Hair & Nails

To the Editor:
Longitudinal melanonychia encompasses a broad spectrum of diseases and often is a complex diagnostic problem. Differential diagnoses include ethnic-type nail pigmentation, which is more frequently seen in darker-skinned individuals; drug-induced pigmentation; subungual hemorrhage; fungal or bacterial infection; nevus; and melanoma.^1,2 Fungal melan-onychia is an uncommon presentation of onychomycosis. Dermoscopy can assist in the evaluation of nail pigmentation caused by fungi to avoid unnecessary nail biopsies.

A 39-year-old man visited the dermatology clinic with a concern for melanoma because of blackish pigmentation of the toenails of 1 month’s duration. He denied history of trauma and was not taking any medications. On physical examination the second and third toenails revealed a 2-mm longitudinal band of black pigment on the lateral side; the fifth toenail showed diffuse black pigment (Figure 1A). The nail plates were thickened. Dermoscopy revealed prominent subungual hyperkeratosis, a homogeneous brown-black band with wide yellow streaks that were wider in the distal ends, and some focal reddish hue. No visible melanin inclusions were observed (Figure 2). These findings were suggestive of fungal infection. Cultures from the diseased nail grew a fungus identified as Trichophyton rubrum. The patient was treated with itraconazole 200 mg daily for 3 months. Clinical cure with disappearance of pigment was obtained at 5-month follow-up (Figure 1B).

Figure 1. Blackish discoloration of the right second, third, and fifth toenails (A). Resolution of pigmentation and subungual hyperkeratosis was achieved at 5-month follow-up after treatment (B).

Figure 2. Top view (A) and front view (B) of a homogeneous brown-black band with subungual hyperkeratosis and wide intervening yellow streaks. Each ruler mark denotes 1 mm.

Our patient illustrates the value of dermoscopy in evaluating melanonychia. The pigmentation of adult-onset melanonychia involving multiple fingers can be divided into nonmelanocytic or melanocytic origin. Causes of the former include subungual hematoma, fungal or bacterial infection, and exogenous pigmentation. The nonmelanocytic pigment often is homogeneously distributed without melanin inclusions under the dermoscope.²

On the contrary, melanin inclusions can be detected as fine granules in pigmentation of melanocytic origin, either from focal melanocytic activation or melanocyte proliferation. Causes of focal melanocytic activation include ethnic-type nail hyperpigmentation; inflammatory nail diseases; or drug-, radiation-, and friction-induced hyperpigmentation. The characteristic dermoscopic features are thin longitudinal gray lines with regular thickness and spacing in a grayish background.^1-3

Melanocyte proliferation can result in a nevus or melanoma of the nail apparatus. Both share dermoscopic features of brown-black longitudinal lines in a brown background. However, the longitudinal lines in melanoma are irregular in coloration, spacing, thickness, and parallelism, in contrast with the regular pattern of a nevus.^1-4 Although patients often are concerned about melanoma, involvement of multiple fingers at the same time is less likely.

In our patient, the homogeneous deep brown color without melanin inclusions favored a nonmel-anocytic origin. The distally wider pigmentation suggested fungal infection because most ungual infections extend from the distal to the proximal part of the nail.^5,6 The focal reddish hue may be related with traumatic hemorrhage from subungual hyperkeratosis.

Cases of fungal melanonychia are being reported at an increasing rate. Some fungal strains are capable of synthesizing melanin, which is associated with virulence and acts as a fungal armor against toxic insults.⁵ In T rubrum, the melanoid variant, the diffusible black pigment infiltrates the nail plate and attributes to the black nail clinically.⁴ The most frequently isolated fungi in fungal melanonychia are T rubrum and Scytalidium dimidiatum⁶; however, Candida species,^7,8 dematiaceous fungus,⁹ and other dermatophytes such as Trichophyton soudanense¹⁰ have been reported to be the cause.⁵

Our patient presented with fungal melanonychia due to T rubrum with dermoscopic features. The prominent subungual hyperkeratosis, distally wider homogeneous brown-black pigmented band, and wide yellow streaks with focal reddish hue all suggested fungal melanonychia. The diagnosis was further confirmed by a good response to antifungal agents.

To the Editor:
Longitudinal melanonychia encompasses a broad spectrum of diseases and often is a complex diagnostic problem. Differential diagnoses include ethnic-type nail pigmentation, which is more frequently seen in darker-skinned individuals; drug-induced pigmentation; subungual hemorrhage; fungal or bacterial infection; nevus; and melanoma.^1,2 Fungal melan-onychia is an uncommon presentation of onychomycosis. Dermoscopy can assist in the evaluation of nail pigmentation caused by fungi to avoid unnecessary nail biopsies.

A 39-year-old man visited the dermatology clinic with a concern for melanoma because of blackish pigmentation of the toenails of 1 month’s duration. He denied history of trauma and was not taking any medications. On physical examination the second and third toenails revealed a 2-mm longitudinal band of black pigment on the lateral side; the fifth toenail showed diffuse black pigment (Figure 1A). The nail plates were thickened. Dermoscopy revealed prominent subungual hyperkeratosis, a homogeneous brown-black band with wide yellow streaks that were wider in the distal ends, and some focal reddish hue. No visible melanin inclusions were observed (Figure 2). These findings were suggestive of fungal infection. Cultures from the diseased nail grew a fungus identified as Trichophyton rubrum. The patient was treated with itraconazole 200 mg daily for 3 months. Clinical cure with disappearance of pigment was obtained at 5-month follow-up (Figure 1B).

Figure 1. Blackish discoloration of the right second, third, and fifth toenails (A). Resolution of pigmentation and subungual hyperkeratosis was achieved at 5-month follow-up after treatment (B).

Figure 2. Top view (A) and front view (B) of a homogeneous brown-black band with subungual hyperkeratosis and wide intervening yellow streaks. Each ruler mark denotes 1 mm.

Our patient illustrates the value of dermoscopy in evaluating melanonychia. The pigmentation of adult-onset melanonychia involving multiple fingers can be divided into nonmelanocytic or melanocytic origin. Causes of the former include subungual hematoma, fungal or bacterial infection, and exogenous pigmentation. The nonmelanocytic pigment often is homogeneously distributed without melanin inclusions under the dermoscope.²

On the contrary, melanin inclusions can be detected as fine granules in pigmentation of melanocytic origin, either from focal melanocytic activation or melanocyte proliferation. Causes of focal melanocytic activation include ethnic-type nail hyperpigmentation; inflammatory nail diseases; or drug-, radiation-, and friction-induced hyperpigmentation. The characteristic dermoscopic features are thin longitudinal gray lines with regular thickness and spacing in a grayish background.^1-3

Melanocyte proliferation can result in a nevus or melanoma of the nail apparatus. Both share dermoscopic features of brown-black longitudinal lines in a brown background. However, the longitudinal lines in melanoma are irregular in coloration, spacing, thickness, and parallelism, in contrast with the regular pattern of a nevus.^1-4 Although patients often are concerned about melanoma, involvement of multiple fingers at the same time is less likely.

In our patient, the homogeneous deep brown color without melanin inclusions favored a nonmel-anocytic origin. The distally wider pigmentation suggested fungal infection because most ungual infections extend from the distal to the proximal part of the nail.^5,6 The focal reddish hue may be related with traumatic hemorrhage from subungual hyperkeratosis.

Cases of fungal melanonychia are being reported at an increasing rate. Some fungal strains are capable of synthesizing melanin, which is associated with virulence and acts as a fungal armor against toxic insults.⁵ In T rubrum, the melanoid variant, the diffusible black pigment infiltrates the nail plate and attributes to the black nail clinically.⁴ The most frequently isolated fungi in fungal melanonychia are T rubrum and Scytalidium dimidiatum⁶; however, Candida species,^7,8 dematiaceous fungus,⁹ and other dermatophytes such as Trichophyton soudanense¹⁰ have been reported to be the cause.⁵

Our patient presented with fungal melanonychia due to T rubrum with dermoscopic features. The prominent subungual hyperkeratosis, distally wider homogeneous brown-black pigmented band, and wide yellow streaks with focal reddish hue all suggested fungal melanonychia. The diagnosis was further confirmed by a good response to antifungal agents.

To the Editor:
Longitudinal melanonychia encompasses a broad spectrum of diseases and often is a complex diagnostic problem. Differential diagnoses include ethnic-type nail pigmentation, which is more frequently seen in darker-skinned individuals; drug-induced pigmentation; subungual hemorrhage; fungal or bacterial infection; nevus; and melanoma.^1,2 Fungal melan-onychia is an uncommon presentation of onychomycosis. Dermoscopy can assist in the evaluation of nail pigmentation caused by fungi to avoid unnecessary nail biopsies.

A 39-year-old man visited the dermatology clinic with a concern for melanoma because of blackish pigmentation of the toenails of 1 month’s duration. He denied history of trauma and was not taking any medications. On physical examination the second and third toenails revealed a 2-mm longitudinal band of black pigment on the lateral side; the fifth toenail showed diffuse black pigment (Figure 1A). The nail plates were thickened. Dermoscopy revealed prominent subungual hyperkeratosis, a homogeneous brown-black band with wide yellow streaks that were wider in the distal ends, and some focal reddish hue. No visible melanin inclusions were observed (Figure 2). These findings were suggestive of fungal infection. Cultures from the diseased nail grew a fungus identified as Trichophyton rubrum. The patient was treated with itraconazole 200 mg daily for 3 months. Clinical cure with disappearance of pigment was obtained at 5-month follow-up (Figure 1B).

Figure 1. Blackish discoloration of the right second, third, and fifth toenails (A). Resolution of pigmentation and subungual hyperkeratosis was achieved at 5-month follow-up after treatment (B).

Figure 2. Top view (A) and front view (B) of a homogeneous brown-black band with subungual hyperkeratosis and wide intervening yellow streaks. Each ruler mark denotes 1 mm.

Our patient illustrates the value of dermoscopy in evaluating melanonychia. The pigmentation of adult-onset melanonychia involving multiple fingers can be divided into nonmelanocytic or melanocytic origin. Causes of the former include subungual hematoma, fungal or bacterial infection, and exogenous pigmentation. The nonmelanocytic pigment often is homogeneously distributed without melanin inclusions under the dermoscope.²

On the contrary, melanin inclusions can be detected as fine granules in pigmentation of melanocytic origin, either from focal melanocytic activation or melanocyte proliferation. Causes of focal melanocytic activation include ethnic-type nail hyperpigmentation; inflammatory nail diseases; or drug-, radiation-, and friction-induced hyperpigmentation. The characteristic dermoscopic features are thin longitudinal gray lines with regular thickness and spacing in a grayish background.^1-3

Melanocyte proliferation can result in a nevus or melanoma of the nail apparatus. Both share dermoscopic features of brown-black longitudinal lines in a brown background. However, the longitudinal lines in melanoma are irregular in coloration, spacing, thickness, and parallelism, in contrast with the regular pattern of a nevus.^1-4 Although patients often are concerned about melanoma, involvement of multiple fingers at the same time is less likely.

In our patient, the homogeneous deep brown color without melanin inclusions favored a nonmel-anocytic origin. The distally wider pigmentation suggested fungal infection because most ungual infections extend from the distal to the proximal part of the nail.^5,6 The focal reddish hue may be related with traumatic hemorrhage from subungual hyperkeratosis.

Cases of fungal melanonychia are being reported at an increasing rate. Some fungal strains are capable of synthesizing melanin, which is associated with virulence and acts as a fungal armor against toxic insults.⁵ In T rubrum, the melanoid variant, the diffusible black pigment infiltrates the nail plate and attributes to the black nail clinically.⁴ The most frequently isolated fungi in fungal melanonychia are T rubrum and Scytalidium dimidiatum⁶; however, Candida species,^7,8 dematiaceous fungus,⁹ and other dermatophytes such as Trichophyton soudanense¹⁰ have been reported to be the cause.⁵

Our patient presented with fungal melanonychia due to T rubrum with dermoscopic features. The prominent subungual hyperkeratosis, distally wider homogeneous brown-black pigmented band, and wide yellow streaks with focal reddish hue all suggested fungal melanonychia. The diagnosis was further confirmed by a good response to antifungal agents.

To the Editor:
Macro- or microtrauma to nails can cause and/or exacerbate chronic diseases such as ingrown nails, onycholysis, onychauxis, onychogryposis, and hallux valgus (bunions). This trauma also can break the anatomic barrier of the hyponychium, thereby creating a portal for dermatophytes and other organisms to penetrate the nail apparatus.¹

For many years, one author (C.R.D.) has used the following demonstration to communicate to patients how improper shoe fit may cause toenail trauma. The patient’s shoe is flipped 180° and placed toe-to-toe with the patient’s foot (Figure). Most patients can comprehend the relationship between their shoe fit and their toenail disease when they see this demonstration. We have termed it toe-to-toe sign.

The foot and shoe are toe-to-toe, demonstrating the narrow toe box in comparison to the actual toes (A). This comparison is accentuated when the shoe is placed over the foot with toes splayed from standing (B).

Narrow toe box is the usual culprit. The toe-to-toe sign best emphasizes this relationship. This sign serves as a powerful tool when demonstrating how much the foot widens when bearing full weight, and how forces of ambulation and foot strike can damage the nails with narrow-toed footwear. This trauma is compounded with high-heeled shoes that force the toes forward. However, proper shoe fit may compete with idealized shoe style. It is not until patients realize the relationship between improper shoe fit, foot strike, and toe/toenail trauma that they can make long-term decisions that favorably impact their toes and toenails.

To the Editor:
Macro- or microtrauma to nails can cause and/or exacerbate chronic diseases such as ingrown nails, onycholysis, onychauxis, onychogryposis, and hallux valgus (bunions). This trauma also can break the anatomic barrier of the hyponychium, thereby creating a portal for dermatophytes and other organisms to penetrate the nail apparatus.¹

For many years, one author (C.R.D.) has used the following demonstration to communicate to patients how improper shoe fit may cause toenail trauma. The patient’s shoe is flipped 180° and placed toe-to-toe with the patient’s foot (Figure). Most patients can comprehend the relationship between their shoe fit and their toenail disease when they see this demonstration. We have termed it toe-to-toe sign.

The foot and shoe are toe-to-toe, demonstrating the narrow toe box in comparison to the actual toes (A). This comparison is accentuated when the shoe is placed over the foot with toes splayed from standing (B).

Narrow toe box is the usual culprit. The toe-to-toe sign best emphasizes this relationship. This sign serves as a powerful tool when demonstrating how much the foot widens when bearing full weight, and how forces of ambulation and foot strike can damage the nails with narrow-toed footwear. This trauma is compounded with high-heeled shoes that force the toes forward. However, proper shoe fit may compete with idealized shoe style. It is not until patients realize the relationship between improper shoe fit, foot strike, and toe/toenail trauma that they can make long-term decisions that favorably impact their toes and toenails.

To the Editor:
Macro- or microtrauma to nails can cause and/or exacerbate chronic diseases such as ingrown nails, onycholysis, onychauxis, onychogryposis, and hallux valgus (bunions). This trauma also can break the anatomic barrier of the hyponychium, thereby creating a portal for dermatophytes and other organisms to penetrate the nail apparatus.¹

For many years, one author (C.R.D.) has used the following demonstration to communicate to patients how improper shoe fit may cause toenail trauma. The patient’s shoe is flipped 180° and placed toe-to-toe with the patient’s foot (Figure). Most patients can comprehend the relationship between their shoe fit and their toenail disease when they see this demonstration. We have termed it toe-to-toe sign.

The foot and shoe are toe-to-toe, demonstrating the narrow toe box in comparison to the actual toes (A). This comparison is accentuated when the shoe is placed over the foot with toes splayed from standing (B).

Narrow toe box is the usual culprit. The toe-to-toe sign best emphasizes this relationship. This sign serves as a powerful tool when demonstrating how much the foot widens when bearing full weight, and how forces of ambulation and foot strike can damage the nails with narrow-toed footwear. This trauma is compounded with high-heeled shoes that force the toes forward. However, proper shoe fit may compete with idealized shoe style. It is not until patients realize the relationship between improper shoe fit, foot strike, and toe/toenail trauma that they can make long-term decisions that favorably impact their toes and toenails.

COEUR D’ALENE, IDAHO – Conventional wisdom holds that onychomycosis is rare in children. Not so.

Fully one-third of children and adolescents who presented with a nail complaint to a prominent dermatologic nail disorders center were diagnosed with mycologically confirmed onychomycosis, Dr. Julie Jefferson reported at the annual meeting of the Society for Pediatric Dermatology.

Courtesy Wikimedia Commons/pepsyrock/ Creative Commons License

That’s a substantially higher prevalence than the 15.5% figure reported by Spanish investigators in a 20-year retrospective study (Mycoses 2011;54:450-3). It’s also well below the 47% prevalence recently reported in Denver in a 5-year retrospective study, where Trychophyton rubrum was the most common pathogen, and the highest prevalence of onychomycosis in the pediatric population was seen in 6- to 10-year-olds (Pediatr. Dermatol. 2014;31:106-8), noted Dr. Jefferson of Johns Hopkins University, Baltimore.

The investigators in both Span and Denver observed that the prevalence of pediatric onychomycosis appears to be increasing in recent years.

Dr. Jefferson presented a retrospective study that included 917 patients up to age 18 years who presented to the Oregon Dermatology and Research Center, Portland, in a recent 6-year period. One or more nail disorders were diagnosed in 11%. The mean age at presentation was 9.4 years, with a mean 2.4-year duration of the condition prior to presentation. Toenails were affected in 47 patients, fingernails in 37, and both in 18. Fourteen patients had two nail disorders, 9 had three, and 2 had four distinct nail disorders.

The etiologies ranged widely, from infections to congenital and hereditary malformations, tumors, inflammatory processes, and systemic diseases.

The most common nail condition was onychomycosis, diagnosed in 34 patients. Thus, 3.7% of all pediatric patients presenting to the dermatology center for any reason were diagnosed with onychomycosis, a higher rate than previously reported by others.

Other conditions included 13 cases of longitudinal melanonychia, 11 of disappearing nail bed, 9 of retronychia, 8 cases of congenital malalignment, 8 cases of trachyonychia, 7 of paronychia, 5 cases of psoriasis, and 2 of lichen planus.

Three of four patients with an ingrown toenail also had congenital malalignment of the affected great toenail, supporting the notion put forth by other investigators that congenital malalignment of the great toenail predisposes to ingrown toenails, according to Dr. Jefferson.

She reported having no financial conflicts related to this study.

[email protected]

COEUR D’ALENE, IDAHO – Conventional wisdom holds that onychomycosis is rare in children. Not so.

Fully one-third of children and adolescents who presented with a nail complaint to a prominent dermatologic nail disorders center were diagnosed with mycologically confirmed onychomycosis, Dr. Julie Jefferson reported at the annual meeting of the Society for Pediatric Dermatology.

Courtesy Wikimedia Commons/pepsyrock/ Creative Commons License

That’s a substantially higher prevalence than the 15.5% figure reported by Spanish investigators in a 20-year retrospective study (Mycoses 2011;54:450-3). It’s also well below the 47% prevalence recently reported in Denver in a 5-year retrospective study, where Trychophyton rubrum was the most common pathogen, and the highest prevalence of onychomycosis in the pediatric population was seen in 6- to 10-year-olds (Pediatr. Dermatol. 2014;31:106-8), noted Dr. Jefferson of Johns Hopkins University, Baltimore.

The investigators in both Span and Denver observed that the prevalence of pediatric onychomycosis appears to be increasing in recent years.

Dr. Jefferson presented a retrospective study that included 917 patients up to age 18 years who presented to the Oregon Dermatology and Research Center, Portland, in a recent 6-year period. One or more nail disorders were diagnosed in 11%. The mean age at presentation was 9.4 years, with a mean 2.4-year duration of the condition prior to presentation. Toenails were affected in 47 patients, fingernails in 37, and both in 18. Fourteen patients had two nail disorders, 9 had three, and 2 had four distinct nail disorders.

The etiologies ranged widely, from infections to congenital and hereditary malformations, tumors, inflammatory processes, and systemic diseases.

The most common nail condition was onychomycosis, diagnosed in 34 patients. Thus, 3.7% of all pediatric patients presenting to the dermatology center for any reason were diagnosed with onychomycosis, a higher rate than previously reported by others.

Other conditions included 13 cases of longitudinal melanonychia, 11 of disappearing nail bed, 9 of retronychia, 8 cases of congenital malalignment, 8 cases of trachyonychia, 7 of paronychia, 5 cases of psoriasis, and 2 of lichen planus.

Three of four patients with an ingrown toenail also had congenital malalignment of the affected great toenail, supporting the notion put forth by other investigators that congenital malalignment of the great toenail predisposes to ingrown toenails, according to Dr. Jefferson.

She reported having no financial conflicts related to this study.

[email protected]

COEUR D’ALENE, IDAHO – Conventional wisdom holds that onychomycosis is rare in children. Not so.

Fully one-third of children and adolescents who presented with a nail complaint to a prominent dermatologic nail disorders center were diagnosed with mycologically confirmed onychomycosis, Dr. Julie Jefferson reported at the annual meeting of the Society for Pediatric Dermatology.

Courtesy Wikimedia Commons/pepsyrock/ Creative Commons License

That’s a substantially higher prevalence than the 15.5% figure reported by Spanish investigators in a 20-year retrospective study (Mycoses 2011;54:450-3). It’s also well below the 47% prevalence recently reported in Denver in a 5-year retrospective study, where Trychophyton rubrum was the most common pathogen, and the highest prevalence of onychomycosis in the pediatric population was seen in 6- to 10-year-olds (Pediatr. Dermatol. 2014;31:106-8), noted Dr. Jefferson of Johns Hopkins University, Baltimore.

The investigators in both Span and Denver observed that the prevalence of pediatric onychomycosis appears to be increasing in recent years.

Dr. Jefferson presented a retrospective study that included 917 patients up to age 18 years who presented to the Oregon Dermatology and Research Center, Portland, in a recent 6-year period. One or more nail disorders were diagnosed in 11%. The mean age at presentation was 9.4 years, with a mean 2.4-year duration of the condition prior to presentation. Toenails were affected in 47 patients, fingernails in 37, and both in 18. Fourteen patients had two nail disorders, 9 had three, and 2 had four distinct nail disorders.

The etiologies ranged widely, from infections to congenital and hereditary malformations, tumors, inflammatory processes, and systemic diseases.

The most common nail condition was onychomycosis, diagnosed in 34 patients. Thus, 3.7% of all pediatric patients presenting to the dermatology center for any reason were diagnosed with onychomycosis, a higher rate than previously reported by others.

Other conditions included 13 cases of longitudinal melanonychia, 11 of disappearing nail bed, 9 of retronychia, 8 cases of congenital malalignment, 8 cases of trachyonychia, 7 of paronychia, 5 cases of psoriasis, and 2 of lichen planus.

Three of four patients with an ingrown toenail also had congenital malalignment of the affected great toenail, supporting the notion put forth by other investigators that congenital malalignment of the great toenail predisposes to ingrown toenails, according to Dr. Jefferson.

She reported having no financial conflicts related to this study.

[email protected]

COEUR D’ALENE, IDAHO – Systemic corticosteroids usually bring an impressive initial response for children with alopecia areata. The big question is, ‘What do you try next?’

Children can’t safely remain on long-term systemic steroids. And the great majority of responders will relapse once steroids are discontinued. The challenge is to find a safe, well-tolerated drug with long-term effectiveness as a maintenance therapy.

"For me, when I look at the list of drugs for maintenance therapy in alopecia areata, which includes cyclosporine, azathioprine, and sulfasalazine, the drug I’m most comfortable giving to children for a prolonged time is methotrexate. That’s why this drug has really become my go-to maintenance therapy for patients with alopecia areata," Dr. Ruth Ann Vleugels said at the annual meeting of the Society for Pediatric Dermatology.

"I will give them 2-3 months of systemic steroids as a boost while their methotrexate kicks in; but after that, it’s maintenance therapy with methotrexate at 1 mg/kg/week," added Dr. Vleugels, director of the Autoimmune Skin Disease Program at Brigham and Women’s Hospital, Boston.

Of course, methotrexate doesn’t work as maintenance therapy for all children with alopecia areata. Patients who don’t respond to the initial several months of combination therapy with systemic steroids won’t respond to maintenance therapy with methotrexate alone.

For those few patients who need second-line maintenance therapy, Dr. Vleugels’ drug of choice is the transplant anti-rejection medication mycophenolate mofetil (CellCept), which is used off-label for alopecia areata. Mycophenolate mofetil also is her rescue agent as maintenance therapy for children with systemic lupus erythematosus, cutaneous lupus erythematosus, juvenile dermatomyositis, and linear morphea with progressive hemifacial atrophy.

In patients with progressive juvenile systemic sclerosis, Dr. Vleugels and her Boston colleagues now use mycophenolate mofetil, rather than methotrexate, as their first-line therapy based upon favorable results in their practice and prospective studies in adults (J. Rheumatol. 2012;39:1241-7).

The mycophenolate mofetil dosing in children with alopecia areata is 600 mg/m² given twice daily, or 1 g twice daily in patients bigger than 1.5 m². She uses half the dose for the first 2-3 weeks, then titrates up to full-dose therapy in order to minimize GI side effects, which she said are far and away the most common adverse effects. Smaller children do best with the liquid formulation.

A common clinical dilemma involves the child who experiences intolerable GI upset on mycophenolate mofetil. Dr. Vleugels offered two suggestions: One is to tell the parents to ignore the package insert and have their child take the drug with meals.

"No one can handle this drug on an empty stomach," she said.

A caveat: mycophenolate mofetil cannot be taken with antacids.

If mealtime dosing doesn’t solve the GI upset problem, the alternative is to switch to mycophenolic acid (Myfortic), which is enteric-coated, has better bioavailability, and is better tolerated. It’s also more expensive than mycophenolate mofetil and will require prior authorization from payers. The dose conversion is as follows: 500 mg mycophenolate mofetil equals 360 mg of mycophenolic acid.

Dr. Vleugels reported having no financial conflicts with regard to her presentation.

[email protected]

COEUR D’ALENE, IDAHO – Systemic corticosteroids usually bring an impressive initial response for children with alopecia areata. The big question is, ‘What do you try next?’

Children can’t safely remain on long-term systemic steroids. And the great majority of responders will relapse once steroids are discontinued. The challenge is to find a safe, well-tolerated drug with long-term effectiveness as a maintenance therapy.

"For me, when I look at the list of drugs for maintenance therapy in alopecia areata, which includes cyclosporine, azathioprine, and sulfasalazine, the drug I’m most comfortable giving to children for a prolonged time is methotrexate. That’s why this drug has really become my go-to maintenance therapy for patients with alopecia areata," Dr. Ruth Ann Vleugels said at the annual meeting of the Society for Pediatric Dermatology.

"I will give them 2-3 months of systemic steroids as a boost while their methotrexate kicks in; but after that, it’s maintenance therapy with methotrexate at 1 mg/kg/week," added Dr. Vleugels, director of the Autoimmune Skin Disease Program at Brigham and Women’s Hospital, Boston.

Of course, methotrexate doesn’t work as maintenance therapy for all children with alopecia areata. Patients who don’t respond to the initial several months of combination therapy with systemic steroids won’t respond to maintenance therapy with methotrexate alone.

For those few patients who need second-line maintenance therapy, Dr. Vleugels’ drug of choice is the transplant anti-rejection medication mycophenolate mofetil (CellCept), which is used off-label for alopecia areata. Mycophenolate mofetil also is her rescue agent as maintenance therapy for children with systemic lupus erythematosus, cutaneous lupus erythematosus, juvenile dermatomyositis, and linear morphea with progressive hemifacial atrophy.

In patients with progressive juvenile systemic sclerosis, Dr. Vleugels and her Boston colleagues now use mycophenolate mofetil, rather than methotrexate, as their first-line therapy based upon favorable results in their practice and prospective studies in adults (J. Rheumatol. 2012;39:1241-7).

The mycophenolate mofetil dosing in children with alopecia areata is 600 mg/m² given twice daily, or 1 g twice daily in patients bigger than 1.5 m². She uses half the dose for the first 2-3 weeks, then titrates up to full-dose therapy in order to minimize GI side effects, which she said are far and away the most common adverse effects. Smaller children do best with the liquid formulation.

A common clinical dilemma involves the child who experiences intolerable GI upset on mycophenolate mofetil. Dr. Vleugels offered two suggestions: One is to tell the parents to ignore the package insert and have their child take the drug with meals.

"No one can handle this drug on an empty stomach," she said.

A caveat: mycophenolate mofetil cannot be taken with antacids.

If mealtime dosing doesn’t solve the GI upset problem, the alternative is to switch to mycophenolic acid (Myfortic), which is enteric-coated, has better bioavailability, and is better tolerated. It’s also more expensive than mycophenolate mofetil and will require prior authorization from payers. The dose conversion is as follows: 500 mg mycophenolate mofetil equals 360 mg of mycophenolic acid.

Dr. Vleugels reported having no financial conflicts with regard to her presentation.

[email protected]

COEUR D’ALENE, IDAHO – Systemic corticosteroids usually bring an impressive initial response for children with alopecia areata. The big question is, ‘What do you try next?’

Children can’t safely remain on long-term systemic steroids. And the great majority of responders will relapse once steroids are discontinued. The challenge is to find a safe, well-tolerated drug with long-term effectiveness as a maintenance therapy.

"For me, when I look at the list of drugs for maintenance therapy in alopecia areata, which includes cyclosporine, azathioprine, and sulfasalazine, the drug I’m most comfortable giving to children for a prolonged time is methotrexate. That’s why this drug has really become my go-to maintenance therapy for patients with alopecia areata," Dr. Ruth Ann Vleugels said at the annual meeting of the Society for Pediatric Dermatology.

"I will give them 2-3 months of systemic steroids as a boost while their methotrexate kicks in; but after that, it’s maintenance therapy with methotrexate at 1 mg/kg/week," added Dr. Vleugels, director of the Autoimmune Skin Disease Program at Brigham and Women’s Hospital, Boston.

Of course, methotrexate doesn’t work as maintenance therapy for all children with alopecia areata. Patients who don’t respond to the initial several months of combination therapy with systemic steroids won’t respond to maintenance therapy with methotrexate alone.

For those few patients who need second-line maintenance therapy, Dr. Vleugels’ drug of choice is the transplant anti-rejection medication mycophenolate mofetil (CellCept), which is used off-label for alopecia areata. Mycophenolate mofetil also is her rescue agent as maintenance therapy for children with systemic lupus erythematosus, cutaneous lupus erythematosus, juvenile dermatomyositis, and linear morphea with progressive hemifacial atrophy.

In patients with progressive juvenile systemic sclerosis, Dr. Vleugels and her Boston colleagues now use mycophenolate mofetil, rather than methotrexate, as their first-line therapy based upon favorable results in their practice and prospective studies in adults (J. Rheumatol. 2012;39:1241-7).

The mycophenolate mofetil dosing in children with alopecia areata is 600 mg/m² given twice daily, or 1 g twice daily in patients bigger than 1.5 m². She uses half the dose for the first 2-3 weeks, then titrates up to full-dose therapy in order to minimize GI side effects, which she said are far and away the most common adverse effects. Smaller children do best with the liquid formulation.

A common clinical dilemma involves the child who experiences intolerable GI upset on mycophenolate mofetil. Dr. Vleugels offered two suggestions: One is to tell the parents to ignore the package insert and have their child take the drug with meals.

"No one can handle this drug on an empty stomach," she said.

A caveat: mycophenolate mofetil cannot be taken with antacids.

If mealtime dosing doesn’t solve the GI upset problem, the alternative is to switch to mycophenolic acid (Myfortic), which is enteric-coated, has better bioavailability, and is better tolerated. It’s also more expensive than mycophenolate mofetil and will require prior authorization from payers. The dose conversion is as follows: 500 mg mycophenolate mofetil equals 360 mg of mycophenolic acid.

Dr. Vleugels reported having no financial conflicts with regard to her presentation.

[email protected]

COEUR D’ALENE, IDAHO – The most important test in determining the cause of diffuse hair loss in children and adolescents is a gentle hair pull, Dr. Elise A. Olsen said at the annual meeting of the Society for Pediatric Dermatology.

"This is something you should do in all patients with alopecia, accompanied by looking under the microscope at the hair you’ve pulled. Grasp a small clump of hair close to the scalp and gently pull through to the ends. It’s important that you do it not just in one area but all over, in various places on the scalp. Coming away with three or four hairs per pull is abnormal. Be especially gentle in young children because you can actually induce what looks like a loose anagen syndrome, confusing the picture," explained Dr. Olsen, professor of dermatology and medicine and director of the hair disorders research and treatment center at Duke University in Durham, N.C.

She described how to use the hair pull and other tools to differentiate between telogen effluvium, alopecia areata, androgenetic alopecia, loose anagen syndrome, and short anagen syndrome.

Telogen effluvium: This condition is characterized by a global decrease in hair density. This global reduction can be confirmed by performing a midline part on the back and top of the scalp, which should show a similarly widened, thinned part.

Microscopic examination of the proximal end of all hairs that come off with hair pulls in an adolescent with telogen effluvium should show them to be telogen hairs.

"If you see any anagen hairs, that’s abnormal, and I would urge you to think about another condition, like loose anagen syndrome or alopecia areata," Dr. Olsen said.

Potential etiologies of telogen effluvium include stress, thyroid disease, medication side effects, vitamin A intake in excess of 15,000 IU/day, and numerous diet or nutritional deficits.

"Diet is incredibly important in figuring out the cause of telogen effluvium, particularly in children and adolescents, where you might be dealing with bulimia, anorexia nervosa, or another abnormal diet," according to the dermatologist.

The relationship between hair loss and iron deficiency is a matter of long-standing controversy. Low iron levels have often been linked to hair loss. As yet, however, there is no well-controlled clinical trial showing that iron replacement improves telogen effluvium in an iron-deficient patient.

Isotretinoin tops the list of medications that can cause telogen effluvium in pediatric patients. Other drugs that need to be considered include sodium valproate, antidepressants, lithium, and medications for attention-deficit/hyperactivity disorder.

Vitamin supplements should be stopped for at least 24 hours before conducting screening laboratory testing in a patient with telogen effluvium. Dr. Olsen recommended ordering a CBC with differential; thyroid-stimulating hormone and free thyroxine; serum ferritin; total iron binding capacity; and an erythrocyte sedimentation rate to screen for occult inflammatory conditions, which would skew the ferritin results. While a serum ferritin less than 40 ng/mL ordinarily has 98% sensitivity and specificity for iron deficiency, the bar rises to less than 70 ng/mL in patients with any kind of underlying systemic inflammation.

Alopecia areata: This form of diffuse hair loss can look clinically just like telogen effluvium. The key distinguishing feature is a positive hair pull showing not only telogen hairs but dystrophic, "exclamation point" anagen hairs as well.

"These anagen hairs are broken off or bayonet-like in appearance, and there’s usually a distortion of the hair shaft diameter as well," she explained.

Scalp dermoscopy will show yellow dots of keratinaceous debris in the empty follicles of patients with alopecia areata, an uncommon condition in children.

Androgenetic alopecia: The most useful clue in differentiating this condition from telogen effluvium is that a midline part will be widened on the central scalp but never over the occiput. The gentle hair pull typically doesn’t yield any hairs except in affected areas on the top portion of the scalp. Any hairs produced via the hair pull will be telogen hairs, and they will typically vary in diameter. Dermoscopy may show perifollicular pigmentation in areas of hair loss.

"If you diagnose alopecia areata in an adolescent, there are some key things you need to discuss with the parents," Dr. Olsen stressed.

For example, their child is likely to have a more rapidly progressive course of hair loss. And affected girls are at increased risk for underlying hyperandrogenemia-related symptoms, including hirsutism, insulin resistance, polycystic ovarian syndrome, and metabolic syndrome. A finding of acanthosis nigricans in a nonobese teen is a very good indicator that they may have underlying insulin resistance.

Loose anagen syndrome: This condition, whose onset is usually before 8 years of age, is characterized by short, very slow-growing hair. The hair pull yields anagen hairs, which under the microscope have a distinctive appearance marked by a rolled-up proximal tip.

Short anagen syndrome: The hallmarks here are decreased hair density, increased shedding, and an inability to grow hair long. On the hair pull, affected patients have an increased number of telogen hairs. The telogen hairs, which are newly regrowing in response to the truncated anagen cycle, will have a tapered tip at the distal end.

Scalp biopsy is of variable utility in diagnosing the cause of diffuse hair loss in young patients. It can be used to make the diagnosis of certain conditions, including acute alopecia areata, trichotillomania, connective tissue disease, infection, tumor, and scarring disorders. However, scalp biopsy can’t be used to make a definitive diagnosis of telogen effluvium, androgenetic alopecia, or long-standing alopecia areata – it can only be suggestive.

Pathologic standards dictate that the scalp biopsy should always be 4 mm. Normal white adults have roughly 36 follicles per 4-mm biopsy. African American adults have about 22. While no standard numbers have been established for children, the number of follicles per biopsy is higher than in adults because of the child’s smaller head size. After all, the number of follicles present at birth is what an individual will carry throughout life, Dr. Olsen explained.

It’s important that patients and parents understand the need for patience regarding hair regrowth, which takes 6-12 months after the cause of alopecia has been identified and eliminated. That means, for example, that in a patient with thyroid disease the clock for regrowth starts ticking not at the time treatment begins, but when the patient becomes euthyroid.

Dr. Olsen reported serving as a consultant to Canfield Scientific and Allergan.

[email protected]

COEUR D’ALENE, IDAHO – The most important test in determining the cause of diffuse hair loss in children and adolescents is a gentle hair pull, Dr. Elise A. Olsen said at the annual meeting of the Society for Pediatric Dermatology.

"This is something you should do in all patients with alopecia, accompanied by looking under the microscope at the hair you’ve pulled. Grasp a small clump of hair close to the scalp and gently pull through to the ends. It’s important that you do it not just in one area but all over, in various places on the scalp. Coming away with three or four hairs per pull is abnormal. Be especially gentle in young children because you can actually induce what looks like a loose anagen syndrome, confusing the picture," explained Dr. Olsen, professor of dermatology and medicine and director of the hair disorders research and treatment center at Duke University in Durham, N.C.

She described how to use the hair pull and other tools to differentiate between telogen effluvium, alopecia areata, androgenetic alopecia, loose anagen syndrome, and short anagen syndrome.

Telogen effluvium: This condition is characterized by a global decrease in hair density. This global reduction can be confirmed by performing a midline part on the back and top of the scalp, which should show a similarly widened, thinned part.

Microscopic examination of the proximal end of all hairs that come off with hair pulls in an adolescent with telogen effluvium should show them to be telogen hairs.

"If you see any anagen hairs, that’s abnormal, and I would urge you to think about another condition, like loose anagen syndrome or alopecia areata," Dr. Olsen said.

Potential etiologies of telogen effluvium include stress, thyroid disease, medication side effects, vitamin A intake in excess of 15,000 IU/day, and numerous diet or nutritional deficits.

"Diet is incredibly important in figuring out the cause of telogen effluvium, particularly in children and adolescents, where you might be dealing with bulimia, anorexia nervosa, or another abnormal diet," according to the dermatologist.

The relationship between hair loss and iron deficiency is a matter of long-standing controversy. Low iron levels have often been linked to hair loss. As yet, however, there is no well-controlled clinical trial showing that iron replacement improves telogen effluvium in an iron-deficient patient.

Isotretinoin tops the list of medications that can cause telogen effluvium in pediatric patients. Other drugs that need to be considered include sodium valproate, antidepressants, lithium, and medications for attention-deficit/hyperactivity disorder.

Vitamin supplements should be stopped for at least 24 hours before conducting screening laboratory testing in a patient with telogen effluvium. Dr. Olsen recommended ordering a CBC with differential; thyroid-stimulating hormone and free thyroxine; serum ferritin; total iron binding capacity; and an erythrocyte sedimentation rate to screen for occult inflammatory conditions, which would skew the ferritin results. While a serum ferritin less than 40 ng/mL ordinarily has 98% sensitivity and specificity for iron deficiency, the bar rises to less than 70 ng/mL in patients with any kind of underlying systemic inflammation.

Alopecia areata: This form of diffuse hair loss can look clinically just like telogen effluvium. The key distinguishing feature is a positive hair pull showing not only telogen hairs but dystrophic, "exclamation point" anagen hairs as well.

"These anagen hairs are broken off or bayonet-like in appearance, and there’s usually a distortion of the hair shaft diameter as well," she explained.

Scalp dermoscopy will show yellow dots of keratinaceous debris in the empty follicles of patients with alopecia areata, an uncommon condition in children.

Androgenetic alopecia: The most useful clue in differentiating this condition from telogen effluvium is that a midline part will be widened on the central scalp but never over the occiput. The gentle hair pull typically doesn’t yield any hairs except in affected areas on the top portion of the scalp. Any hairs produced via the hair pull will be telogen hairs, and they will typically vary in diameter. Dermoscopy may show perifollicular pigmentation in areas of hair loss.

"If you diagnose alopecia areata in an adolescent, there are some key things you need to discuss with the parents," Dr. Olsen stressed.

For example, their child is likely to have a more rapidly progressive course of hair loss. And affected girls are at increased risk for underlying hyperandrogenemia-related symptoms, including hirsutism, insulin resistance, polycystic ovarian syndrome, and metabolic syndrome. A finding of acanthosis nigricans in a nonobese teen is a very good indicator that they may have underlying insulin resistance.

Loose anagen syndrome: This condition, whose onset is usually before 8 years of age, is characterized by short, very slow-growing hair. The hair pull yields anagen hairs, which under the microscope have a distinctive appearance marked by a rolled-up proximal tip.

Short anagen syndrome: The hallmarks here are decreased hair density, increased shedding, and an inability to grow hair long. On the hair pull, affected patients have an increased number of telogen hairs. The telogen hairs, which are newly regrowing in response to the truncated anagen cycle, will have a tapered tip at the distal end.

Scalp biopsy is of variable utility in diagnosing the cause of diffuse hair loss in young patients. It can be used to make the diagnosis of certain conditions, including acute alopecia areata, trichotillomania, connective tissue disease, infection, tumor, and scarring disorders. However, scalp biopsy can’t be used to make a definitive diagnosis of telogen effluvium, androgenetic alopecia, or long-standing alopecia areata – it can only be suggestive.

Pathologic standards dictate that the scalp biopsy should always be 4 mm. Normal white adults have roughly 36 follicles per 4-mm biopsy. African American adults have about 22. While no standard numbers have been established for children, the number of follicles per biopsy is higher than in adults because of the child’s smaller head size. After all, the number of follicles present at birth is what an individual will carry throughout life, Dr. Olsen explained.

It’s important that patients and parents understand the need for patience regarding hair regrowth, which takes 6-12 months after the cause of alopecia has been identified and eliminated. That means, for example, that in a patient with thyroid disease the clock for regrowth starts ticking not at the time treatment begins, but when the patient becomes euthyroid.

Dr. Olsen reported serving as a consultant to Canfield Scientific and Allergan.

[email protected]

COEUR D’ALENE, IDAHO – The most important test in determining the cause of diffuse hair loss in children and adolescents is a gentle hair pull, Dr. Elise A. Olsen said at the annual meeting of the Society for Pediatric Dermatology.

"This is something you should do in all patients with alopecia, accompanied by looking under the microscope at the hair you’ve pulled. Grasp a small clump of hair close to the scalp and gently pull through to the ends. It’s important that you do it not just in one area but all over, in various places on the scalp. Coming away with three or four hairs per pull is abnormal. Be especially gentle in young children because you can actually induce what looks like a loose anagen syndrome, confusing the picture," explained Dr. Olsen, professor of dermatology and medicine and director of the hair disorders research and treatment center at Duke University in Durham, N.C.

She described how to use the hair pull and other tools to differentiate between telogen effluvium, alopecia areata, androgenetic alopecia, loose anagen syndrome, and short anagen syndrome.

Telogen effluvium: This condition is characterized by a global decrease in hair density. This global reduction can be confirmed by performing a midline part on the back and top of the scalp, which should show a similarly widened, thinned part.

Microscopic examination of the proximal end of all hairs that come off with hair pulls in an adolescent with telogen effluvium should show them to be telogen hairs.

"If you see any anagen hairs, that’s abnormal, and I would urge you to think about another condition, like loose anagen syndrome or alopecia areata," Dr. Olsen said.

Potential etiologies of telogen effluvium include stress, thyroid disease, medication side effects, vitamin A intake in excess of 15,000 IU/day, and numerous diet or nutritional deficits.

"Diet is incredibly important in figuring out the cause of telogen effluvium, particularly in children and adolescents, where you might be dealing with bulimia, anorexia nervosa, or another abnormal diet," according to the dermatologist.

The relationship between hair loss and iron deficiency is a matter of long-standing controversy. Low iron levels have often been linked to hair loss. As yet, however, there is no well-controlled clinical trial showing that iron replacement improves telogen effluvium in an iron-deficient patient.

Isotretinoin tops the list of medications that can cause telogen effluvium in pediatric patients. Other drugs that need to be considered include sodium valproate, antidepressants, lithium, and medications for attention-deficit/hyperactivity disorder.

Vitamin supplements should be stopped for at least 24 hours before conducting screening laboratory testing in a patient with telogen effluvium. Dr. Olsen recommended ordering a CBC with differential; thyroid-stimulating hormone and free thyroxine; serum ferritin; total iron binding capacity; and an erythrocyte sedimentation rate to screen for occult inflammatory conditions, which would skew the ferritin results. While a serum ferritin less than 40 ng/mL ordinarily has 98% sensitivity and specificity for iron deficiency, the bar rises to less than 70 ng/mL in patients with any kind of underlying systemic inflammation.

Alopecia areata: This form of diffuse hair loss can look clinically just like telogen effluvium. The key distinguishing feature is a positive hair pull showing not only telogen hairs but dystrophic, "exclamation point" anagen hairs as well.

"These anagen hairs are broken off or bayonet-like in appearance, and there’s usually a distortion of the hair shaft diameter as well," she explained.

Scalp dermoscopy will show yellow dots of keratinaceous debris in the empty follicles of patients with alopecia areata, an uncommon condition in children.

Androgenetic alopecia: The most useful clue in differentiating this condition from telogen effluvium is that a midline part will be widened on the central scalp but never over the occiput. The gentle hair pull typically doesn’t yield any hairs except in affected areas on the top portion of the scalp. Any hairs produced via the hair pull will be telogen hairs, and they will typically vary in diameter. Dermoscopy may show perifollicular pigmentation in areas of hair loss.

"If you diagnose alopecia areata in an adolescent, there are some key things you need to discuss with the parents," Dr. Olsen stressed.

For example, their child is likely to have a more rapidly progressive course of hair loss. And affected girls are at increased risk for underlying hyperandrogenemia-related symptoms, including hirsutism, insulin resistance, polycystic ovarian syndrome, and metabolic syndrome. A finding of acanthosis nigricans in a nonobese teen is a very good indicator that they may have underlying insulin resistance.

Loose anagen syndrome: This condition, whose onset is usually before 8 years of age, is characterized by short, very slow-growing hair. The hair pull yields anagen hairs, which under the microscope have a distinctive appearance marked by a rolled-up proximal tip.

Short anagen syndrome: The hallmarks here are decreased hair density, increased shedding, and an inability to grow hair long. On the hair pull, affected patients have an increased number of telogen hairs. The telogen hairs, which are newly regrowing in response to the truncated anagen cycle, will have a tapered tip at the distal end.

Scalp biopsy is of variable utility in diagnosing the cause of diffuse hair loss in young patients. It can be used to make the diagnosis of certain conditions, including acute alopecia areata, trichotillomania, connective tissue disease, infection, tumor, and scarring disorders. However, scalp biopsy can’t be used to make a definitive diagnosis of telogen effluvium, androgenetic alopecia, or long-standing alopecia areata – it can only be suggestive.

Pathologic standards dictate that the scalp biopsy should always be 4 mm. Normal white adults have roughly 36 follicles per 4-mm biopsy. African American adults have about 22. While no standard numbers have been established for children, the number of follicles per biopsy is higher than in adults because of the child’s smaller head size. After all, the number of follicles present at birth is what an individual will carry throughout life, Dr. Olsen explained.

It’s important that patients and parents understand the need for patience regarding hair regrowth, which takes 6-12 months after the cause of alopecia has been identified and eliminated. That means, for example, that in a patient with thyroid disease the clock for regrowth starts ticking not at the time treatment begins, but when the patient becomes euthyroid.

Dr. Olsen reported serving as a consultant to Canfield Scientific and Allergan.

[email protected]

The Diagnosis: Onychomadesis

The nail changes were characteristic of onychomadesis. Systemic illness in this patient most likely resulted in temporary arrest of nail matrix activity, leading to separation of the proximal nail plate from the proximal nail fold, which gave rise to a deep transverse sulcus.¹ Conversely, Beau lines are characterized by transverse grooves that move distally as the nail grows. Onychomadesis also is seen in pemphigus vulgaris, which could be due to an autoimmune disease inhibiting normal nail plate growth and development of blisters beneath the nail causing detachment of the nail plate.² Drug-induced Beau lines or onychomadesis are most frequently caused by chemotherapeutic agents (taxanes) and retinoids, which reflect an arrest in epithelial proliferation.³ Familial cases also have been described.⁴ Management of the nail abnormality should focus on the underlying medical problem or triggering factor. In our patient, hypertension and kidney disease were managed by a low-salt diet, oral antihypertensives, and iron replacement.

The Diagnosis: Onychomadesis

The nail changes were characteristic of onychomadesis. Systemic illness in this patient most likely resulted in temporary arrest of nail matrix activity, leading to separation of the proximal nail plate from the proximal nail fold, which gave rise to a deep transverse sulcus.¹ Conversely, Beau lines are characterized by transverse grooves that move distally as the nail grows. Onychomadesis also is seen in pemphigus vulgaris, which could be due to an autoimmune disease inhibiting normal nail plate growth and development of blisters beneath the nail causing detachment of the nail plate.² Drug-induced Beau lines or onychomadesis are most frequently caused by chemotherapeutic agents (taxanes) and retinoids, which reflect an arrest in epithelial proliferation.³ Familial cases also have been described.⁴ Management of the nail abnormality should focus on the underlying medical problem or triggering factor. In our patient, hypertension and kidney disease were managed by a low-salt diet, oral antihypertensives, and iron replacement.

The Diagnosis: Onychomadesis

The nail changes were characteristic of onychomadesis. Systemic illness in this patient most likely resulted in temporary arrest of nail matrix activity, leading to separation of the proximal nail plate from the proximal nail fold, which gave rise to a deep transverse sulcus.¹ Conversely, Beau lines are characterized by transverse grooves that move distally as the nail grows. Onychomadesis also is seen in pemphigus vulgaris, which could be due to an autoimmune disease inhibiting normal nail plate growth and development of blisters beneath the nail causing detachment of the nail plate.² Drug-induced Beau lines or onychomadesis are most frequently caused by chemotherapeutic agents (taxanes) and retinoids, which reflect an arrest in epithelial proliferation.³ Familial cases also have been described.⁴ Management of the nail abnormality should focus on the underlying medical problem or triggering factor. In our patient, hypertension and kidney disease were managed by a low-salt diet, oral antihypertensives, and iron replacement.

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

[email protected]

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

[email protected]

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

[email protected]

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

[email protected]

A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

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A 25-year-old man with plaque psoriasis and virtually no hair of any sort now sports a full head of hair plus body hair after treatment with the arthritis drug tofacitinib, according to Dr. Brittany G. Craiglow and Dr. Brett A. King of Yale University, New Haven, Conn.

The treatment has been so successful that Dr. King has submitted a proposal for a clinical trial involving a cream form of tofacitinib as a treatment for alopecia areata, according to a statement from the university.

Tofacitinib is approved only for the treatment of adult patients with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate, but it is in clinical development for the treatment of psoriasis.

Dr. Craiglow and Dr. King began treating the patient with 10 mg oral tofacitinib (Xeljanz) daily. At baseline, the patient had been diagnosed with plaque psoriasis and alopecia universalis. His only body hair was a small amount of hair within the psoriasis plaques on his head, the researchers said (J. Invest. Dermatol. 2014 June 18 [doi:10.1038/jid.2014.260]). 

After 2 months of tofacitinib dosed at 5 mg twice daily, the psoriasis on the patient’s scalp, torso, and elbows showed some improvement, and there was some hair growth on his face and scalp. The researchers increased the dose to 10 mg in the morning and 5 mg at night. After 3 more months, the patient had complete regrowth of scalp hair, as well as some growth of eyebrows, eyelashes, armpit hair, and pubic hair. After 8 months, the patient had full regrowth of all body hair, with the exception of hair on the arms and legs (which had been sparse prior to his alopecia diagnosis, the researchers said).

Although the hair growth has been dramatic, improvements in the patient’s psoriasis have been slower, likely because of the dosage.

“While we considered increasing the dose of tofacitinib, the patient is so pleased with the regrowth of his hair (and is not particularly bothered by the remaining psoriasis) that he has chosen to continue at the present dose,” the researchers noted.

The researchers considered using tofacitinib to treat the patient’s alopecia universalis based on the research of Angela M. Christiano, Ph.D., of Columbia University, New York, in which the drug reversed hair loss in a mouse model of alopecia areata.

The patient has reported no side effects, and lab testing has shown no abnormalities in complete blood count, serum creatinine, electrolytes, liver function, glucose, or lipids, the researchers noted.
The researchers had no financial conflicts to disclose.

[email protected]