcers. Silver has a predilection for granular deposition in stromal tissues and basement membranes with sparing of the epidermis, manifesting as progressive, permanent, blue to slate gray discoloration of sunexposed skin, mucous membranes, and nail beds.¹ The patient was advised to discontinue use of colloidal silver to avoid development of further pigmentary changes. The appearance of his nails remained unchanged in the months following initial presentation, as expected, since argyria pigmentation is not anticipated to reverse upon colloidal silver cessation.

Nail involvement may be an early presentation of generalized argyria or may be found in isolation, as seen in our patient. Early recognition and patient education are essential to minimize cumulative silver deposition. Although dyspigmentation may impact psychosocial well-being secondary to aesthetic concerns, there is limited research supporting adverse systemic effects of argyria confined to the nail beds. Similarly, the majority of generalized cases are not associated with systemic complications; however, potential toxicities, as described in isolated case reports without conclusive causal relationships, include nyctalopia, renal or hepatic toxicity, pulmonary fibrosis, and neuropsychiatric events.^1-6 Successful treatment of cutaneous argyria has been reported with the 1064-nm Q-switched Nd:YAG laser; however, there have been no reported treatments for nail bed involvement.⁷ Due to the absence of systemic symptoms, additional mucocutaneous dyspigmentation, or cosmetic concerns regarding nail bed lunulae discoloration in our patient, no further intervention was pursued, except for continued colloidal silver cessation.

The differential diagnosis of blue-gray nail bed dyspigmentation is broad and includes cyanosis secondary to cardiopulmonary disease, drug-induced dyspigmentation, Wilson disease, argyria, chrysiasis, hereditary acrolabial telangiectasia, and pseudomonal infection or chloronychia.^1,8,9 Etiologic insight may be provided from a thorough review of prescription and over-the-counter medications as well as careful attention to the distribution of dyspigmentation. Medications commonly associated with bluish nail bed dyspigmentation include antimalarials, amiodarone, minocycline, clofazimine, chlorpromazine/phenothiazines, and various chemotherapeutic drugs; our patient was not taking any of these.^1,9

Cyanotic nail bed dyspigmentation secondary to cardiopulmonary disease likely manifests with more diffuse nail bed dyspigmentation and is not confined solely to the lunulae. Only drug-induced dyspigmentation, classically due to phenolphthalein-containing laxatives; Wilson disease; and argyria have a tendency to spare the distal nail bed, which is a presentation termed azure lunulae.⁸ The toenails typically are spared in argyria, while toenail involvement is variable in Wilson disease, and additional systemic symptoms—including hepatic, ophthalmologic, and neuropsychiatric—as well as potential family history would be expected.⁸ Phenolphthalein is no longer available in over-the-counter laxatives, as it was formally banned by the US Food and Drug Administration in 1999 due to concerns of carcinogenicity.¹⁰

Hereditary acrolabial telangiectasia is a familial condition with autosomal-dominant inheritance that can manifest similarly to argyria with blue-gray discoloration of the proximal nail bed; however, this condition also would demonstrate involvement of the vermilion border and nipple areolae, often with associated telangiectasia and migraine headaches.¹¹

Chloronychia (also known as green nail syndrome) is an infection of the nail bed with Pseudomonas aeruginosa that more commonly presents with greenblack discoloration with variable involvement of the fingernails and toenails. Chloronychia, often with associated onycholysis, typically is found in individuals with repeated exposure to water, soaps, and detergents.¹² Our patient’s long-standing and unwavering nail bed appearance, involvement of all fingernail lunulae, lack of additional symptoms, and disclosed use of over-the-counter colloidal silver supported a clinical diagnosis of argyriainduced azure lunulae.

Argyria-induced azure lunulae secondary to colloidal silver exposure is an uncommon yet clinically significant cause of nail bed dyspigmentation. Prompt identification and cessation of the offending agent can prevent progression of mucocutaneous dyspigmentation and avoid potential long-term sequelae from systemic deposition.

The Diagnosis: Argyria-Induced Azure Lunulae

Argyria is an acquired condition resulting from excessive exogenous exposure to silver with subsequent gastrointestinal absorption and pigmentary tissue deposition. Upon further questioning, our patient disclosed a lifetime history of colloidal silver use, both as a topical antiseptic agent and intraorally for aphthous ulcers. Silver has a predilection for granular deposition in stromal tissues and basement membranes with sparing of the epidermis, manifesting as progressive, permanent, blue to slate gray discoloration of sunexposed skin, mucous membranes, and nail beds.¹ The patient was advised to discontinue use of colloidal silver to avoid development of further pigmentary changes. The appearance of his nails remained unchanged in the months following initial presentation, as expected, since argyria pigmentation is not anticipated to reverse upon colloidal silver cessation.

Nail involvement may be an early presentation of generalized argyria or may be found in isolation, as seen in our patient. Early recognition and patient education are essential to minimize cumulative silver deposition. Although dyspigmentation may impact psychosocial well-being secondary to aesthetic concerns, there is limited research supporting adverse systemic effects of argyria confined to the nail beds. Similarly, the majority of generalized cases are not associated with systemic complications; however, potential toxicities, as described in isolated case reports without conclusive causal relationships, include nyctalopia, renal or hepatic toxicity, pulmonary fibrosis, and neuropsychiatric events.^1-6 Successful treatment of cutaneous argyria has been reported with the 1064-nm Q-switched Nd:YAG laser; however, there have been no reported treatments for nail bed involvement.⁷ Due to the absence of systemic symptoms, additional mucocutaneous dyspigmentation, or cosmetic concerns regarding nail bed lunulae discoloration in our patient, no further intervention was pursued, except for continued colloidal silver cessation.

The differential diagnosis of blue-gray nail bed dyspigmentation is broad and includes cyanosis secondary to cardiopulmonary disease, drug-induced dyspigmentation, Wilson disease, argyria, chrysiasis, hereditary acrolabial telangiectasia, and pseudomonal infection or chloronychia.^1,8,9 Etiologic insight may be provided from a thorough review of prescription and over-the-counter medications as well as careful attention to the distribution of dyspigmentation. Medications commonly associated with bluish nail bed dyspigmentation include antimalarials, amiodarone, minocycline, clofazimine, chlorpromazine/phenothiazines, and various chemotherapeutic drugs; our patient was not taking any of these.^1,9

Cyanotic nail bed dyspigmentation secondary to cardiopulmonary disease likely manifests with more diffuse nail bed dyspigmentation and is not confined solely to the lunulae. Only drug-induced dyspigmentation, classically due to phenolphthalein-containing laxatives; Wilson disease; and argyria have a tendency to spare the distal nail bed, which is a presentation termed azure lunulae.⁸ The toenails typically are spared in argyria, while toenail involvement is variable in Wilson disease, and additional systemic symptoms—including hepatic, ophthalmologic, and neuropsychiatric—as well as potential family history would be expected.⁸ Phenolphthalein is no longer available in over-the-counter laxatives, as it was formally banned by the US Food and Drug Administration in 1999 due to concerns of carcinogenicity.¹⁰

Hereditary acrolabial telangiectasia is a familial condition with autosomal-dominant inheritance that can manifest similarly to argyria with blue-gray discoloration of the proximal nail bed; however, this condition also would demonstrate involvement of the vermilion border and nipple areolae, often with associated telangiectasia and migraine headaches.¹¹

Chloronychia (also known as green nail syndrome) is an infection of the nail bed with Pseudomonas aeruginosa that more commonly presents with greenblack discoloration with variable involvement of the fingernails and toenails. Chloronychia, often with associated onycholysis, typically is found in individuals with repeated exposure to water, soaps, and detergents.¹² Our patient’s long-standing and unwavering nail bed appearance, involvement of all fingernail lunulae, lack of additional symptoms, and disclosed use of over-the-counter colloidal silver supported a clinical diagnosis of argyriainduced azure lunulae.

Argyria-induced azure lunulae secondary to colloidal silver exposure is an uncommon yet clinically significant cause of nail bed dyspigmentation. Prompt identification and cessation of the offending agent can prevent progression of mucocutaneous dyspigmentation and avoid potential long-term sequelae from systemic deposition.

In late December 2023, Brazil’s National Health Surveillance Agency (ANVISA) suspended the commercialization of approximately 1200 hair creams because of reports of eye irritation and temporary blindness.

A similar measure encompassing all hair creams sold in the country had already been announced by the agency in March. However, after a few weeks, ANVISA issued a resolution with rules for the products’ commercialization, allowing them back on the shelves.

With the new resolution, the sale of products that do not comply with the standards has once again been suspended. The reason is that reports of adverse events have reemerged. These events include temporary vision loss, headaches, and burning, tearing, itching, redness, and swelling of the eyes. According to reports, these adverse effects occurred mainly in people who used the specific products before swimming in the sea or in pools, or even going out in the rain.

The banned products contain 20% or more ethoxylated alcohols in their formulations. Products containing methylchloroisothiazolinone and methylisothiazolinone were already prohibited. These substances, used as preservatives, are considered toxic to the skin and mucous membranes, potentially causing allergies and burns to the eyes and skin. They also have a high pulmonary and neurological toxicity. All these substances are eye irritants and can cause chemical keratitis. In extreme cases, corneal ulcers may develop, leading to vision loss.

The Brazilian Council of Ophthalmology also issued a warning on these products. It emphasized that, in addition to the sales prohibition, consumers should check the labels of hair creams to make sure that these toxic substances are not present in the product formulation.

The ANVISA website contains a list of creams that are considered safe and have not had their commercialization suspended, along with links to adverse event notifications reported by healthcare professionals or consumers.

For consumers who have recently used hair creams, the agency advises careful hair washing, including tilting the head backward to prevent the product from coming into contact with the eye area. If there is accidental eye contact, the eyes should be washed with plenty of water.

If there are any undesired effects after using these products, users should immediately seek the nearest healthcare service. Treatment should be individualized, possibly including ocular occlusion and the use of eye drops containing antibiotics or corticosteroids, among other medications.

Not every patient has easy access to an ophthalmologist in an emergency, so it is crucial for general practitioners to be prepared for initial care. In this regard, one of the most important measures is eye washing with copious amounts of clean water or saline solution for 5-10 minutes.

Eye itching is a frequent manifestation of using hair creams, and scratching the area may worsen the condition. Ocular occlusion can protect the cornea until an evaluation can be performed by a specialist.

Although we prefer our patients to stay away from these creams, it is also important to disseminate this information and advise them to read labels and use safe cosmetics.
 

This article was translated from the Medscape Portuguese edition. A version of this article appeared on Medscape.com.

In late December 2023, Brazil’s National Health Surveillance Agency (ANVISA) suspended the commercialization of approximately 1200 hair creams because of reports of eye irritation and temporary blindness.

A similar measure encompassing all hair creams sold in the country had already been announced by the agency in March. However, after a few weeks, ANVISA issued a resolution with rules for the products’ commercialization, allowing them back on the shelves.

With the new resolution, the sale of products that do not comply with the standards has once again been suspended. The reason is that reports of adverse events have reemerged. These events include temporary vision loss, headaches, and burning, tearing, itching, redness, and swelling of the eyes. According to reports, these adverse effects occurred mainly in people who used the specific products before swimming in the sea or in pools, or even going out in the rain.

The banned products contain 20% or more ethoxylated alcohols in their formulations. Products containing methylchloroisothiazolinone and methylisothiazolinone were already prohibited. These substances, used as preservatives, are considered toxic to the skin and mucous membranes, potentially causing allergies and burns to the eyes and skin. They also have a high pulmonary and neurological toxicity. All these substances are eye irritants and can cause chemical keratitis. In extreme cases, corneal ulcers may develop, leading to vision loss.

The Brazilian Council of Ophthalmology also issued a warning on these products. It emphasized that, in addition to the sales prohibition, consumers should check the labels of hair creams to make sure that these toxic substances are not present in the product formulation.

The ANVISA website contains a list of creams that are considered safe and have not had their commercialization suspended, along with links to adverse event notifications reported by healthcare professionals or consumers.

For consumers who have recently used hair creams, the agency advises careful hair washing, including tilting the head backward to prevent the product from coming into contact with the eye area. If there is accidental eye contact, the eyes should be washed with plenty of water.

If there are any undesired effects after using these products, users should immediately seek the nearest healthcare service. Treatment should be individualized, possibly including ocular occlusion and the use of eye drops containing antibiotics or corticosteroids, among other medications.

Not every patient has easy access to an ophthalmologist in an emergency, so it is crucial for general practitioners to be prepared for initial care. In this regard, one of the most important measures is eye washing with copious amounts of clean water or saline solution for 5-10 minutes.

Eye itching is a frequent manifestation of using hair creams, and scratching the area may worsen the condition. Ocular occlusion can protect the cornea until an evaluation can be performed by a specialist.

Although we prefer our patients to stay away from these creams, it is also important to disseminate this information and advise them to read labels and use safe cosmetics.
 

This article was translated from the Medscape Portuguese edition. A version of this article appeared on Medscape.com.

In late December 2023, Brazil’s National Health Surveillance Agency (ANVISA) suspended the commercialization of approximately 1200 hair creams because of reports of eye irritation and temporary blindness.

A similar measure encompassing all hair creams sold in the country had already been announced by the agency in March. However, after a few weeks, ANVISA issued a resolution with rules for the products’ commercialization, allowing them back on the shelves.

With the new resolution, the sale of products that do not comply with the standards has once again been suspended. The reason is that reports of adverse events have reemerged. These events include temporary vision loss, headaches, and burning, tearing, itching, redness, and swelling of the eyes. According to reports, these adverse effects occurred mainly in people who used the specific products before swimming in the sea or in pools, or even going out in the rain.

The banned products contain 20% or more ethoxylated alcohols in their formulations. Products containing methylchloroisothiazolinone and methylisothiazolinone were already prohibited. These substances, used as preservatives, are considered toxic to the skin and mucous membranes, potentially causing allergies and burns to the eyes and skin. They also have a high pulmonary and neurological toxicity. All these substances are eye irritants and can cause chemical keratitis. In extreme cases, corneal ulcers may develop, leading to vision loss.

The Brazilian Council of Ophthalmology also issued a warning on these products. It emphasized that, in addition to the sales prohibition, consumers should check the labels of hair creams to make sure that these toxic substances are not present in the product formulation.

The ANVISA website contains a list of creams that are considered safe and have not had their commercialization suspended, along with links to adverse event notifications reported by healthcare professionals or consumers.

For consumers who have recently used hair creams, the agency advises careful hair washing, including tilting the head backward to prevent the product from coming into contact with the eye area. If there is accidental eye contact, the eyes should be washed with plenty of water.

If there are any undesired effects after using these products, users should immediately seek the nearest healthcare service. Treatment should be individualized, possibly including ocular occlusion and the use of eye drops containing antibiotics or corticosteroids, among other medications.

Not every patient has easy access to an ophthalmologist in an emergency, so it is crucial for general practitioners to be prepared for initial care. In this regard, one of the most important measures is eye washing with copious amounts of clean water or saline solution for 5-10 minutes.

Eye itching is a frequent manifestation of using hair creams, and scratching the area may worsen the condition. Ocular occlusion can protect the cornea until an evaluation can be performed by a specialist.

Although we prefer our patients to stay away from these creams, it is also important to disseminate this information and advise them to read labels and use safe cosmetics.
 

This article was translated from the Medscape Portuguese edition. A version of this article appeared on Medscape.com.

ORLANDO, FLORIDA — There are subtleties and nuances to diagnosing, treating, and monitoring the progress of treatment of hair loss in children. Moreover, hair loss in children can be challenging because it can be caused by a range of conditions, some common and others relatively rare.

Michelle Oboite, MD, shared tips on how to distinguish types of hair loss, when to treat with medications such as topical corticosteroids or Janus kinase (JAK) inhibitors, and why shared decision-making is important, at the ODAC Dermatology, Aesthetic & Surgical Conference.

What these conditions share is that they can negatively affect the quality of life for a child or teenager when the condition leads to anxiety, teasing, or bullying. “It is very isolating to have this condition that everyone in the world can see that you have and judge you for it,” said Dr. Oboite, an attending physician in the dermatology section of Children’s Hospital of Philadelphia.

While alopecia areata, tinea capitis, and trichotillomania are more common, other causes of hair loss in children include androgenetic alopecia, primary scarring alopecias, such as central centrifugal cicatricial alopecia, and dissecting cellulitis. Others are lichen planopilaris and genetic conditions, including loose anagen syndrome, uncombable hair syndrome, and “something so rare” — it has no acronym — autosomal recessive hypotrichosis with recurrent skin vesicles, Dr. Oboite said.
 

Alopecia Areata

Alopecia areata can differ from child to child and can appear in different stages: A localized patch stage, a diffuse patchy stage, or alopecia universalis. In this last stage, the child has already lost most or all the hair on the scalp and eyebrows, as well as the eyelashes.

The decision to treat or not to treat, particularly in younger children, should be on the basis of shared decision-making between a healthcare provider and caregiver, said Dr. Oboite, who is also an assistant professor of clinical dermatology at the University of Pennsylvania, Philadelphia.

Some younger children may not experience any negative impact from the condition, so waiting until they are older is an option.

Also, consider the impact of treatment on a child. Some therapies require frequent blood draws for monitoring, and some topical therapies that are applied multiple times a day “can be very overwhelming” for young children, Dr. Oboite said.

Most children with alopecia areata are healthy and do not need extensive screening laboratory testing. However, one exception is if thyroid dysfunction, commonly associated with alopecia areata, is suspected.

For alopecia areata, Dr. Oboite recommends starting with topical therapies, either topical corticosteroids (as first line) or topical JAK inhibitors (either topical ruxolitinib or compounded topical tofacitinib, both off-label for this indication).

Topical corticosteroids can be effective, but “you want to be thoughtful of the strength you’re using, the application frequency, and then the total amount of surface area that you’re treating,” Dr. Oboite said. Too potent or too much of a topical corticosteroid increases the risk for atrophy and systemic absorption, respectively. To reduce the risk, she reserves the use of ultrahigh-potency topical corticosteroids, such as clobetasol, for children ages 10 years or older. For children younger than 10 years, she recommends using mid-high-potency topical corticosteroids instead.

She recommends once-a-day application around bedtime 5 days a week, generally Monday through Friday to make it easier to remember.

“For children who have over 50% of the scalp involved, I do consider systemic therapy,” Dr. Oboite said. This can include oral steroids such as dexamethasone, prednisone, or prednisolone. For children with recalcitrant disease, she is more likely to use the oral JAK inhibitor ritlecitinib because it was recently approved by the Food and Drug Administration for treating severe alopecia areata in children 12 years and older and in adults.

Another strategy Dr. Oboite uses is to add low-dose oral minoxidil as an adjuvant to other systemic therapy. “I find that it helps with faster hair regrowth,” she said.
 

Tinea Capitis

Oral treatment is indicated for tinea capitis. “Topicals just don’t really clear this,” Dr. Oboite said. Also, talk to patients and families about preventing reinfection with the dermatophyte that causes this condition. “Make sure we’re cleaning hats, combs, brushes, and pillowcases. That is really important.”

Some patients can develop a widespread rash while on treatment. But in most cases, it’s not an adverse reaction to the medication but rather an indication that the body’s response is revving up, she noted.

Griseofulvin 20 mg/kg/d is one treatment option. Another is terbinafine (using weight-based dosing). A tip with terbinafine is that because the tablet needs to be crushed for a young child, “you can put it in anything, besides applesauce or yogurt with fruit on the bottom, which can be acidic and reduce the effectiveness of the medication,” Dr. Oboite said.

For cases of severe, inflammatory tinea capitis such as a kerion, “I will say you have to hold the hands of these patients, the journey can be long,” she added.
 

Trichotillomania

Trichotillomania occurs when someone cannot stop pulling their own hair, and in the early phases, it can be confused with alopecia areata. A thorough history and examination of the patient can help distinguish the two conditions. Sometimes a child or teen has a history of anxiety-related behaviors like nail biting that points to trichotillomania. Another tip is to use a dermatoscope to help distinguish hair loss conditions because it avoids having to do as many biopsies in children.

Redirection therapy can work for younger children, and cognitive behavioral therapy (CBT) can help older children with trichotillomania. In response to a question during the Q&A period, Dr. Oboite said psychiatrists or psychologists can perform CBT. If it takes time to get an appointment, there are some CBT apps that can help in the meantime, she said.

“One thing really important is to not blame the child,” Dr. Oboite said. “Most children don’t even know that they’re doing this. This is often not a behavior that is being done on purpose.”

Androgenetic Alopecia

Rarely, children and teenagers can also present with androgenetic alopecia, which Dr. Oboite has successfully treated with topical minoxidil, applied once a day before increasing to twice a day if tolerated. “I will tell them that when they pick it up, it will say ‘you should not use in children.’ But it actually can be used in children safely.”

Low-dose oral minoxidil is another option. Both treatments require a commitment by patients and parents because they are “taking this for a long time.”
 

Loose Anagen and Uncombable Hair Syndromes

A rare genetic form of hair loss is called loose anagen syndrome. Children with this disorder will have thin hair that is easily pulled out without a lot of force. Their hair appears to typically only grow to a certain length (such as to the nape of the neck) and then stops.

Another genetic hair loss condition is uncombable hair syndrome. It can cause hair to grow out of the scalp in all directions, and as the name suggests, it is almost impossible to comb or brush down. Along with loose anagen syndrome, uncombable hair syndrome tends to improve as the child gets older. “The key point here is telling parents that it can get better with time,” Dr. Oboite said.
 

A Condition With No Well-Known Acronym

She described a child she treated who had hair that never grew and was easily broken. The patient’s skin was prone to bruising, and her fingernails would easily fall off after trauma; her dentist noted that she had no buds for adult teeth on x-rays. These different presentations are important because hair, teeth, and nails all come from the same ectoderm germ line in embryo development, Dr. Oboite said.

Exome sequencing revealed the girl had a very rare diagnosis called autosomal recessive hypotrichosis with recurrent skin vesicles. “So, it is really important to recognize that children who are presenting with hair issues can have a genetic, underlying condition,” she said. Examining the skin, nails, and teeth, in addition to the hair, can be clues to these very rare diagnoses.

Some of these hair loss conditions in children can be challenging to diagnose and manage, Dr. Oboite said. “So don’t be afraid to ask for help on complex or rare cases.” Pediatric dermatologists “are always happy to help you. Hair loss is daunting, and hair loss in children can be even more daunting,” but the rewards of accurate diagnosis and successful treatment can be great, she said.

Dr. Oboite reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

ORLANDO, FLORIDA — There are subtleties and nuances to diagnosing, treating, and monitoring the progress of treatment of hair loss in children. Moreover, hair loss in children can be challenging because it can be caused by a range of conditions, some common and others relatively rare.

Michelle Oboite, MD, shared tips on how to distinguish types of hair loss, when to treat with medications such as topical corticosteroids or Janus kinase (JAK) inhibitors, and why shared decision-making is important, at the ODAC Dermatology, Aesthetic & Surgical Conference.

What these conditions share is that they can negatively affect the quality of life for a child or teenager when the condition leads to anxiety, teasing, or bullying. “It is very isolating to have this condition that everyone in the world can see that you have and judge you for it,” said Dr. Oboite, an attending physician in the dermatology section of Children’s Hospital of Philadelphia.

While alopecia areata, tinea capitis, and trichotillomania are more common, other causes of hair loss in children include androgenetic alopecia, primary scarring alopecias, such as central centrifugal cicatricial alopecia, and dissecting cellulitis. Others are lichen planopilaris and genetic conditions, including loose anagen syndrome, uncombable hair syndrome, and “something so rare” — it has no acronym — autosomal recessive hypotrichosis with recurrent skin vesicles, Dr. Oboite said.
 

Alopecia Areata

Alopecia areata can differ from child to child and can appear in different stages: A localized patch stage, a diffuse patchy stage, or alopecia universalis. In this last stage, the child has already lost most or all the hair on the scalp and eyebrows, as well as the eyelashes.

The decision to treat or not to treat, particularly in younger children, should be on the basis of shared decision-making between a healthcare provider and caregiver, said Dr. Oboite, who is also an assistant professor of clinical dermatology at the University of Pennsylvania, Philadelphia.

Some younger children may not experience any negative impact from the condition, so waiting until they are older is an option.

Also, consider the impact of treatment on a child. Some therapies require frequent blood draws for monitoring, and some topical therapies that are applied multiple times a day “can be very overwhelming” for young children, Dr. Oboite said.

Most children with alopecia areata are healthy and do not need extensive screening laboratory testing. However, one exception is if thyroid dysfunction, commonly associated with alopecia areata, is suspected.

For alopecia areata, Dr. Oboite recommends starting with topical therapies, either topical corticosteroids (as first line) or topical JAK inhibitors (either topical ruxolitinib or compounded topical tofacitinib, both off-label for this indication).

Topical corticosteroids can be effective, but “you want to be thoughtful of the strength you’re using, the application frequency, and then the total amount of surface area that you’re treating,” Dr. Oboite said. Too potent or too much of a topical corticosteroid increases the risk for atrophy and systemic absorption, respectively. To reduce the risk, she reserves the use of ultrahigh-potency topical corticosteroids, such as clobetasol, for children ages 10 years or older. For children younger than 10 years, she recommends using mid-high-potency topical corticosteroids instead.

She recommends once-a-day application around bedtime 5 days a week, generally Monday through Friday to make it easier to remember.

“For children who have over 50% of the scalp involved, I do consider systemic therapy,” Dr. Oboite said. This can include oral steroids such as dexamethasone, prednisone, or prednisolone. For children with recalcitrant disease, she is more likely to use the oral JAK inhibitor ritlecitinib because it was recently approved by the Food and Drug Administration for treating severe alopecia areata in children 12 years and older and in adults.

Another strategy Dr. Oboite uses is to add low-dose oral minoxidil as an adjuvant to other systemic therapy. “I find that it helps with faster hair regrowth,” she said.
 

Tinea Capitis

Oral treatment is indicated for tinea capitis. “Topicals just don’t really clear this,” Dr. Oboite said. Also, talk to patients and families about preventing reinfection with the dermatophyte that causes this condition. “Make sure we’re cleaning hats, combs, brushes, and pillowcases. That is really important.”

Some patients can develop a widespread rash while on treatment. But in most cases, it’s not an adverse reaction to the medication but rather an indication that the body’s response is revving up, she noted.

Griseofulvin 20 mg/kg/d is one treatment option. Another is terbinafine (using weight-based dosing). A tip with terbinafine is that because the tablet needs to be crushed for a young child, “you can put it in anything, besides applesauce or yogurt with fruit on the bottom, which can be acidic and reduce the effectiveness of the medication,” Dr. Oboite said.

For cases of severe, inflammatory tinea capitis such as a kerion, “I will say you have to hold the hands of these patients, the journey can be long,” she added.
 

Trichotillomania

Trichotillomania occurs when someone cannot stop pulling their own hair, and in the early phases, it can be confused with alopecia areata. A thorough history and examination of the patient can help distinguish the two conditions. Sometimes a child or teen has a history of anxiety-related behaviors like nail biting that points to trichotillomania. Another tip is to use a dermatoscope to help distinguish hair loss conditions because it avoids having to do as many biopsies in children.

Redirection therapy can work for younger children, and cognitive behavioral therapy (CBT) can help older children with trichotillomania. In response to a question during the Q&A period, Dr. Oboite said psychiatrists or psychologists can perform CBT. If it takes time to get an appointment, there are some CBT apps that can help in the meantime, she said.

“One thing really important is to not blame the child,” Dr. Oboite said. “Most children don’t even know that they’re doing this. This is often not a behavior that is being done on purpose.”

Androgenetic Alopecia

Rarely, children and teenagers can also present with androgenetic alopecia, which Dr. Oboite has successfully treated with topical minoxidil, applied once a day before increasing to twice a day if tolerated. “I will tell them that when they pick it up, it will say ‘you should not use in children.’ But it actually can be used in children safely.”

Low-dose oral minoxidil is another option. Both treatments require a commitment by patients and parents because they are “taking this for a long time.”
 

Loose Anagen and Uncombable Hair Syndromes

A rare genetic form of hair loss is called loose anagen syndrome. Children with this disorder will have thin hair that is easily pulled out without a lot of force. Their hair appears to typically only grow to a certain length (such as to the nape of the neck) and then stops.

Another genetic hair loss condition is uncombable hair syndrome. It can cause hair to grow out of the scalp in all directions, and as the name suggests, it is almost impossible to comb or brush down. Along with loose anagen syndrome, uncombable hair syndrome tends to improve as the child gets older. “The key point here is telling parents that it can get better with time,” Dr. Oboite said.
 

A Condition With No Well-Known Acronym

She described a child she treated who had hair that never grew and was easily broken. The patient’s skin was prone to bruising, and her fingernails would easily fall off after trauma; her dentist noted that she had no buds for adult teeth on x-rays. These different presentations are important because hair, teeth, and nails all come from the same ectoderm germ line in embryo development, Dr. Oboite said.

Exome sequencing revealed the girl had a very rare diagnosis called autosomal recessive hypotrichosis with recurrent skin vesicles. “So, it is really important to recognize that children who are presenting with hair issues can have a genetic, underlying condition,” she said. Examining the skin, nails, and teeth, in addition to the hair, can be clues to these very rare diagnoses.

Some of these hair loss conditions in children can be challenging to diagnose and manage, Dr. Oboite said. “So don’t be afraid to ask for help on complex or rare cases.” Pediatric dermatologists “are always happy to help you. Hair loss is daunting, and hair loss in children can be even more daunting,” but the rewards of accurate diagnosis and successful treatment can be great, she said.

Dr. Oboite reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

ORLANDO, FLORIDA — There are subtleties and nuances to diagnosing, treating, and monitoring the progress of treatment of hair loss in children. Moreover, hair loss in children can be challenging because it can be caused by a range of conditions, some common and others relatively rare.

Michelle Oboite, MD, shared tips on how to distinguish types of hair loss, when to treat with medications such as topical corticosteroids or Janus kinase (JAK) inhibitors, and why shared decision-making is important, at the ODAC Dermatology, Aesthetic & Surgical Conference.

What these conditions share is that they can negatively affect the quality of life for a child or teenager when the condition leads to anxiety, teasing, or bullying. “It is very isolating to have this condition that everyone in the world can see that you have and judge you for it,” said Dr. Oboite, an attending physician in the dermatology section of Children’s Hospital of Philadelphia.

While alopecia areata, tinea capitis, and trichotillomania are more common, other causes of hair loss in children include androgenetic alopecia, primary scarring alopecias, such as central centrifugal cicatricial alopecia, and dissecting cellulitis. Others are lichen planopilaris and genetic conditions, including loose anagen syndrome, uncombable hair syndrome, and “something so rare” — it has no acronym — autosomal recessive hypotrichosis with recurrent skin vesicles, Dr. Oboite said.
 

Alopecia Areata

Alopecia areata can differ from child to child and can appear in different stages: A localized patch stage, a diffuse patchy stage, or alopecia universalis. In this last stage, the child has already lost most or all the hair on the scalp and eyebrows, as well as the eyelashes.

The decision to treat or not to treat, particularly in younger children, should be on the basis of shared decision-making between a healthcare provider and caregiver, said Dr. Oboite, who is also an assistant professor of clinical dermatology at the University of Pennsylvania, Philadelphia.

Some younger children may not experience any negative impact from the condition, so waiting until they are older is an option.

Also, consider the impact of treatment on a child. Some therapies require frequent blood draws for monitoring, and some topical therapies that are applied multiple times a day “can be very overwhelming” for young children, Dr. Oboite said.

Most children with alopecia areata are healthy and do not need extensive screening laboratory testing. However, one exception is if thyroid dysfunction, commonly associated with alopecia areata, is suspected.

For alopecia areata, Dr. Oboite recommends starting with topical therapies, either topical corticosteroids (as first line) or topical JAK inhibitors (either topical ruxolitinib or compounded topical tofacitinib, both off-label for this indication).

Topical corticosteroids can be effective, but “you want to be thoughtful of the strength you’re using, the application frequency, and then the total amount of surface area that you’re treating,” Dr. Oboite said. Too potent or too much of a topical corticosteroid increases the risk for atrophy and systemic absorption, respectively. To reduce the risk, she reserves the use of ultrahigh-potency topical corticosteroids, such as clobetasol, for children ages 10 years or older. For children younger than 10 years, she recommends using mid-high-potency topical corticosteroids instead.

She recommends once-a-day application around bedtime 5 days a week, generally Monday through Friday to make it easier to remember.

“For children who have over 50% of the scalp involved, I do consider systemic therapy,” Dr. Oboite said. This can include oral steroids such as dexamethasone, prednisone, or prednisolone. For children with recalcitrant disease, she is more likely to use the oral JAK inhibitor ritlecitinib because it was recently approved by the Food and Drug Administration for treating severe alopecia areata in children 12 years and older and in adults.

Another strategy Dr. Oboite uses is to add low-dose oral minoxidil as an adjuvant to other systemic therapy. “I find that it helps with faster hair regrowth,” she said.
 

Tinea Capitis

Oral treatment is indicated for tinea capitis. “Topicals just don’t really clear this,” Dr. Oboite said. Also, talk to patients and families about preventing reinfection with the dermatophyte that causes this condition. “Make sure we’re cleaning hats, combs, brushes, and pillowcases. That is really important.”

Some patients can develop a widespread rash while on treatment. But in most cases, it’s not an adverse reaction to the medication but rather an indication that the body’s response is revving up, she noted.

Griseofulvin 20 mg/kg/d is one treatment option. Another is terbinafine (using weight-based dosing). A tip with terbinafine is that because the tablet needs to be crushed for a young child, “you can put it in anything, besides applesauce or yogurt with fruit on the bottom, which can be acidic and reduce the effectiveness of the medication,” Dr. Oboite said.

For cases of severe, inflammatory tinea capitis such as a kerion, “I will say you have to hold the hands of these patients, the journey can be long,” she added.
 

Trichotillomania

Trichotillomania occurs when someone cannot stop pulling their own hair, and in the early phases, it can be confused with alopecia areata. A thorough history and examination of the patient can help distinguish the two conditions. Sometimes a child or teen has a history of anxiety-related behaviors like nail biting that points to trichotillomania. Another tip is to use a dermatoscope to help distinguish hair loss conditions because it avoids having to do as many biopsies in children.

Redirection therapy can work for younger children, and cognitive behavioral therapy (CBT) can help older children with trichotillomania. In response to a question during the Q&A period, Dr. Oboite said psychiatrists or psychologists can perform CBT. If it takes time to get an appointment, there are some CBT apps that can help in the meantime, she said.

“One thing really important is to not blame the child,” Dr. Oboite said. “Most children don’t even know that they’re doing this. This is often not a behavior that is being done on purpose.”

Androgenetic Alopecia

Rarely, children and teenagers can also present with androgenetic alopecia, which Dr. Oboite has successfully treated with topical minoxidil, applied once a day before increasing to twice a day if tolerated. “I will tell them that when they pick it up, it will say ‘you should not use in children.’ But it actually can be used in children safely.”

Low-dose oral minoxidil is another option. Both treatments require a commitment by patients and parents because they are “taking this for a long time.”
 

Loose Anagen and Uncombable Hair Syndromes

A rare genetic form of hair loss is called loose anagen syndrome. Children with this disorder will have thin hair that is easily pulled out without a lot of force. Their hair appears to typically only grow to a certain length (such as to the nape of the neck) and then stops.

Another genetic hair loss condition is uncombable hair syndrome. It can cause hair to grow out of the scalp in all directions, and as the name suggests, it is almost impossible to comb or brush down. Along with loose anagen syndrome, uncombable hair syndrome tends to improve as the child gets older. “The key point here is telling parents that it can get better with time,” Dr. Oboite said.
 

A Condition With No Well-Known Acronym

She described a child she treated who had hair that never grew and was easily broken. The patient’s skin was prone to bruising, and her fingernails would easily fall off after trauma; her dentist noted that she had no buds for adult teeth on x-rays. These different presentations are important because hair, teeth, and nails all come from the same ectoderm germ line in embryo development, Dr. Oboite said.

Exome sequencing revealed the girl had a very rare diagnosis called autosomal recessive hypotrichosis with recurrent skin vesicles. “So, it is really important to recognize that children who are presenting with hair issues can have a genetic, underlying condition,” she said. Examining the skin, nails, and teeth, in addition to the hair, can be clues to these very rare diagnoses.

Some of these hair loss conditions in children can be challenging to diagnose and manage, Dr. Oboite said. “So don’t be afraid to ask for help on complex or rare cases.” Pediatric dermatologists “are always happy to help you. Hair loss is daunting, and hair loss in children can be even more daunting,” but the rewards of accurate diagnosis and successful treatment can be great, she said.

Dr. Oboite reported no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Men who have smoked or currently smoke are significantly more likely to develop androgenetic alopecia (AGA) than men who have never smoked, according to a new study.

In addition, the odds of developing AGA are higher among those who smoke at least 10 cigarettes per day than among those who smoke less, the study authors found.

“Men who smoke are more likely to develop and experience progression of male pattern hair loss,” lead author Aditya Gupta, MD, PhD, professor of medicine at the University of Toronto, Toronto, and director of clinical research at Mediprobe Research Inc., London, Ontario, Canada, told this news organization.

“Our patients with male pattern baldness need to be educated about the negative effects of smoking, given that this condition can have a profound negative psychological impact on those who suffer from it,” he said.

The study was published online in the Journal of Cosmetic Dermatology.
 

Analyzing Smoking’s Effects

Smoking generally has been accepted as a risk factor for the development and progression of AGA or the most common form of hair loss. The research evidence on this association has been inconsistent, however, the authors wrote.

The investigators conducted a review and meta-analysis of eight observational studies to understand the links between smoking and AGA. Ever-smokers were defined as current and former smokers.

Overall, based on six studies, men who have ever smoked are 1.8 times more likely (P < .05) to develop AGA.

Based on two studies, men who smoke 10 or more cigarettes daily are about twice as likely (P < .05) to develop AGA than those who smoke up to 10 cigarettes per day.

Based on four studies, ever smoking is associated with 1.3 times higher odds of AGA progressing from mild (ie, Norwood-Hamilton stages I-III) to more severe (stages IV-VII) than among those who have never smoked.

Based on two studies, there’s no association between AGA progression and smoking intensity (as defined as smoking up to 20 cigarettes daily vs smoking 20 or more cigarettes per day).

“Though our pooled analysis found no significant association between smoking intensity and severity of male AGA, a positive correlation may exist and be detected through an analysis that is statistically better powered,” said Dr. Gupta.

The investigators noted the limitations of their analysis, such as its reliance on observational studies and its lack of data about nicotine levels, smoking intensity, and smoking cessation among study participants.

Additional studies are needed to better understand the links between smoking and hair loss, said Dr. Gupta, as well as the effects of smoking cessation.

Improving Practice and Research

Commenting on the findings for this news organization, Arash Babadjouni, MD, a dermatologist at Midwestern University, Glendale, Arizona, said, “Smoking is not only a preventable cause of significant systemic disease but also affects the follicular growth cycle and fiber pigmentation. The prevalence of hair loss and premature hair graying is higher in smokers than nonsmokers.”

Dr. Babadjouni, who wasn’t involved with this study, has researched the associations between smoking and hair loss and premature hair graying.

“Evidence of this association can be used to clinically promote smoking cessation and emphasize the consequences of smoking on hair,” he said. “Smoking status should be assessed in patients who are presenting to their dermatologist and physicians alike for evaluation of alopecia and premature hair graying.”

The study was conducted without outside funding, and the authors declared no conflicts of interest. Dr. Babadjouni reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Men who have smoked or currently smoke are significantly more likely to develop androgenetic alopecia (AGA) than men who have never smoked, according to a new study.

In addition, the odds of developing AGA are higher among those who smoke at least 10 cigarettes per day than among those who smoke less, the study authors found.

“Men who smoke are more likely to develop and experience progression of male pattern hair loss,” lead author Aditya Gupta, MD, PhD, professor of medicine at the University of Toronto, Toronto, and director of clinical research at Mediprobe Research Inc., London, Ontario, Canada, told this news organization.

“Our patients with male pattern baldness need to be educated about the negative effects of smoking, given that this condition can have a profound negative psychological impact on those who suffer from it,” he said.

The study was published online in the Journal of Cosmetic Dermatology.
 

Analyzing Smoking’s Effects

Smoking generally has been accepted as a risk factor for the development and progression of AGA or the most common form of hair loss. The research evidence on this association has been inconsistent, however, the authors wrote.

The investigators conducted a review and meta-analysis of eight observational studies to understand the links between smoking and AGA. Ever-smokers were defined as current and former smokers.

Overall, based on six studies, men who have ever smoked are 1.8 times more likely (P < .05) to develop AGA.

Based on two studies, men who smoke 10 or more cigarettes daily are about twice as likely (P < .05) to develop AGA than those who smoke up to 10 cigarettes per day.

Based on four studies, ever smoking is associated with 1.3 times higher odds of AGA progressing from mild (ie, Norwood-Hamilton stages I-III) to more severe (stages IV-VII) than among those who have never smoked.

Based on two studies, there’s no association between AGA progression and smoking intensity (as defined as smoking up to 20 cigarettes daily vs smoking 20 or more cigarettes per day).

“Though our pooled analysis found no significant association between smoking intensity and severity of male AGA, a positive correlation may exist and be detected through an analysis that is statistically better powered,” said Dr. Gupta.

The investigators noted the limitations of their analysis, such as its reliance on observational studies and its lack of data about nicotine levels, smoking intensity, and smoking cessation among study participants.

Additional studies are needed to better understand the links between smoking and hair loss, said Dr. Gupta, as well as the effects of smoking cessation.

Improving Practice and Research

Commenting on the findings for this news organization, Arash Babadjouni, MD, a dermatologist at Midwestern University, Glendale, Arizona, said, “Smoking is not only a preventable cause of significant systemic disease but also affects the follicular growth cycle and fiber pigmentation. The prevalence of hair loss and premature hair graying is higher in smokers than nonsmokers.”

Dr. Babadjouni, who wasn’t involved with this study, has researched the associations between smoking and hair loss and premature hair graying.

“Evidence of this association can be used to clinically promote smoking cessation and emphasize the consequences of smoking on hair,” he said. “Smoking status should be assessed in patients who are presenting to their dermatologist and physicians alike for evaluation of alopecia and premature hair graying.”

The study was conducted without outside funding, and the authors declared no conflicts of interest. Dr. Babadjouni reported no relevant disclosures.

A version of this article appeared on Medscape.com.

Men who have smoked or currently smoke are significantly more likely to develop androgenetic alopecia (AGA) than men who have never smoked, according to a new study.

In addition, the odds of developing AGA are higher among those who smoke at least 10 cigarettes per day than among those who smoke less, the study authors found.

“Men who smoke are more likely to develop and experience progression of male pattern hair loss,” lead author Aditya Gupta, MD, PhD, professor of medicine at the University of Toronto, Toronto, and director of clinical research at Mediprobe Research Inc., London, Ontario, Canada, told this news organization.

“Our patients with male pattern baldness need to be educated about the negative effects of smoking, given that this condition can have a profound negative psychological impact on those who suffer from it,” he said.

The study was published online in the Journal of Cosmetic Dermatology.
 

Analyzing Smoking’s Effects

Smoking generally has been accepted as a risk factor for the development and progression of AGA or the most common form of hair loss. The research evidence on this association has been inconsistent, however, the authors wrote.

The investigators conducted a review and meta-analysis of eight observational studies to understand the links between smoking and AGA. Ever-smokers were defined as current and former smokers.

Overall, based on six studies, men who have ever smoked are 1.8 times more likely (P < .05) to develop AGA.

Based on two studies, men who smoke 10 or more cigarettes daily are about twice as likely (P < .05) to develop AGA than those who smoke up to 10 cigarettes per day.

Based on four studies, ever smoking is associated with 1.3 times higher odds of AGA progressing from mild (ie, Norwood-Hamilton stages I-III) to more severe (stages IV-VII) than among those who have never smoked.

Based on two studies, there’s no association between AGA progression and smoking intensity (as defined as smoking up to 20 cigarettes daily vs smoking 20 or more cigarettes per day).

“Though our pooled analysis found no significant association between smoking intensity and severity of male AGA, a positive correlation may exist and be detected through an analysis that is statistically better powered,” said Dr. Gupta.

The investigators noted the limitations of their analysis, such as its reliance on observational studies and its lack of data about nicotine levels, smoking intensity, and smoking cessation among study participants.

Additional studies are needed to better understand the links between smoking and hair loss, said Dr. Gupta, as well as the effects of smoking cessation.

Improving Practice and Research

Commenting on the findings for this news organization, Arash Babadjouni, MD, a dermatologist at Midwestern University, Glendale, Arizona, said, “Smoking is not only a preventable cause of significant systemic disease but also affects the follicular growth cycle and fiber pigmentation. The prevalence of hair loss and premature hair graying is higher in smokers than nonsmokers.”

Dr. Babadjouni, who wasn’t involved with this study, has researched the associations between smoking and hair loss and premature hair graying.

“Evidence of this association can be used to clinically promote smoking cessation and emphasize the consequences of smoking on hair,” he said. “Smoking status should be assessed in patients who are presenting to their dermatologist and physicians alike for evaluation of alopecia and premature hair graying.”

The study was conducted without outside funding, and the authors declared no conflicts of interest. Dr. Babadjouni reported no relevant disclosures.

A version of this article appeared on Medscape.com.

A member of the Lamiaceae family, Salvia rosmarinus (rosemary),* an aromatic plant native to the Mediterranean region and now cultivated globally, has been used for centuries in cuisine and medicine, with several well-established biological activities.^1-3 Thought to contribute to preventing hair loss, rosemary oil was also used for hundreds of years in hair rinses in the Mediterranean area.⁴ In traditional Iranian medicine, rosemary essential oil has been topically applied as an analgesic, anti-inflammatory, and anti-acne remedy.⁵ Rosemary is known to absorb UV light well and to impart antibacterial and antifungal activity, as well as help maintain skin homeostasis.³ It is also used and under further study for its anti-inflammatory, antioxidant, anti-infective, and anticancer activity.^2,6-9 The health benefits of rosemary are typically ascribed to its constituent carnosol/carnosic and ursolic acids.⁷In part 1 of this update on rosemary, the focus will be on chemical constituents, wound healing, anticancer activity, and hair care potential.

Chemical Constituents

The key chemical components of S. rosmarinus include bitter principle, resin, tannic acid, flavonoids, and volatile oils (made up of borneol, bornyl acetate, camphene, cineol, pinene, and camphor).¹⁰ Other important constituents of rosemary oil, in particular, include p-Cymene, linalool, gamma-terpinene, thymol, beta-pinene, alpha-pinene, eucalyptol, and carnosic acid.⁹ Volatile oils of rosemary have been used in various oils and lotions to treat wounds and with the intention of stimulating hair growth.¹⁰

Wound Healing

In a 2022 study in 60 adult male rats, Bulhões and colleagues found that the use of rosemary leaf essential oil-based ointments on skin lesions spurred wound healing, decreased inflammation, and enhanced angiogenesis as well as collagen fiber density.¹¹

Three years earlier, Labib and colleagues studied the wound healing capacity of three chitosan-based topical formulations containing either tea tree essential oil, rosemary essential oil, or a mixture of both oils in an excision wound model in rats.

HUIZENG HU/Moment/Getty Images

The combination preparation was found to be the most effective in fostering various stages of wound healing, with significant increases in wound contraction percentage observed in the combination group compared with either group treated using individual essential oils or the untreated animals.¹²

A 2010 in vivo study by Abu-Al-Basal using BALB/c mice with diabetes revealed that the topical application of rosemary essential oil for three days reduced inflammation, enhanced wound contraction and re-epithelialization, and promoted angiogenesis, granulation tissue regeneration, and collagen deposition.¹³

Anticancer Activity

Using a 7,12-dimethlybenz(a)anthracene (DMBA)-initiated and croton oil-promoted model in 2006, Sancheti and Goyal determined that rosemary extract administered orally at a dose rate of 500 mg/kg body weight/mouse significantly inhibited two-stage skin tumorigenesis in mice.¹⁴ Nearly a decade later, Cattaneo and colleagues determined that a rosemary hydroalcoholic extract displayed antiproliferative effects on the human melanoma A375 cell line.⁸

The polyphenols carnosic acid and rosmarinic acid are most often cited as the sources of the reputed anticancer effects of rosemary.¹⁵

Hair Health

Early in 2023, Begum and colleagues developed a 1% hair lotion including a methanolic extract of the aerial part of S. rosmarinus that they assessed for potential hair growth activity in C57BL/6 mice. Using water as a control and 2% minoxidil hair lotion as standard, the investigators determined that their rosemary hair lotion demonstrated significant hair growth promotion, exceeding that seen in the mice treated with the drug standard.¹

Baumann Cosmetic &amp; Research Institute

In a randomized controlled study in C57BL/6NCrSlc mice a decade earlier, Murata and colleagues evaluated the anti-androgenic activity and hair growth potential imparted by topical rosemary oil compared with finasteride and minoxidil. Rosemary oil leaf extract, with 12-O-methylcarnosic acid as its most active component, robustly suppressed 5alpha-reductase and stimulated hair growth in vivo in both the androgenetic alopecia/testosterone-treated mouse model, as well as the hair growth activating mouse model as compared with minoxidil. Further, the inhibitory activity of rosemary was 82.4% and 94.6% at 200 mcg/mL and 500 mcg/mL, respectively, whereas finasteride demonstrated 81.9% at 250 nM.¹⁶

A human study two years later was even more encouraging. Panahi and colleagues conducted a randomized comparative trial with 100 patients to investigate the effects of rosemary oil as opposed to minoxidil 2% for the treatment of androgenetic alopecia over 6 months. By 6 months, significantly greater hair counts were observed in both groups compared with baseline and 3-month readings, but no significant variations between groups. No differences were found in the frequency of dryness, greasiness, or dandruff at any time point or between groups. Scalp itching was significantly greater at the 3- and 6-month points in both groups, particularly in the minoxidil group at both of those time points. The investigators concluded that rosemary oil compared well with minoxidil as androgenetic alopecia therapy.¹⁷

Conclusion

Rosemary has been used in traditional medicine for hundreds of years and it has been a common ingredient in cosmetic and cosmeceutical formulations for more than 20 years. Recent findings suggest a broad array of applications in modern medicine, particularly dermatology. The next column will focus on the most recent studies pertaining to the antioxidant and anti-aging activity of this aromatic shrub.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a SaaS company used to generate skin care routines in office and as a ecommerce solution. Write to her at dermnews@mdedge.com.

References

1. Begum A et al. Adv Biomed Res. 2023 Mar 21;12:60.

2. de Oliveira JR et al. J Biomed Sci. 2019 Jan 9;26(1):5.

3. González-Minero FJ et al. Cosmetics. 2020 Oct 3;7(4):77.

4. Dinkins J et al. Int J Dermatol. 2023 Aug;62(8):980-5.

5. Akbari J et al. Pharm Biol. 2015;53(10):1442-7.

6. Allegra A et al. Nutrients. 2020 Jun 10;12(6):1739.

7. de Macedo LM et al. Plants (Basel). 2020 May 21;9(5):651.

8. Cattaneo L et al. PLoS One. 2015 Jul 15;10(7):e0132439.

9. Borges RS et al. J Ethnopharmacol. 2019 Jan 30;229:29-45.

10. Begum A et al. Acta Sci Pol Technol Aliment. 2013 Jan-Mar;12(1):61-73.

11. Bulhões AAVC et al. Acta Cir Bras. 2022 Apr 8;37(1):e370104.

12. Labib RM et al. PLoS One. 2019 Sep 16;14(9):e0219561.

13. Abu-Al-Basal MA. J Ethnopharmacol. 2010 Sep 15;131(2):443-50.

14. Sancheti G and Goyal PK. Phytother Res. 2006 Nov;20(11):981-6.

15. Moore J et al. Nutrients. 2016 Nov 17;8(11):731.

16. Murata K et al. Phytother Res. 2013 Feb;27(2):212-7.

17. Panahi Y et al. Skinmed. 2015 Jan-Feb;13(1):15-21.

*Correction, 2/27: This column was updated with the more recent name for rosemary, Salvia rosmarinus.

A member of the Lamiaceae family, Salvia rosmarinus (rosemary),* an aromatic plant native to the Mediterranean region and now cultivated globally, has been used for centuries in cuisine and medicine, with several well-established biological activities.^1-3 Thought to contribute to preventing hair loss, rosemary oil was also used for hundreds of years in hair rinses in the Mediterranean area.⁴ In traditional Iranian medicine, rosemary essential oil has been topically applied as an analgesic, anti-inflammatory, and anti-acne remedy.⁵ Rosemary is known to absorb UV light well and to impart antibacterial and antifungal activity, as well as help maintain skin homeostasis.³ It is also used and under further study for its anti-inflammatory, antioxidant, anti-infective, and anticancer activity.^2,6-9 The health benefits of rosemary are typically ascribed to its constituent carnosol/carnosic and ursolic acids.⁷In part 1 of this update on rosemary, the focus will be on chemical constituents, wound healing, anticancer activity, and hair care potential.

Chemical Constituents

The key chemical components of S. rosmarinus include bitter principle, resin, tannic acid, flavonoids, and volatile oils (made up of borneol, bornyl acetate, camphene, cineol, pinene, and camphor).¹⁰ Other important constituents of rosemary oil, in particular, include p-Cymene, linalool, gamma-terpinene, thymol, beta-pinene, alpha-pinene, eucalyptol, and carnosic acid.⁹ Volatile oils of rosemary have been used in various oils and lotions to treat wounds and with the intention of stimulating hair growth.¹⁰

Wound Healing

In a 2022 study in 60 adult male rats, Bulhões and colleagues found that the use of rosemary leaf essential oil-based ointments on skin lesions spurred wound healing, decreased inflammation, and enhanced angiogenesis as well as collagen fiber density.¹¹

Three years earlier, Labib and colleagues studied the wound healing capacity of three chitosan-based topical formulations containing either tea tree essential oil, rosemary essential oil, or a mixture of both oils in an excision wound model in rats.

HUIZENG HU/Moment/Getty Images

The combination preparation was found to be the most effective in fostering various stages of wound healing, with significant increases in wound contraction percentage observed in the combination group compared with either group treated using individual essential oils or the untreated animals.¹²

A 2010 in vivo study by Abu-Al-Basal using BALB/c mice with diabetes revealed that the topical application of rosemary essential oil for three days reduced inflammation, enhanced wound contraction and re-epithelialization, and promoted angiogenesis, granulation tissue regeneration, and collagen deposition.¹³

Anticancer Activity

Using a 7,12-dimethlybenz(a)anthracene (DMBA)-initiated and croton oil-promoted model in 2006, Sancheti and Goyal determined that rosemary extract administered orally at a dose rate of 500 mg/kg body weight/mouse significantly inhibited two-stage skin tumorigenesis in mice.¹⁴ Nearly a decade later, Cattaneo and colleagues determined that a rosemary hydroalcoholic extract displayed antiproliferative effects on the human melanoma A375 cell line.⁸

The polyphenols carnosic acid and rosmarinic acid are most often cited as the sources of the reputed anticancer effects of rosemary.¹⁵

Hair Health

Early in 2023, Begum and colleagues developed a 1% hair lotion including a methanolic extract of the aerial part of S. rosmarinus that they assessed for potential hair growth activity in C57BL/6 mice. Using water as a control and 2% minoxidil hair lotion as standard, the investigators determined that their rosemary hair lotion demonstrated significant hair growth promotion, exceeding that seen in the mice treated with the drug standard.¹

Baumann Cosmetic &amp; Research Institute

In a randomized controlled study in C57BL/6NCrSlc mice a decade earlier, Murata and colleagues evaluated the anti-androgenic activity and hair growth potential imparted by topical rosemary oil compared with finasteride and minoxidil. Rosemary oil leaf extract, with 12-O-methylcarnosic acid as its most active component, robustly suppressed 5alpha-reductase and stimulated hair growth in vivo in both the androgenetic alopecia/testosterone-treated mouse model, as well as the hair growth activating mouse model as compared with minoxidil. Further, the inhibitory activity of rosemary was 82.4% and 94.6% at 200 mcg/mL and 500 mcg/mL, respectively, whereas finasteride demonstrated 81.9% at 250 nM.¹⁶

A human study two years later was even more encouraging. Panahi and colleagues conducted a randomized comparative trial with 100 patients to investigate the effects of rosemary oil as opposed to minoxidil 2% for the treatment of androgenetic alopecia over 6 months. By 6 months, significantly greater hair counts were observed in both groups compared with baseline and 3-month readings, but no significant variations between groups. No differences were found in the frequency of dryness, greasiness, or dandruff at any time point or between groups. Scalp itching was significantly greater at the 3- and 6-month points in both groups, particularly in the minoxidil group at both of those time points. The investigators concluded that rosemary oil compared well with minoxidil as androgenetic alopecia therapy.¹⁷

Conclusion

Rosemary has been used in traditional medicine for hundreds of years and it has been a common ingredient in cosmetic and cosmeceutical formulations for more than 20 years. Recent findings suggest a broad array of applications in modern medicine, particularly dermatology. The next column will focus on the most recent studies pertaining to the antioxidant and anti-aging activity of this aromatic shrub.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a SaaS company used to generate skin care routines in office and as a ecommerce solution. Write to her at dermnews@mdedge.com.

References

1. Begum A et al. Adv Biomed Res. 2023 Mar 21;12:60.

2. de Oliveira JR et al. J Biomed Sci. 2019 Jan 9;26(1):5.

3. González-Minero FJ et al. Cosmetics. 2020 Oct 3;7(4):77.

4. Dinkins J et al. Int J Dermatol. 2023 Aug;62(8):980-5.

5. Akbari J et al. Pharm Biol. 2015;53(10):1442-7.

6. Allegra A et al. Nutrients. 2020 Jun 10;12(6):1739.

7. de Macedo LM et al. Plants (Basel). 2020 May 21;9(5):651.

8. Cattaneo L et al. PLoS One. 2015 Jul 15;10(7):e0132439.

9. Borges RS et al. J Ethnopharmacol. 2019 Jan 30;229:29-45.

10. Begum A et al. Acta Sci Pol Technol Aliment. 2013 Jan-Mar;12(1):61-73.

11. Bulhões AAVC et al. Acta Cir Bras. 2022 Apr 8;37(1):e370104.

12. Labib RM et al. PLoS One. 2019 Sep 16;14(9):e0219561.

13. Abu-Al-Basal MA. J Ethnopharmacol. 2010 Sep 15;131(2):443-50.

14. Sancheti G and Goyal PK. Phytother Res. 2006 Nov;20(11):981-6.

15. Moore J et al. Nutrients. 2016 Nov 17;8(11):731.

16. Murata K et al. Phytother Res. 2013 Feb;27(2):212-7.

17. Panahi Y et al. Skinmed. 2015 Jan-Feb;13(1):15-21.

*Correction, 2/27: This column was updated with the more recent name for rosemary, Salvia rosmarinus.

A member of the Lamiaceae family, Salvia rosmarinus (rosemary),* an aromatic plant native to the Mediterranean region and now cultivated globally, has been used for centuries in cuisine and medicine, with several well-established biological activities.^1-3 Thought to contribute to preventing hair loss, rosemary oil was also used for hundreds of years in hair rinses in the Mediterranean area.⁴ In traditional Iranian medicine, rosemary essential oil has been topically applied as an analgesic, anti-inflammatory, and anti-acne remedy.⁵ Rosemary is known to absorb UV light well and to impart antibacterial and antifungal activity, as well as help maintain skin homeostasis.³ It is also used and under further study for its anti-inflammatory, antioxidant, anti-infective, and anticancer activity.^2,6-9 The health benefits of rosemary are typically ascribed to its constituent carnosol/carnosic and ursolic acids.⁷In part 1 of this update on rosemary, the focus will be on chemical constituents, wound healing, anticancer activity, and hair care potential.

Chemical Constituents

The key chemical components of S. rosmarinus include bitter principle, resin, tannic acid, flavonoids, and volatile oils (made up of borneol, bornyl acetate, camphene, cineol, pinene, and camphor).¹⁰ Other important constituents of rosemary oil, in particular, include p-Cymene, linalool, gamma-terpinene, thymol, beta-pinene, alpha-pinene, eucalyptol, and carnosic acid.⁹ Volatile oils of rosemary have been used in various oils and lotions to treat wounds and with the intention of stimulating hair growth.¹⁰

Wound Healing

In a 2022 study in 60 adult male rats, Bulhões and colleagues found that the use of rosemary leaf essential oil-based ointments on skin lesions spurred wound healing, decreased inflammation, and enhanced angiogenesis as well as collagen fiber density.¹¹

Three years earlier, Labib and colleagues studied the wound healing capacity of three chitosan-based topical formulations containing either tea tree essential oil, rosemary essential oil, or a mixture of both oils in an excision wound model in rats.

HUIZENG HU/Moment/Getty Images

The combination preparation was found to be the most effective in fostering various stages of wound healing, with significant increases in wound contraction percentage observed in the combination group compared with either group treated using individual essential oils or the untreated animals.¹²

A 2010 in vivo study by Abu-Al-Basal using BALB/c mice with diabetes revealed that the topical application of rosemary essential oil for three days reduced inflammation, enhanced wound contraction and re-epithelialization, and promoted angiogenesis, granulation tissue regeneration, and collagen deposition.¹³

Anticancer Activity

Using a 7,12-dimethlybenz(a)anthracene (DMBA)-initiated and croton oil-promoted model in 2006, Sancheti and Goyal determined that rosemary extract administered orally at a dose rate of 500 mg/kg body weight/mouse significantly inhibited two-stage skin tumorigenesis in mice.¹⁴ Nearly a decade later, Cattaneo and colleagues determined that a rosemary hydroalcoholic extract displayed antiproliferative effects on the human melanoma A375 cell line.⁸

The polyphenols carnosic acid and rosmarinic acid are most often cited as the sources of the reputed anticancer effects of rosemary.¹⁵

Hair Health

Early in 2023, Begum and colleagues developed a 1% hair lotion including a methanolic extract of the aerial part of S. rosmarinus that they assessed for potential hair growth activity in C57BL/6 mice. Using water as a control and 2% minoxidil hair lotion as standard, the investigators determined that their rosemary hair lotion demonstrated significant hair growth promotion, exceeding that seen in the mice treated with the drug standard.¹

Baumann Cosmetic &amp; Research Institute

In a randomized controlled study in C57BL/6NCrSlc mice a decade earlier, Murata and colleagues evaluated the anti-androgenic activity and hair growth potential imparted by topical rosemary oil compared with finasteride and minoxidil. Rosemary oil leaf extract, with 12-O-methylcarnosic acid as its most active component, robustly suppressed 5alpha-reductase and stimulated hair growth in vivo in both the androgenetic alopecia/testosterone-treated mouse model, as well as the hair growth activating mouse model as compared with minoxidil. Further, the inhibitory activity of rosemary was 82.4% and 94.6% at 200 mcg/mL and 500 mcg/mL, respectively, whereas finasteride demonstrated 81.9% at 250 nM.¹⁶

A human study two years later was even more encouraging. Panahi and colleagues conducted a randomized comparative trial with 100 patients to investigate the effects of rosemary oil as opposed to minoxidil 2% for the treatment of androgenetic alopecia over 6 months. By 6 months, significantly greater hair counts were observed in both groups compared with baseline and 3-month readings, but no significant variations between groups. No differences were found in the frequency of dryness, greasiness, or dandruff at any time point or between groups. Scalp itching was significantly greater at the 3- and 6-month points in both groups, particularly in the minoxidil group at both of those time points. The investigators concluded that rosemary oil compared well with minoxidil as androgenetic alopecia therapy.¹⁷

Conclusion

Rosemary has been used in traditional medicine for hundreds of years and it has been a common ingredient in cosmetic and cosmeceutical formulations for more than 20 years. Recent findings suggest a broad array of applications in modern medicine, particularly dermatology. The next column will focus on the most recent studies pertaining to the antioxidant and anti-aging activity of this aromatic shrub.

Dr. Baumann is a private practice dermatologist, researcher, author, and entrepreneur in Miami. She founded the division of cosmetic dermatology at the University of Miami in 1997. The third edition of her bestselling textbook, “Cosmetic Dermatology,” was published in 2022. Dr. Baumann has received funding for advisory boards and/or clinical research trials from Allergan, Galderma, Johnson & Johnson, and Burt’s Bees. She is the CEO of Skin Type Solutions Inc., a SaaS company used to generate skin care routines in office and as a ecommerce solution. Write to her at dermnews@mdedge.com.

References

1. Begum A et al. Adv Biomed Res. 2023 Mar 21;12:60.

2. de Oliveira JR et al. J Biomed Sci. 2019 Jan 9;26(1):5.

3. González-Minero FJ et al. Cosmetics. 2020 Oct 3;7(4):77.

4. Dinkins J et al. Int J Dermatol. 2023 Aug;62(8):980-5.

5. Akbari J et al. Pharm Biol. 2015;53(10):1442-7.

6. Allegra A et al. Nutrients. 2020 Jun 10;12(6):1739.

7. de Macedo LM et al. Plants (Basel). 2020 May 21;9(5):651.

8. Cattaneo L et al. PLoS One. 2015 Jul 15;10(7):e0132439.

9. Borges RS et al. J Ethnopharmacol. 2019 Jan 30;229:29-45.

10. Begum A et al. Acta Sci Pol Technol Aliment. 2013 Jan-Mar;12(1):61-73.

11. Bulhões AAVC et al. Acta Cir Bras. 2022 Apr 8;37(1):e370104.

12. Labib RM et al. PLoS One. 2019 Sep 16;14(9):e0219561.

13. Abu-Al-Basal MA. J Ethnopharmacol. 2010 Sep 15;131(2):443-50.

14. Sancheti G and Goyal PK. Phytother Res. 2006 Nov;20(11):981-6.

15. Moore J et al. Nutrients. 2016 Nov 17;8(11):731.

16. Murata K et al. Phytother Res. 2013 Feb;27(2):212-7.

17. Panahi Y et al. Skinmed. 2015 Jan-Feb;13(1):15-21.

*Correction, 2/27: This column was updated with the more recent name for rosemary, Salvia rosmarinus.