Hair & Nails

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.¹ Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.² Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.³ Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.^4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.^6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.⁶

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).⁸ Another study by Hall et al⁹ of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al⁶ investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al¹⁰ examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.¹¹ Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.¹² Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.¹³ Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.¹⁴ The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan¹⁵ revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.¹⁶

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling¹⁷ demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.^18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.^20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard²² shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.²² Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.^23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.²⁵ Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.^26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.²⁸ Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).⁸ Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.¹ Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.² Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.³ Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.^4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.^6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.⁶

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).⁸ Another study by Hall et al⁹ of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al⁶ investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al¹⁰ examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.¹¹ Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.¹² Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.¹³ Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.¹⁴ The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan¹⁵ revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.¹⁶

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling¹⁷ demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.^18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.^20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard²² shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.²² Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.^23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.²⁵ Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.^26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.²⁸ Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).⁸ Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

One of the most common concerns among black patients is hair- and scalp-related disease. As increasing numbers of black patients opt to see dermatologists, it is imperative that all dermatologists be adequately trained to address the concerns of this patient population. When patients ask for help with common skin diseases of the hair and scalp, there are details that must be included in diagnosis, treatment, and hair care recommendations to reach goals for excellence in patient care. Herein, we provide must-know information to effectively approach this patient population.

Seborrheic Dermatitis

A study utilizing data from the National Ambulatory Medical Care Survey from 1993 to 2009 revealed seborrheic dermatitis (SD) as the second most common diagnosis for black patients who visit a dermatologist.¹ Prevalence data from a population of 1408 white, black, and Chinese patients from the United States and China revealed scalp flaking in 81% to 95% of black patients, 66% to 82% in white patients, and 30% to 42% in Chinese patients.² Seborrheic dermatitis has a notable prevalence in black women and often is considered normal by patients. It can be exacerbated by infrequent shampooing (ranging from once per month or longer in between shampoos) and the inappropriate use of hair oils and pomades; it also has been associated with hair breakage, lichen simplex chronicus, and folliculitis. Seborrheic dermatitis must be distinguished from other disorders including sarcoidosis, psoriasis, discoid lupus erythematosus, tinea capitis, and lichen simplex chronicus.

Although there is a paucity of literature on the treatment of SD in black patients, components of treatment are similar to those recommended for other populations. Black women are advised to carefully utilize antidandruff shampoos containing zinc pyrithione, selenium sulfide, or tar to avoid hair shaft damage and dryness. Ketoconazole shampoo rarely is recommended and may be more appropriately used in men and boys, as hair fragility is less of a concern for them. The shampoo should be applied directly to the scalp rather than the hair shafts to minimize dryness, with no particular elongated contact time needed for these medicated shampoos to be effective. Because conditioners can wash off the active ingredients in therapeutic shampoos, antidandruff conditioners are recommended. Potent or ultrapotent topical corticosteroids applied to the scalp 3 to 4 times weekly initially will control the symptoms of itching as well as scaling, and mid-potency topical corticosteroid oil may be used at weekly intervals.

Hairline and facial involvement of SD often co-occurs, and low-potency topical steroids may be applied to the affected areas twice daily for 3 to 4 weeks, which may be repeated for flares. Topical calcineurin inhibitors or antifungal creams such as ketoconazole or econazole may then provide effective control. Encouraging patients to increase shampooing to once weekly or every 2 weeks and discontinue use of scalp pomades and oils also is recommended. Patients must know that an itchy scaly scalp represents a treatable disorder. 

Acquired Trichorrhexis Nodosa

Hair fragility and breakage is common and multifactorial in black patients. Hair shaft breakage can occur on the vertex scalp in central centrifugal cicatricial alopecia (CCCA), with random localized breakage due to scratching in SD. Heat, hair colorants, and chemical relaxers may result in diffuse damage and breakage.³ Sodium-, potassium-, and guanine hydroxide–containing chemical relaxers change the physical properties of the hair by rearranging disulfide bonds. They remove the monomolecular layer of fatty acids covalently bound to the cuticle that help prevent penetration of water into the hair shaft. Additionally, chemical relaxers weaken the hair shaft and decrease tensile strength.

Unlike hair relaxers, colorants are less likely to lead to catastrophic hair breakage after a single use and require frequent use, which leads to cumulative damage. Thermal straightening is another cause of hair-shaft weakening in black patients.^4,5 Flat irons and curling irons can cause substantially more damage than blow-dryers due to the amount of heat generated. Flat irons may reach a high temperature of 230ºC (450ºF) as compared to 100°C (210°F) for a blow-dryer. Even the simple act of combing the hair can cause hair breakage, as demonstrated in African volunteers whose hair remained short in contrast to white and Asian volunteers, despite the fact that they had not cut their hair for 1 or more years.^6,7 These volunteers had many hair strand knots that led to breakage during combing and hair grooming.⁶

There is no known prevalence data for acquired trichorrhexis nodosa, though a study of 30 white and black women demonstrated that broken hairs were significantly increased in black women (P=.0001).⁸ Another study by Hall et al⁹ of 103 black women showed that 55% of the women reported breakage of hair shafts with normal styling. Khumalo et al⁶ investigated hair shaft fragility and reported no trichothiodystrophy; the authors concluded that the cause of the hair fragility likely was physical trauma or an undiscovered structural abnormality. Franbourg et al¹⁰ examined the structure of hair fibers in white, Asian, and black patients and found no differences, but microfractures were only present in black patients and were determined to be the cause of hair breakage. These studies underscore the need for specific questioning of the patient on hair care including combing, washing, drying, and using products and chemicals.

The approach to the treatment of hair breakage involves correcting underlying abnormalities (eg, iron deficiency, hypothyroidism, nutritional deficiencies). Patients should “give their hair a rest” by discontinuing use of heat, colorants, and chemical relaxers. For patients who are unable to comply, advising them to stop these processes for 6 to 12 months will allow for repair of the hair shaft. To minimize damage from colorants, recommend semipermanent, demipermanent, or temporary dyes. Patients should be counseled to stop bleaching their hair or using permanent colorants. The use of heat protectant products on the hair before styling as well as layering moisturizing regimens starting with a moisturizing shampoo followed by a leave-in, dimethicone-containing conditioner marketed for dry damaged hair is suggested. Dimethicone thinly coats the hair shaft to restore hydrophobicity, smoothes cuticular scales, decreases frizz, and protects the hair from damage. Use of a 2-in-1 shampoo and conditioner containing anionic surfactants and wide-toothed, smooth (no jagged edges in the grooves) combs along with rare brushing are recommended. The hair may be worn in its natural state, but straightening with heat should be avoided. Air drying the hair can minimize breakage, but if thermal styling is necessary, patients should turn the temperature setting of the flat or curling iron down. Protective hair care practices may include placing a loosely sewn-in hair weave that will allow for good hair care, wearing loose braids, or using a wig. Serial trimming of the hair every 6 to 8 weeks is recommended. Improvement may take time, and patients should be advised of this timeline to prevent frustration.

Acne Keloidalis Nuchae

Acne keloidalis nuchae (AKN) is characterized by papules and pustules located on the occipital scalp and/or the nape of the neck, which may result in keloidal papules and plaques. The etiology is unknown, but ingrown hairs, genetics, trauma, infection, inflammation, and androgen hormones have been proposed to play a role.¹¹ Although AKN may occur in black women, it is primarily a disorder in black men. The diagnosis is made based primarily on clinical findings, and a history of short haircuts may support the diagnosis. Treatment is tailored to the severity of the disease (Table 1). Avoidance of short haircuts and irritation from shirt collars may be helpful. Patients should be advised that the condition is controllable but not curable.

Pseudofolliculitis Barbae

Pseudofolliculitis barbae (PFB) is characterized by papules and pustules in the beard region that may result in postinflammatory hyperpigmentation, keloidal scar formation, and/or linear scarring. The coarse curled hairs characteristic of black men penetrate the follicle before exiting the skin and penetrate the skin after exiting the follicle, resulting in inflammation. Shaving methods and genetics also may contribute to the development of PFB. As with AKN, diagnosis is made clinically and does not require a skin biopsy. Important components of the patient’s history that should be obtained are hair removal practices and the use of over-the-counter products (eg, shave [pre and post] moisturizers, exfoliants, shaving creams or gels, keratin-softening agents containing α- or β-hydroxy acids). A bacterial culture may be appropriate if a notable pustular component is present. The patient should be advised to discontinue shaving if possible, which may require a physician’s letter explaining the necessity to the patient’s employer. Pseudofolliculitis barbae often can be prevented or lessened with the right hair removal strategy. Because there is not one optimal hair removal strategy that suits every patient, encourage the patient to experiment with different hair removal techniques, from depilatories to electric shavers, foil-guard razors, and multiple-blade razors. Preshave hydration and postshave moisturiza-tion also should be encouraged.¹² Benzoyl peroxide–containing shave gels and cleansers, as well as moisturizers containing glycolic, salicylic, and phytic acids, may minimize ingrown hairs, papules, and inflammation.

Other useful topical agents include eflornithine hydrochloride to decrease hair growth, retinoids to soften hair fibers, mild topical steroids to reduce inflammation, and/or topical erythromycin or clindamycin if pustules are present.¹³ Oral antibiotics such as doxycycline, minocycline, or erythromycin can be added for more severe cases of inflammation or infection. Procedural interventions include laser hair removal to prevent PFB and intralesional triamcinolone 10 to 40 mg/cc every 4 to 6 weeks, with the total volume depending on the size and number of lesions.

Alopecia

Alopecia is the sixth most common diagnosis seen in black patients visiting a dermatologist.¹⁴ The physician’s response to the patient’s chief concern of hair loss is key to building a relationship of confidence and trust. Trivializing the concern or dismissing it will undermine the physician-patient relationship. A survey by Gathers and Mahan¹⁵ revealed that 68% of patients thought that physicians did not understand their hair.

Hair loss negatively impacts quality of life, and a study of 50 black South African women with alopecia demonstrated a notable disease burden. Factors with the highest impact were those related to self-image, relationships, and interactions with others.¹⁶

It is not unusual for black women to have multiple types of alopecia identified in one biopsy specimen. Wohltmann and Sperling¹⁷ demonstrated 2 or more different types of alopecia in more than 10% of biopsy specimens of alopecia, including CCCA, androgenetic alopecia, end-stage traction alopecia, telogen effluvium, and tinea capitis. A complete history, physical examination, and appropriate procedures (eg, hair pull test, dermatoscopic examination and scalp biopsy) likely will yield an accurate diagnosis. Table 2 highlights important questions that should be asked about the patient’s history.

Physical examination of the scalp including dermatoscopic examination and a hair pull test as well as an evaluation of other hair-bearing areas may suggest a diagnosis that can be confirmed with a scalp biopsy.^18,19 Selection of a biopsy site at the periphery of the alopecic area that includes hair and consultation with a dermatopathologist familiar with features of CCCA, traction, and traumatic alopecia are important for making an accurate diagnosis.

Tinea Capitis in Black Pediatric Patients

Tinea capitis, a fungal infection of the scalp and hair, is one of the most common issues in children with skin of color. Clinical presentation may include widely distributed scaling, annular scaly plaques, annular patches of alopecia studded with black dots (broken hairs), and/or annular inflammatory plaques. Although scalp hyperkeratosis often is a hallmark of pediatric tinea capitis, it is not diagnostic. The differential diagnosis of pediatric scalp hyperkeratosis/scaling includes tinea capitis, SD, atopic dermatitis, psoriasis, and sebopsoriasis.^20,21 Clues to accurate diagnosis of tinea capitis may be found by examination of the adult who combs the child’s hair, as erythematous annular scaly plaques representing tinea corporis may be observed on the forearms or thighs. Although the thighs are a seemingly unusual location, the frequent practice of the child sitting on the floor between the legs of the adult during hairstyling provides a point of contact for the transmission of tinea from the child’s scalp to the thighs or forearms of the adult. Once tinea capitis is clinically suspected, the diagnosis is confirmed by a fungal culture. Adequate sampling is obtained by clipping hairs in an area of scaling for submission and vigorously rubbing the area of black dots or hyperkeratosis with a cotton swab.

Hubbard²² shed light on the decision to treat tinea capitis empirically or await the culture results. One hundred consecutive children (98 were black) presented with the constellation of scalp alopecia, scaling, pruritus, and occipital lymphadenopathy. Sixty-eight of those children had positive fungal cultures, and of them, 60 had both occipital lymphadenopathy and scaling and 55 had both occipital lymphadenopathy and alopecia.²² Thus, occipital lymphadenopathy in conjunction with alopecia and/or scaling is predictive of tinea capitis in this population and suggests that the initiation of treatment prior to confirmative culture results is appropriate.

The mainstay of treatment for tinea capitis is griseofulvin, but it is often underdosed and not continued for an adequate period of time to ensure clearance of the infection. Griseofulvin microsize (125 mg/5 mL) at the dosage of 20 to 25 mg/kg once daily for 8 to 12 weeks is recommended instead of a lower-dosed 4- to 6-week course.^23,24

Options for treating a child with residual disease include increasing and/or extending the griseofulvin dosage, encouraging ingestion of fatty foods to enhance absorption, dividing the dosage of griseofulvin from once daily to twice daily, changing therapy to oral terbinafine due to resistance to griseofulvin, examining siblings as a source of reinfection, and reviewing the positive fungal culture report to distinguish Trichophyton tonsurans versus Microsporum canis as the causative agent and adjust treatment accordingly. Although griseofulvin is the first-line treatment for M canis, terbinafine, which is approved for children 4 years and older for tineacapitis, is most efficacious for T tonsurans.²⁵ Treatment with terbinafine is weight based and should extend for 2 to 4 weeksfor T tonsurans and 8 to 12 weeks for M canis.

Antifungal shampoos may help reduce household spread of tinea and decrease transmissible fungal spores, but they may cause hair dryness and breakage.^26,27 Antifungal shampoos can be applied directly onto the scalp for a 5- to 10-minute contact time and rinsed, and then the hair should be shampooed with a moisturizing shampoo followed by a moisturizing conditioner. Hair conditioners may decrease household spread of tinea capitis and should be used by the patient and other members of the household.²⁸ Infection control may be enhanced by advising parents to dispose of hair pomades and washing hair accessories, combs, and brushes in hot soapy water, preferably in the dishwasher.

Hair Growth

The inability of the hair of black children to grow long is a common concern for parents of toddlers and preschool-aged children. Although the hair does grow, it grows more slowly than hair in white children (0.259 vs 0.330 mm per day), and it is likely to break faster than it is growing in black versus white children (146.6 vs 13.13 total broken hairs).⁸ Reassurance that the hair is indeed growing and that the length will increase as the child matures is important. Avoidance of hairstyles that promote traction and use of hair extensions, as well as use of moisturizing shampoos and conditioners, may minimize breakage and support the growth of healthy hair.

Conclusion

Hair- and scalp-related disease in black adults and children is commonly encountered in dermatology practice. It is important to understand the intrinsic characteristics of facial and scalp hair as well as hair care practices in this patient population that differ from those of white and Asian populations, such as frequency of shampooing, products, and styling. Familiarity with these differences may aid in effective diagnosis, treatment, and hair care recommendations in patients with these conditions.

Minoxidil 5% foam costs a mean of 40% more when it’s marketed to women instead of men, according to a review of 24 pharmacies in four northeastern states.

The statistically significant difference – $11.27/30 mL versus $8.05/30 mL – “could be a result of differential pricing by gender or could reflect production costs that are not related to medication strength,” reported the investigators from the University of Pennsylvania, Philadelphia. Also, the formulation for women, approved in 2014, is still on-patent and available only as Rogaine, whereas generics are available for the men’s foam (JAMA Dermatol. 2017 Jun 7. doi: 10.1001/jamadermatol.2017.1394).

The team also found that women’s 2% minoxidil solution costs about the same as men’s 5% minoxidil solution, despite the difference in strength ($7.61/30 mL versus $7.63/30 mL).

“These are products with the exact same ingredients. They come in different amounts and packaging based on gender, so, for the most part, women probably do not even realize they are paying more,” lead author Jules Lipoff, MD, of the department of dermatology, said in a University of Pennsylvania press release. “We recommend that our female patients buy the male version of the product because it doesn’t seem right to ask a woman to pay more when the products are, for all intents and purposes, identical,” he said.

Gender-based price differences – the “pink tax” – have been documented in consumer products before. A 2015 report found that women pay about 13% more than men for equivalent personal products in New York City. “However, to our knowledge, gender-based price differences for medications have not been previously studied,” the investigators said.

Pricing data came from CVS, Kroger, Rite Aid, Target, Walgreens, and Walmart pharmacies in Pennsylvania, New York, Ohio, and Indiana. The analysis included 14 OTC minoxidil preparations marketed to women and 27 marketed to men. Products were matched based on concentration and inactive ingredients to arrive at overall prices. When prices varied for the same product at different stores in the same chain, the mean price was used.

Dr. Lipoff reported receiving a grant from Pfizer. No other disclosures were reported.
 

[email protected]

Minoxidil 5% foam costs a mean of 40% more when it’s marketed to women instead of men, according to a review of 24 pharmacies in four northeastern states.

The statistically significant difference – $11.27/30 mL versus $8.05/30 mL – “could be a result of differential pricing by gender or could reflect production costs that are not related to medication strength,” reported the investigators from the University of Pennsylvania, Philadelphia. Also, the formulation for women, approved in 2014, is still on-patent and available only as Rogaine, whereas generics are available for the men’s foam (JAMA Dermatol. 2017 Jun 7. doi: 10.1001/jamadermatol.2017.1394).

The team also found that women’s 2% minoxidil solution costs about the same as men’s 5% minoxidil solution, despite the difference in strength ($7.61/30 mL versus $7.63/30 mL).

“These are products with the exact same ingredients. They come in different amounts and packaging based on gender, so, for the most part, women probably do not even realize they are paying more,” lead author Jules Lipoff, MD, of the department of dermatology, said in a University of Pennsylvania press release. “We recommend that our female patients buy the male version of the product because it doesn’t seem right to ask a woman to pay more when the products are, for all intents and purposes, identical,” he said.

Gender-based price differences – the “pink tax” – have been documented in consumer products before. A 2015 report found that women pay about 13% more than men for equivalent personal products in New York City. “However, to our knowledge, gender-based price differences for medications have not been previously studied,” the investigators said.

Pricing data came from CVS, Kroger, Rite Aid, Target, Walgreens, and Walmart pharmacies in Pennsylvania, New York, Ohio, and Indiana. The analysis included 14 OTC minoxidil preparations marketed to women and 27 marketed to men. Products were matched based on concentration and inactive ingredients to arrive at overall prices. When prices varied for the same product at different stores in the same chain, the mean price was used.

Dr. Lipoff reported receiving a grant from Pfizer. No other disclosures were reported.
 

[email protected]

Minoxidil 5% foam costs a mean of 40% more when it’s marketed to women instead of men, according to a review of 24 pharmacies in four northeastern states.

The statistically significant difference – $11.27/30 mL versus $8.05/30 mL – “could be a result of differential pricing by gender or could reflect production costs that are not related to medication strength,” reported the investigators from the University of Pennsylvania, Philadelphia. Also, the formulation for women, approved in 2014, is still on-patent and available only as Rogaine, whereas generics are available for the men’s foam (JAMA Dermatol. 2017 Jun 7. doi: 10.1001/jamadermatol.2017.1394).

The team also found that women’s 2% minoxidil solution costs about the same as men’s 5% minoxidil solution, despite the difference in strength ($7.61/30 mL versus $7.63/30 mL).

“These are products with the exact same ingredients. They come in different amounts and packaging based on gender, so, for the most part, women probably do not even realize they are paying more,” lead author Jules Lipoff, MD, of the department of dermatology, said in a University of Pennsylvania press release. “We recommend that our female patients buy the male version of the product because it doesn’t seem right to ask a woman to pay more when the products are, for all intents and purposes, identical,” he said.

Gender-based price differences – the “pink tax” – have been documented in consumer products before. A 2015 report found that women pay about 13% more than men for equivalent personal products in New York City. “However, to our knowledge, gender-based price differences for medications have not been previously studied,” the investigators said.

Pricing data came from CVS, Kroger, Rite Aid, Target, Walgreens, and Walmart pharmacies in Pennsylvania, New York, Ohio, and Indiana. The analysis included 14 OTC minoxidil preparations marketed to women and 27 marketed to men. Products were matched based on concentration and inactive ingredients to arrive at overall prices. When prices varied for the same product at different stores in the same chain, the mean price was used.

Dr. Lipoff reported receiving a grant from Pfizer. No other disclosures were reported.
 

[email protected]

Real-time PCR techniques for identifying the pathogens responsible for onychomycosis can offer some advantages over conventional diagnostic approaches but also have their limitations, say the authors of a study published in Mycoses.

Anissa Z. Hafirassou of Frères-Mentouri, Constantine University, Algeria, and colleagues analyzed nail samples from 70 patients with clinical signs of onychomycosis and 15 healthy controls using four different real-time PCR assays – a panfungal, a pandermatophyte, an assay for Candida and one for Aspergillus – and conventional methods.

copyright Metin Cengiz Bar/Thinkstock

Real-time PCR techniques for identifying the pathogens responsible for onychomycosis can offer some advantages over conventional diagnostic approaches but also have their limitations, say the authors of a study published in Mycoses.

Anissa Z. Hafirassou of Frères-Mentouri, Constantine University, Algeria, and colleagues analyzed nail samples from 70 patients with clinical signs of onychomycosis and 15 healthy controls using four different real-time PCR assays – a panfungal, a pandermatophyte, an assay for Candida and one for Aspergillus – and conventional methods.

copyright Metin Cengiz Bar/Thinkstock

Real-time PCR techniques for identifying the pathogens responsible for onychomycosis can offer some advantages over conventional diagnostic approaches but also have their limitations, say the authors of a study published in Mycoses.

Anissa Z. Hafirassou of Frères-Mentouri, Constantine University, Algeria, and colleagues analyzed nail samples from 70 patients with clinical signs of onychomycosis and 15 healthy controls using four different real-time PCR assays – a panfungal, a pandermatophyte, an assay for Candida and one for Aspergillus – and conventional methods.

copyright Metin Cengiz Bar/Thinkstock

In the absence of a typical presentation, combining direct microscopy plus nail clipping histopathology – two diagnostic tests with different sensitivities and specificities – raises the likelihood of correctly diagnosing onychomycosis, according to a report published in Mycoses.

It is often difficult to diagnose nail diseases based solely on clinical features, and laboratory techniques for diagnosing onychomycoses in particular “remain a challenge,” said Fernanda G. Lavorato, MD, of Universidade do Estado do Rio de Janeiro, and her associates.

Isolating filamentous fungi in cultures is considered the preferred method for diagnosing the disorder, but this method lacks sensitivity and is not always accessible, since some dermatologic centers don’t have a mycology laboratory with personnel trained in sample collection and fungal processing.

copyright Manuel-F-O/Thinkstock

In the absence of a typical presentation, combining direct microscopy plus nail clipping histopathology – two diagnostic tests with different sensitivities and specificities – raises the likelihood of correctly diagnosing onychomycosis, according to a report published in Mycoses.

It is often difficult to diagnose nail diseases based solely on clinical features, and laboratory techniques for diagnosing onychomycoses in particular “remain a challenge,” said Fernanda G. Lavorato, MD, of Universidade do Estado do Rio de Janeiro, and her associates.

Isolating filamentous fungi in cultures is considered the preferred method for diagnosing the disorder, but this method lacks sensitivity and is not always accessible, since some dermatologic centers don’t have a mycology laboratory with personnel trained in sample collection and fungal processing.

copyright Manuel-F-O/Thinkstock

In the absence of a typical presentation, combining direct microscopy plus nail clipping histopathology – two diagnostic tests with different sensitivities and specificities – raises the likelihood of correctly diagnosing onychomycosis, according to a report published in Mycoses.

It is often difficult to diagnose nail diseases based solely on clinical features, and laboratory techniques for diagnosing onychomycoses in particular “remain a challenge,” said Fernanda G. Lavorato, MD, of Universidade do Estado do Rio de Janeiro, and her associates.

Isolating filamentous fungi in cultures is considered the preferred method for diagnosing the disorder, but this method lacks sensitivity and is not always accessible, since some dermatologic centers don’t have a mycology laboratory with personnel trained in sample collection and fungal processing.

copyright Manuel-F-O/Thinkstock

SYDNEY – Responses to treatments for lichen planopilaris varied widely, and decreased with second- and third-line therapies, in a retrospective study, Karolina Kerkemeyer, MD, said at the annual meeting of the Australasian College of Dermatologists.

An analysis of computerized medical records for 32 patients who had been treated for lichen planopilaris at a tertiary referral hair center in Australia was conducted from 2012 to 2016 by Dr. Kerkemeyer of the University of Notre Dame Australia, Werribee, and Jack Green, MD, of the Skin and Cancer Foundation and St. Vincent’s Hospital in Melbourne. The study excluded patients with a dual diagnosis, or those followed for less than 12 months.

[email protected]

SYDNEY – Responses to treatments for lichen planopilaris varied widely, and decreased with second- and third-line therapies, in a retrospective study, Karolina Kerkemeyer, MD, said at the annual meeting of the Australasian College of Dermatologists.

An analysis of computerized medical records for 32 patients who had been treated for lichen planopilaris at a tertiary referral hair center in Australia was conducted from 2012 to 2016 by Dr. Kerkemeyer of the University of Notre Dame Australia, Werribee, and Jack Green, MD, of the Skin and Cancer Foundation and St. Vincent’s Hospital in Melbourne. The study excluded patients with a dual diagnosis, or those followed for less than 12 months.

[email protected]

SYDNEY – Responses to treatments for lichen planopilaris varied widely, and decreased with second- and third-line therapies, in a retrospective study, Karolina Kerkemeyer, MD, said at the annual meeting of the Australasian College of Dermatologists.

An analysis of computerized medical records for 32 patients who had been treated for lichen planopilaris at a tertiary referral hair center in Australia was conducted from 2012 to 2016 by Dr. Kerkemeyer of the University of Notre Dame Australia, Werribee, and Jack Green, MD, of the Skin and Cancer Foundation and St. Vincent’s Hospital in Melbourne. The study excluded patients with a dual diagnosis, or those followed for less than 12 months.

[email protected]

PORTLAND – Alopecia areata can resist treatment stubbornly, but dermatologists might soon have better tools to predict response to therapy.

Personalized gene sequencing is key to this type of precision medicine, but conventional sequencing can be “extremely cumbersome and clinically impractical,” James C. Chen, PhD, said at the annual meeting of the Society for Investigative Dermatology.

PORTLAND – Alopecia areata can resist treatment stubbornly, but dermatologists might soon have better tools to predict response to therapy.

Personalized gene sequencing is key to this type of precision medicine, but conventional sequencing can be “extremely cumbersome and clinically impractical,” James C. Chen, PhD, said at the annual meeting of the Society for Investigative Dermatology.

PORTLAND – Alopecia areata can resist treatment stubbornly, but dermatologists might soon have better tools to predict response to therapy.

Personalized gene sequencing is key to this type of precision medicine, but conventional sequencing can be “extremely cumbersome and clinically impractical,” James C. Chen, PhD, said at the annual meeting of the Society for Investigative Dermatology.

Besides skin wrinkling, volume shifts, and photoaging, graying hair can also be a telltale sign of aging. While it was recently a fashionable trend for younger persons to dye their hair white or gray, graying hair can make a younger person appear older, even in those with naturally premature graying of the hair.

In a study recently published in Genes & Development, researchers at the University of Texas Southwestern Medical Center, Dallas, identified hair shaft progenitors in the matrix that are specific to the hair shaft and not to follicular epithelial cells.¹ These hair shaft progenitors express transcription factor KROX20, which expresses stem cell growth factor necessary for hair pigmentation by maintenance of differentiated melanocytes. When KROX20+ is depleted, hair growth is halted and hair turns gray, proving its important role in both hair growth and graying pathways.

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
 

References:

1. Genes Dev. 2017 May 2. doi: 10.1101/gad.298703.117.

2. Nat Commun. 2016 Mar 1;7:10815.

Besides skin wrinkling, volume shifts, and photoaging, graying hair can also be a telltale sign of aging. While it was recently a fashionable trend for younger persons to dye their hair white or gray, graying hair can make a younger person appear older, even in those with naturally premature graying of the hair.

In a study recently published in Genes & Development, researchers at the University of Texas Southwestern Medical Center, Dallas, identified hair shaft progenitors in the matrix that are specific to the hair shaft and not to follicular epithelial cells.¹ These hair shaft progenitors express transcription factor KROX20, which expresses stem cell growth factor necessary for hair pigmentation by maintenance of differentiated melanocytes. When KROX20+ is depleted, hair growth is halted and hair turns gray, proving its important role in both hair growth and graying pathways.

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
 

References:

1. Genes Dev. 2017 May 2. doi: 10.1101/gad.298703.117.

2. Nat Commun. 2016 Mar 1;7:10815.

Besides skin wrinkling, volume shifts, and photoaging, graying hair can also be a telltale sign of aging. While it was recently a fashionable trend for younger persons to dye their hair white or gray, graying hair can make a younger person appear older, even in those with naturally premature graying of the hair.

In a study recently published in Genes & Development, researchers at the University of Texas Southwestern Medical Center, Dallas, identified hair shaft progenitors in the matrix that are specific to the hair shaft and not to follicular epithelial cells.¹ These hair shaft progenitors express transcription factor KROX20, which expresses stem cell growth factor necessary for hair pigmentation by maintenance of differentiated melanocytes. When KROX20+ is depleted, hair growth is halted and hair turns gray, proving its important role in both hair growth and graying pathways.

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
 

References:

1. Genes Dev. 2017 May 2. doi: 10.1101/gad.298703.117.

2. Nat Commun. 2016 Mar 1;7:10815.

Central centrifugal cicatricial alopecia (CCCA) can affect adolescents, and a study of six biopsy-proven cases indicates CCCA has a genetic component, Ariana N. Eginli and her colleagues report in Pediatric Dermatology.

CCCA, a scarring alopecia that disproportionately affects middle-aged women of African descent, has been attributed to hair care and styling practices. In this series, however, five of the six patients had a maternal history of CCCA, and only one had used chemical products or styling tools. “Specifically, the early onset of CCCA in these patients with natural virgin hair raises the possibility of genetic anticipation,” wrote Ms. Eginli of Wake Forest Baptist Health, Winston-Salem, N.C., and her coauthors. “Therefore, recognizing that CCCA can present in children, particularly in those with a positive family history, is of utmost importance in controlling further disease progression and improving their quality of life.”

Courtesy RegionalDerm.com

Ms. Eginli had no disclosures. One of her colleagues is a consultant for and has received grant support from various drug companies.

[email protected]

On Twitter @eaztweets

Central centrifugal cicatricial alopecia (CCCA) can affect adolescents, and a study of six biopsy-proven cases indicates CCCA has a genetic component, Ariana N. Eginli and her colleagues report in Pediatric Dermatology.

CCCA, a scarring alopecia that disproportionately affects middle-aged women of African descent, has been attributed to hair care and styling practices. In this series, however, five of the six patients had a maternal history of CCCA, and only one had used chemical products or styling tools. “Specifically, the early onset of CCCA in these patients with natural virgin hair raises the possibility of genetic anticipation,” wrote Ms. Eginli of Wake Forest Baptist Health, Winston-Salem, N.C., and her coauthors. “Therefore, recognizing that CCCA can present in children, particularly in those with a positive family history, is of utmost importance in controlling further disease progression and improving their quality of life.”

Courtesy RegionalDerm.com

Ms. Eginli had no disclosures. One of her colleagues is a consultant for and has received grant support from various drug companies.

[email protected]

On Twitter @eaztweets

Central centrifugal cicatricial alopecia (CCCA) can affect adolescents, and a study of six biopsy-proven cases indicates CCCA has a genetic component, Ariana N. Eginli and her colleagues report in Pediatric Dermatology.

CCCA, a scarring alopecia that disproportionately affects middle-aged women of African descent, has been attributed to hair care and styling practices. In this series, however, five of the six patients had a maternal history of CCCA, and only one had used chemical products or styling tools. “Specifically, the early onset of CCCA in these patients with natural virgin hair raises the possibility of genetic anticipation,” wrote Ms. Eginli of Wake Forest Baptist Health, Winston-Salem, N.C., and her coauthors. “Therefore, recognizing that CCCA can present in children, particularly in those with a positive family history, is of utmost importance in controlling further disease progression and improving their quality of life.”

Courtesy RegionalDerm.com

Ms. Eginli had no disclosures. One of her colleagues is a consultant for and has received grant support from various drug companies.

[email protected]

On Twitter @eaztweets

PORTLAND, ORE. – Janus kinase inhibitors are relatively safe and can produce a full head of hair in patients with moderate to severe alopecia areata (AA), although patients tend to shed hair after stopping treatment, Julian Mackay-Wiggan, MD, said at the annual meeting of the Society for Investigative Dermatology.

“At this point, there are 17 publications in the literature, from clinical trials to case reports, looking at JAK [Janus kinase] inhibitors in patients with alopecia areata,” said Dr. Mackay-Wiggan of the department of dermatology, Columbia University, New York, where she specializes in hair disorders. “Pretty much all report very positive findings. It definitely appears that Janus kinase inhibitors can play a very significant role in treatment.”

Amy Karon/Frontline Medical News

Lab of Dr. Angela Christiano/Columbia University Medical Center

PORTLAND, ORE. – Janus kinase inhibitors are relatively safe and can produce a full head of hair in patients with moderate to severe alopecia areata (AA), although patients tend to shed hair after stopping treatment, Julian Mackay-Wiggan, MD, said at the annual meeting of the Society for Investigative Dermatology.

“At this point, there are 17 publications in the literature, from clinical trials to case reports, looking at JAK [Janus kinase] inhibitors in patients with alopecia areata,” said Dr. Mackay-Wiggan of the department of dermatology, Columbia University, New York, where she specializes in hair disorders. “Pretty much all report very positive findings. It definitely appears that Janus kinase inhibitors can play a very significant role in treatment.”

Amy Karon/Frontline Medical News

Lab of Dr. Angela Christiano/Columbia University Medical Center

PORTLAND, ORE. – Janus kinase inhibitors are relatively safe and can produce a full head of hair in patients with moderate to severe alopecia areata (AA), although patients tend to shed hair after stopping treatment, Julian Mackay-Wiggan, MD, said at the annual meeting of the Society for Investigative Dermatology.

“At this point, there are 17 publications in the literature, from clinical trials to case reports, looking at JAK [Janus kinase] inhibitors in patients with alopecia areata,” said Dr. Mackay-Wiggan of the department of dermatology, Columbia University, New York, where she specializes in hair disorders. “Pretty much all report very positive findings. It definitely appears that Janus kinase inhibitors can play a very significant role in treatment.”

Amy Karon/Frontline Medical News

Lab of Dr. Angela Christiano/Columbia University Medical Center

To the Editor:

An 85-year-old woman with a history of hypertension, hyperlipidemia, stroke, hypothyroidism, chronic obstructive pulmonary disease, and chronic myeloproliferative disorder presented to our clinic for evaluation of brown lesions on the hands and discoloration of the fingernails and toenails of 4 months’ duration. Six months prior to visiting our clinic she was admitted to the hospital for a pulmonary embolism. On admission she was noted to have a platelet count of more than 2 million/μL (reference range, 150,000–350,000/μL). She received urgent plasmapheresis and started hydroxyurea 500 mg twice daily, which she continued as an outpatient.

On physical examination at our clinic she had diffusely scattered red and brown macules on the bilateral palms and transverse hyperpigmented bands of various intensities on all fingernails and toenails (Figure). Her platelet count was 372,000/μL, white blood cell count was 5200/μL (reference range, 4500–11,000/μL), hemoglobin was 12.6 g/dL (reference range, 14.0–17.5 g/dL), hematocrit was 39.0% (reference range, 41%–50%), and mean corpuscular volume was 87.5 fL per red cell (reference range, 80–96 fL per red cell).

The patient was diagnosed with hydroxyurea-induced nail hyperpigmentation and was counseled on the benign nature of the condition. Three months later her platelet count decreased to below 100,000/μL, and hydroxyurea was discontinued. She noticed considerable improvement in the lesions on the hands and nails with the cessation of hydroxyurea.

Hydroxyurea is a cytostatic agent that has been used for more than 40 years in the treatment of myeloproliferative disorders including chronic myelogenous leukemia, polycythemia vera, essential thrombocythemia, and sickle cell anemia.¹ It inhibits ribonucleoside diphosphate reductase and promotes cell death in the S phase of the cell cycle.^1-3

Several adverse cutaneous reactions have been associated with hydroxyurea including increased pigmentation, hyperkeratosis, skin atrophy, xerosis, lichenoid eruptions, palmoplantar keratoderma, cutaneous vasculitis, alopecia, chronic leg ulcers, cutaneous carcinomas, and melanonychia.^3,4

Hydroxyurea-induced melanonychia most often occurs after several months of therapy but has been reported to occur as early as 4 months and as late as 5 years after initiating the drug.^1,4-6 The prevalence of melanonychia in the general population has been estimated at 1% and is thought to increase to approximately 4% in patients treated with hydroxyurea.^1,2,6,7 The prevalence of affected individuals increases with age; it is more common in females as well as black and Hispanic patients.²

Multiple patterns of hydroxyurea-induced melanonychia have been described, including longitudinal bands, transverse bands, and diffuse hyperpigmentation.^1-3,6 By far the most common pattern described in the literature is longitudinal banding^1-3,8; transverse bands are more rare. Although there are sporadic case reports linking the transverse bands with hydroxyurea, these bands occur more frequently with systemic chemotherapy such as doxorubicin and cyclosphosphamide.^1,6

The exact pathogenesis of hydroxyurea-induced melanonychia remains unclear, though it is thought to result from focal melanogenesis in the nail bed or matrix followed by deposition of melanin granules on the nail plate.^5,8 When these melanocytes are activated, melanosomes filled with melanin are transferred to differentiating matrix cells, which migrate distally as they become nail plate oncocytes, resulting in a visible band of pigmentation in the nail plate.² There also may be a genetic and photosensitivity component.^1,2

Prior case series have described spontaneous remission of nail hyperpigmentation following discontinuation of hydroxyurea therapy.¹ In many patients, however, the chronic nature of the myeloproliferative disorder and lack of alternative treatments make a therapeutic change difficult. Although the melanonychia itself is benign, it may precede the appearance of more serious mucocutaneous side effects, such as skin ulceration or development of cutaneous carcinomas, so careful monitoring should be performed.²

Our patient presented with melanonychia that was transverse, polydactylic, monochromic, stable in size and shape, and associated with palmar hyperpigmentation. Of note, the pigmentation remitted over time along with discontinuation of the drug. Although this presentation did not warrant a nail matrix biopsy, it should be noted that patients with single nail melanonychia suspicious for melanoma should have a biopsy, even with concomitant use of hydroxyurea.² Although transverse melanonychia most commonly is associated with other systemic chemotherapeutics, in the absence of such medications hydroxyurea was the likely culprit in our patient. The palmar hyperpigmentation, which has previously been reported with hydroxyurea use, further solidifies the diagnosis.

To the Editor:

An 85-year-old woman with a history of hypertension, hyperlipidemia, stroke, hypothyroidism, chronic obstructive pulmonary disease, and chronic myeloproliferative disorder presented to our clinic for evaluation of brown lesions on the hands and discoloration of the fingernails and toenails of 4 months’ duration. Six months prior to visiting our clinic she was admitted to the hospital for a pulmonary embolism. On admission she was noted to have a platelet count of more than 2 million/μL (reference range, 150,000–350,000/μL). She received urgent plasmapheresis and started hydroxyurea 500 mg twice daily, which she continued as an outpatient.

On physical examination at our clinic she had diffusely scattered red and brown macules on the bilateral palms and transverse hyperpigmented bands of various intensities on all fingernails and toenails (Figure). Her platelet count was 372,000/μL, white blood cell count was 5200/μL (reference range, 4500–11,000/μL), hemoglobin was 12.6 g/dL (reference range, 14.0–17.5 g/dL), hematocrit was 39.0% (reference range, 41%–50%), and mean corpuscular volume was 87.5 fL per red cell (reference range, 80–96 fL per red cell).

The patient was diagnosed with hydroxyurea-induced nail hyperpigmentation and was counseled on the benign nature of the condition. Three months later her platelet count decreased to below 100,000/μL, and hydroxyurea was discontinued. She noticed considerable improvement in the lesions on the hands and nails with the cessation of hydroxyurea.

Hydroxyurea is a cytostatic agent that has been used for more than 40 years in the treatment of myeloproliferative disorders including chronic myelogenous leukemia, polycythemia vera, essential thrombocythemia, and sickle cell anemia.¹ It inhibits ribonucleoside diphosphate reductase and promotes cell death in the S phase of the cell cycle.^1-3

Several adverse cutaneous reactions have been associated with hydroxyurea including increased pigmentation, hyperkeratosis, skin atrophy, xerosis, lichenoid eruptions, palmoplantar keratoderma, cutaneous vasculitis, alopecia, chronic leg ulcers, cutaneous carcinomas, and melanonychia.^3,4

Hydroxyurea-induced melanonychia most often occurs after several months of therapy but has been reported to occur as early as 4 months and as late as 5 years after initiating the drug.^1,4-6 The prevalence of melanonychia in the general population has been estimated at 1% and is thought to increase to approximately 4% in patients treated with hydroxyurea.^1,2,6,7 The prevalence of affected individuals increases with age; it is more common in females as well as black and Hispanic patients.²

Multiple patterns of hydroxyurea-induced melanonychia have been described, including longitudinal bands, transverse bands, and diffuse hyperpigmentation.^1-3,6 By far the most common pattern described in the literature is longitudinal banding^1-3,8; transverse bands are more rare. Although there are sporadic case reports linking the transverse bands with hydroxyurea, these bands occur more frequently with systemic chemotherapy such as doxorubicin and cyclosphosphamide.^1,6

The exact pathogenesis of hydroxyurea-induced melanonychia remains unclear, though it is thought to result from focal melanogenesis in the nail bed or matrix followed by deposition of melanin granules on the nail plate.^5,8 When these melanocytes are activated, melanosomes filled with melanin are transferred to differentiating matrix cells, which migrate distally as they become nail plate oncocytes, resulting in a visible band of pigmentation in the nail plate.² There also may be a genetic and photosensitivity component.^1,2

Prior case series have described spontaneous remission of nail hyperpigmentation following discontinuation of hydroxyurea therapy.¹ In many patients, however, the chronic nature of the myeloproliferative disorder and lack of alternative treatments make a therapeutic change difficult. Although the melanonychia itself is benign, it may precede the appearance of more serious mucocutaneous side effects, such as skin ulceration or development of cutaneous carcinomas, so careful monitoring should be performed.²

Our patient presented with melanonychia that was transverse, polydactylic, monochromic, stable in size and shape, and associated with palmar hyperpigmentation. Of note, the pigmentation remitted over time along with discontinuation of the drug. Although this presentation did not warrant a nail matrix biopsy, it should be noted that patients with single nail melanonychia suspicious for melanoma should have a biopsy, even with concomitant use of hydroxyurea.² Although transverse melanonychia most commonly is associated with other systemic chemotherapeutics, in the absence of such medications hydroxyurea was the likely culprit in our patient. The palmar hyperpigmentation, which has previously been reported with hydroxyurea use, further solidifies the diagnosis.

To the Editor:

An 85-year-old woman with a history of hypertension, hyperlipidemia, stroke, hypothyroidism, chronic obstructive pulmonary disease, and chronic myeloproliferative disorder presented to our clinic for evaluation of brown lesions on the hands and discoloration of the fingernails and toenails of 4 months’ duration. Six months prior to visiting our clinic she was admitted to the hospital for a pulmonary embolism. On admission she was noted to have a platelet count of more than 2 million/μL (reference range, 150,000–350,000/μL). She received urgent plasmapheresis and started hydroxyurea 500 mg twice daily, which she continued as an outpatient.

On physical examination at our clinic she had diffusely scattered red and brown macules on the bilateral palms and transverse hyperpigmented bands of various intensities on all fingernails and toenails (Figure). Her platelet count was 372,000/μL, white blood cell count was 5200/μL (reference range, 4500–11,000/μL), hemoglobin was 12.6 g/dL (reference range, 14.0–17.5 g/dL), hematocrit was 39.0% (reference range, 41%–50%), and mean corpuscular volume was 87.5 fL per red cell (reference range, 80–96 fL per red cell).

The patient was diagnosed with hydroxyurea-induced nail hyperpigmentation and was counseled on the benign nature of the condition. Three months later her platelet count decreased to below 100,000/μL, and hydroxyurea was discontinued. She noticed considerable improvement in the lesions on the hands and nails with the cessation of hydroxyurea.

Hydroxyurea is a cytostatic agent that has been used for more than 40 years in the treatment of myeloproliferative disorders including chronic myelogenous leukemia, polycythemia vera, essential thrombocythemia, and sickle cell anemia.¹ It inhibits ribonucleoside diphosphate reductase and promotes cell death in the S phase of the cell cycle.^1-3

Several adverse cutaneous reactions have been associated with hydroxyurea including increased pigmentation, hyperkeratosis, skin atrophy, xerosis, lichenoid eruptions, palmoplantar keratoderma, cutaneous vasculitis, alopecia, chronic leg ulcers, cutaneous carcinomas, and melanonychia.^3,4

Hydroxyurea-induced melanonychia most often occurs after several months of therapy but has been reported to occur as early as 4 months and as late as 5 years after initiating the drug.^1,4-6 The prevalence of melanonychia in the general population has been estimated at 1% and is thought to increase to approximately 4% in patients treated with hydroxyurea.^1,2,6,7 The prevalence of affected individuals increases with age; it is more common in females as well as black and Hispanic patients.²

Multiple patterns of hydroxyurea-induced melanonychia have been described, including longitudinal bands, transverse bands, and diffuse hyperpigmentation.^1-3,6 By far the most common pattern described in the literature is longitudinal banding^1-3,8; transverse bands are more rare. Although there are sporadic case reports linking the transverse bands with hydroxyurea, these bands occur more frequently with systemic chemotherapy such as doxorubicin and cyclosphosphamide.^1,6

The exact pathogenesis of hydroxyurea-induced melanonychia remains unclear, though it is thought to result from focal melanogenesis in the nail bed or matrix followed by deposition of melanin granules on the nail plate.^5,8 When these melanocytes are activated, melanosomes filled with melanin are transferred to differentiating matrix cells, which migrate distally as they become nail plate oncocytes, resulting in a visible band of pigmentation in the nail plate.² There also may be a genetic and photosensitivity component.^1,2

Prior case series have described spontaneous remission of nail hyperpigmentation following discontinuation of hydroxyurea therapy.¹ In many patients, however, the chronic nature of the myeloproliferative disorder and lack of alternative treatments make a therapeutic change difficult. Although the melanonychia itself is benign, it may precede the appearance of more serious mucocutaneous side effects, such as skin ulceration or development of cutaneous carcinomas, so careful monitoring should be performed.²

Our patient presented with melanonychia that was transverse, polydactylic, monochromic, stable in size and shape, and associated with palmar hyperpigmentation. Of note, the pigmentation remitted over time along with discontinuation of the drug. Although this presentation did not warrant a nail matrix biopsy, it should be noted that patients with single nail melanonychia suspicious for melanoma should have a biopsy, even with concomitant use of hydroxyurea.² Although transverse melanonychia most commonly is associated with other systemic chemotherapeutics, in the absence of such medications hydroxyurea was the likely culprit in our patient. The palmar hyperpigmentation, which has previously been reported with hydroxyurea use, further solidifies the diagnosis.