Hair & Nails

Piebaldism is a rare autosomal dominant disorder characterized by congenital poliosis and leukoderma. We present a case of a 10-year-old girl with a typical clinical presentation, followed by a concise review of the literature discussing the etiology, clinical features, diagnosis, and management of the condition.

Case Report
A 10-year-old girl presented for evaluation of a white forelock and multiple white patches of skin on the trunk and extremities (Figure). The white forelock was present at birth and a few white patches appeared on the chest at 3 months of age. During the subsequent 4 years, the white patches gradually progressed to involve the central forehead, abdomen, and extremities. Multiple frecklelike macules also appeared within the patches and the surrounding healthy skin.

Physical examination revealed a healthy girl with a prominent, large, diamond-shaped, depigmented patch on the central forehead that was associated with a white forelock. The hairs of the medial eyebrows and the eyelashes also were depigmented. Large, irregularly shaped, depigmented patches were present on the trunk and anterior extremities. There were multiple hyperpigmented macules overlying both the depigmented patches and the adjacent normally pigmented skin. The rest of the physical examination and the results of routine blood tests and urinalysis were unremarkable. The patient's mother and 4 siblings also were born with a white forelock. Similar depigmented patches on the trunk and extremities with a similar pattern and distribution were noted in all of them. Neither the patient nor her mother and siblings had midfacial anomalies, deafness, or heterochromia irides.

Comment
Piebaldism is a rare autosomal dominant disorder of melanocyte development resulting from mutations of the c-kit protooncogene.1,2 The disorder is characterized clinically by congenital poliosis and leukoderma. A white forelock is present at birth and may be the only manifestation in most affected individuals.3 The white forelock may have a triangular or diamond shape, and the underlying skin of the scalp also is amelanotic. Typical piebald lesions are typified by well-circumscribed, irregular, chalk white patches, often with hyperpigmented frecklelike macules noted on both depigmented and unaffected adjacent skin.4 The lesions often exhibit a classic distribution, involving the central forehead and anterior trunk, with extension to the flanks and anterior midarms, midknees, and midlegs. The medial third of the eyebrows and eyelashes also may be affected in severe cases.4 Characteristically, there is sparing of the dorsal midline, hands, feet, and periorificial areas. Piebaldism generally is a static disorder of pigmentation, though contraction of the affected areas with time or the appearance of new hyperpigmented macular lesions has been described.5 Progression of the depigmented patches has been reported in isolated cases with a novel Val620Ala mutation in Kit.6 Piebaldism rarely is associated with other disorders such as Hirschsprung disease, neurofibromatosis type 1, congenital dyserythropoietic anemia type II, Diamond-Blackfan anemia, and Grover disease.7-11 Individual case reports with associated deafness also have been described.12 Histopathologic evaluation of the depigmented lesions reveals absent or considerably reduced melanocytes. The hyperpigmented macules have a normal number of melanocytes and an increased number of melanosomes in the melanocytes and keratinocytes.4 The molecular basis of piebaldism was traced by Giebel and Spritz1 and Fleischman et al13 to mutations of the c-kit protooncogene. To date, 14 point mutations, 9 deletion mutations, 2 nucleotide splicing mutations, and 3 insertions of Kit have been described.6,14 c-kit Mutations are found in about 75% of patients with piebaldism.14 Mutations in the slug gene, which is a zinc-finger neural crest transcription factor, have been reported in piebaldism that lacked mutations in Kit.15 The human kit gene encodes the tyrosine kinase transmembrane cellular receptor for mast/stem cell growth factor, which is a critical factor for melanoblast migration, proliferation, differentiation, and survival.6 It would be pertinent to note here that the severity of the phenotype in piebaldism correlates with the site of the mutation within the kit gene. The most severe phenotypes are caused by mutations involving the intracellular tyrosine kinase domain, whereas the mildest phenotypes result from mutations involving the amino-terminal extracellular ligand-binding domain.6 The differential diagnosis of piebaldism includes any condition that may present with a depigmented lesion. Vitiligo is characterized by acquired depigmentation, typically in an acral and periorificial distribution. Piebaldism generally is distinguished from vitiligo by the presence of lesions from birth, hyperpigmented macules within and at the border of depigmented areas, and its static course. Moreover, piebaldism spares the dorsal midline, hands, feet, and periorificial areas. Waardenburg syndrome is an autosomal dominant disorder characterized by a congenital white forelock, lateral displacement of the medial canthi, a hypertrophic nasal root, heterochromia irides, and sensorineural hearing loss.16 At least 4 types of Waardenburg syndrome have been described based on the clinical and genetic criteria. The presence of hyperpigmented patches within the islands of depigmentation and on healthy skin; the absence of midfacial lesions, heterochromia irides, and deafness; and the location of depigmented patches on the trunk and extremities help to distinguish piebaldism from the various forms of Waardenburg syndrome.16 Ziprkowski-Margolis syndrome is a rare X-linked recessive syndrome characterized by deaf-mutism, heterochromic irides, piebaldlike hypomelanosis, and hyperpigmented macules, with a geographic appearance developing mainly on the trunk and extremities.17 Woolf syndrome is an autosomal recessive disorder consisting of piebaldism and deafness. Audiometry is crucial to exclude this diagnosis.18 Depending on its presentation, other conditions to consider include Addison disease, albinism, and systemic sclerosis, as well as use of depigmenting agents. Piebaldism is considered a relatively benign disorder, but it may have psychological impact because it is socially disabling, which presents a therapeutic challenge. Depigmented skin in piebaldism generally is considered unresponsive to medical or light therapy. Of note, the diagnosis of piebaldism should alert the clinician to the possibility of Waardenburg syndrome as determined by the results of ocular and auditory examinations. Sunscreens are recommended to avoid sunburns and to reduce the carcinogenic potential. To camouflage the exposed areas, makeup or temporary pigmenting agents such as the tanning product dihydroxyacetone may be used.19 The lesions of piebaldism do not respond to the topical agents used to treat vitiligo. Different surgical techniques have been tried, with variable success, including thin split-thickness grafts, minigrafting, transplant of autologous cultured melanocytes, and a combination of dermabrasion and grafting of the pigmented skin into the depigmented areas.20,21 Guerra et al22 reported achromic epidermis removed with the erbium:YAG laser and autologous cultured epidermal grafts were applied to the recipient bed in 6 patients. Autologous cultured epidermis, bearing a controlled number of melanocytes, induced repigmentation of all piebald lesions. The mean percentage repigmentation was 95.45%.22

Piebaldism is a rare autosomal dominant disorder characterized by congenital poliosis and leukoderma. We present a case of a 10-year-old girl with a typical clinical presentation, followed by a concise review of the literature discussing the etiology, clinical features, diagnosis, and management of the condition.

Case Report
A 10-year-old girl presented for evaluation of a white forelock and multiple white patches of skin on the trunk and extremities (Figure). The white forelock was present at birth and a few white patches appeared on the chest at 3 months of age. During the subsequent 4 years, the white patches gradually progressed to involve the central forehead, abdomen, and extremities. Multiple frecklelike macules also appeared within the patches and the surrounding healthy skin.

Physical examination revealed a healthy girl with a prominent, large, diamond-shaped, depigmented patch on the central forehead that was associated with a white forelock. The hairs of the medial eyebrows and the eyelashes also were depigmented. Large, irregularly shaped, depigmented patches were present on the trunk and anterior extremities. There were multiple hyperpigmented macules overlying both the depigmented patches and the adjacent normally pigmented skin. The rest of the physical examination and the results of routine blood tests and urinalysis were unremarkable. The patient's mother and 4 siblings also were born with a white forelock. Similar depigmented patches on the trunk and extremities with a similar pattern and distribution were noted in all of them. Neither the patient nor her mother and siblings had midfacial anomalies, deafness, or heterochromia irides.

Comment
Piebaldism is a rare autosomal dominant disorder of melanocyte development resulting from mutations of the c-kit protooncogene.1,2 The disorder is characterized clinically by congenital poliosis and leukoderma. A white forelock is present at birth and may be the only manifestation in most affected individuals.3 The white forelock may have a triangular or diamond shape, and the underlying skin of the scalp also is amelanotic. Typical piebald lesions are typified by well-circumscribed, irregular, chalk white patches, often with hyperpigmented frecklelike macules noted on both depigmented and unaffected adjacent skin.4 The lesions often exhibit a classic distribution, involving the central forehead and anterior trunk, with extension to the flanks and anterior midarms, midknees, and midlegs. The medial third of the eyebrows and eyelashes also may be affected in severe cases.4 Characteristically, there is sparing of the dorsal midline, hands, feet, and periorificial areas. Piebaldism generally is a static disorder of pigmentation, though contraction of the affected areas with time or the appearance of new hyperpigmented macular lesions has been described.5 Progression of the depigmented patches has been reported in isolated cases with a novel Val620Ala mutation in Kit.6 Piebaldism rarely is associated with other disorders such as Hirschsprung disease, neurofibromatosis type 1, congenital dyserythropoietic anemia type II, Diamond-Blackfan anemia, and Grover disease.7-11 Individual case reports with associated deafness also have been described.12 Histopathologic evaluation of the depigmented lesions reveals absent or considerably reduced melanocytes. The hyperpigmented macules have a normal number of melanocytes and an increased number of melanosomes in the melanocytes and keratinocytes.4 The molecular basis of piebaldism was traced by Giebel and Spritz1 and Fleischman et al13 to mutations of the c-kit protooncogene. To date, 14 point mutations, 9 deletion mutations, 2 nucleotide splicing mutations, and 3 insertions of Kit have been described.6,14 c-kit Mutations are found in about 75% of patients with piebaldism.14 Mutations in the slug gene, which is a zinc-finger neural crest transcription factor, have been reported in piebaldism that lacked mutations in Kit.15 The human kit gene encodes the tyrosine kinase transmembrane cellular receptor for mast/stem cell growth factor, which is a critical factor for melanoblast migration, proliferation, differentiation, and survival.6 It would be pertinent to note here that the severity of the phenotype in piebaldism correlates with the site of the mutation within the kit gene. The most severe phenotypes are caused by mutations involving the intracellular tyrosine kinase domain, whereas the mildest phenotypes result from mutations involving the amino-terminal extracellular ligand-binding domain.6 The differential diagnosis of piebaldism includes any condition that may present with a depigmented lesion. Vitiligo is characterized by acquired depigmentation, typically in an acral and periorificial distribution. Piebaldism generally is distinguished from vitiligo by the presence of lesions from birth, hyperpigmented macules within and at the border of depigmented areas, and its static course. Moreover, piebaldism spares the dorsal midline, hands, feet, and periorificial areas. Waardenburg syndrome is an autosomal dominant disorder characterized by a congenital white forelock, lateral displacement of the medial canthi, a hypertrophic nasal root, heterochromia irides, and sensorineural hearing loss.16 At least 4 types of Waardenburg syndrome have been described based on the clinical and genetic criteria. The presence of hyperpigmented patches within the islands of depigmentation and on healthy skin; the absence of midfacial lesions, heterochromia irides, and deafness; and the location of depigmented patches on the trunk and extremities help to distinguish piebaldism from the various forms of Waardenburg syndrome.16 Ziprkowski-Margolis syndrome is a rare X-linked recessive syndrome characterized by deaf-mutism, heterochromic irides, piebaldlike hypomelanosis, and hyperpigmented macules, with a geographic appearance developing mainly on the trunk and extremities.17 Woolf syndrome is an autosomal recessive disorder consisting of piebaldism and deafness. Audiometry is crucial to exclude this diagnosis.18 Depending on its presentation, other conditions to consider include Addison disease, albinism, and systemic sclerosis, as well as use of depigmenting agents. Piebaldism is considered a relatively benign disorder, but it may have psychological impact because it is socially disabling, which presents a therapeutic challenge. Depigmented skin in piebaldism generally is considered unresponsive to medical or light therapy. Of note, the diagnosis of piebaldism should alert the clinician to the possibility of Waardenburg syndrome as determined by the results of ocular and auditory examinations. Sunscreens are recommended to avoid sunburns and to reduce the carcinogenic potential. To camouflage the exposed areas, makeup or temporary pigmenting agents such as the tanning product dihydroxyacetone may be used.19 The lesions of piebaldism do not respond to the topical agents used to treat vitiligo. Different surgical techniques have been tried, with variable success, including thin split-thickness grafts, minigrafting, transplant of autologous cultured melanocytes, and a combination of dermabrasion and grafting of the pigmented skin into the depigmented areas.20,21 Guerra et al22 reported achromic epidermis removed with the erbium:YAG laser and autologous cultured epidermal grafts were applied to the recipient bed in 6 patients. Autologous cultured epidermis, bearing a controlled number of melanocytes, induced repigmentation of all piebald lesions. The mean percentage repigmentation was 95.45%.22

Piebaldism is a rare autosomal dominant disorder characterized by congenital poliosis and leukoderma. We present a case of a 10-year-old girl with a typical clinical presentation, followed by a concise review of the literature discussing the etiology, clinical features, diagnosis, and management of the condition.

Case Report
A 10-year-old girl presented for evaluation of a white forelock and multiple white patches of skin on the trunk and extremities (Figure). The white forelock was present at birth and a few white patches appeared on the chest at 3 months of age. During the subsequent 4 years, the white patches gradually progressed to involve the central forehead, abdomen, and extremities. Multiple frecklelike macules also appeared within the patches and the surrounding healthy skin.

Physical examination revealed a healthy girl with a prominent, large, diamond-shaped, depigmented patch on the central forehead that was associated with a white forelock. The hairs of the medial eyebrows and the eyelashes also were depigmented. Large, irregularly shaped, depigmented patches were present on the trunk and anterior extremities. There were multiple hyperpigmented macules overlying both the depigmented patches and the adjacent normally pigmented skin. The rest of the physical examination and the results of routine blood tests and urinalysis were unremarkable. The patient's mother and 4 siblings also were born with a white forelock. Similar depigmented patches on the trunk and extremities with a similar pattern and distribution were noted in all of them. Neither the patient nor her mother and siblings had midfacial anomalies, deafness, or heterochromia irides.

Comment
Piebaldism is a rare autosomal dominant disorder of melanocyte development resulting from mutations of the c-kit protooncogene.1,2 The disorder is characterized clinically by congenital poliosis and leukoderma. A white forelock is present at birth and may be the only manifestation in most affected individuals.3 The white forelock may have a triangular or diamond shape, and the underlying skin of the scalp also is amelanotic. Typical piebald lesions are typified by well-circumscribed, irregular, chalk white patches, often with hyperpigmented frecklelike macules noted on both depigmented and unaffected adjacent skin.4 The lesions often exhibit a classic distribution, involving the central forehead and anterior trunk, with extension to the flanks and anterior midarms, midknees, and midlegs. The medial third of the eyebrows and eyelashes also may be affected in severe cases.4 Characteristically, there is sparing of the dorsal midline, hands, feet, and periorificial areas. Piebaldism generally is a static disorder of pigmentation, though contraction of the affected areas with time or the appearance of new hyperpigmented macular lesions has been described.5 Progression of the depigmented patches has been reported in isolated cases with a novel Val620Ala mutation in Kit.6 Piebaldism rarely is associated with other disorders such as Hirschsprung disease, neurofibromatosis type 1, congenital dyserythropoietic anemia type II, Diamond-Blackfan anemia, and Grover disease.7-11 Individual case reports with associated deafness also have been described.12 Histopathologic evaluation of the depigmented lesions reveals absent or considerably reduced melanocytes. The hyperpigmented macules have a normal number of melanocytes and an increased number of melanosomes in the melanocytes and keratinocytes.4 The molecular basis of piebaldism was traced by Giebel and Spritz1 and Fleischman et al13 to mutations of the c-kit protooncogene. To date, 14 point mutations, 9 deletion mutations, 2 nucleotide splicing mutations, and 3 insertions of Kit have been described.6,14 c-kit Mutations are found in about 75% of patients with piebaldism.14 Mutations in the slug gene, which is a zinc-finger neural crest transcription factor, have been reported in piebaldism that lacked mutations in Kit.15 The human kit gene encodes the tyrosine kinase transmembrane cellular receptor for mast/stem cell growth factor, which is a critical factor for melanoblast migration, proliferation, differentiation, and survival.6 It would be pertinent to note here that the severity of the phenotype in piebaldism correlates with the site of the mutation within the kit gene. The most severe phenotypes are caused by mutations involving the intracellular tyrosine kinase domain, whereas the mildest phenotypes result from mutations involving the amino-terminal extracellular ligand-binding domain.6 The differential diagnosis of piebaldism includes any condition that may present with a depigmented lesion. Vitiligo is characterized by acquired depigmentation, typically in an acral and periorificial distribution. Piebaldism generally is distinguished from vitiligo by the presence of lesions from birth, hyperpigmented macules within and at the border of depigmented areas, and its static course. Moreover, piebaldism spares the dorsal midline, hands, feet, and periorificial areas. Waardenburg syndrome is an autosomal dominant disorder characterized by a congenital white forelock, lateral displacement of the medial canthi, a hypertrophic nasal root, heterochromia irides, and sensorineural hearing loss.16 At least 4 types of Waardenburg syndrome have been described based on the clinical and genetic criteria. The presence of hyperpigmented patches within the islands of depigmentation and on healthy skin; the absence of midfacial lesions, heterochromia irides, and deafness; and the location of depigmented patches on the trunk and extremities help to distinguish piebaldism from the various forms of Waardenburg syndrome.16 Ziprkowski-Margolis syndrome is a rare X-linked recessive syndrome characterized by deaf-mutism, heterochromic irides, piebaldlike hypomelanosis, and hyperpigmented macules, with a geographic appearance developing mainly on the trunk and extremities.17 Woolf syndrome is an autosomal recessive disorder consisting of piebaldism and deafness. Audiometry is crucial to exclude this diagnosis.18 Depending on its presentation, other conditions to consider include Addison disease, albinism, and systemic sclerosis, as well as use of depigmenting agents. Piebaldism is considered a relatively benign disorder, but it may have psychological impact because it is socially disabling, which presents a therapeutic challenge. Depigmented skin in piebaldism generally is considered unresponsive to medical or light therapy. Of note, the diagnosis of piebaldism should alert the clinician to the possibility of Waardenburg syndrome as determined by the results of ocular and auditory examinations. Sunscreens are recommended to avoid sunburns and to reduce the carcinogenic potential. To camouflage the exposed areas, makeup or temporary pigmenting agents such as the tanning product dihydroxyacetone may be used.19 The lesions of piebaldism do not respond to the topical agents used to treat vitiligo. Different surgical techniques have been tried, with variable success, including thin split-thickness grafts, minigrafting, transplant of autologous cultured melanocytes, and a combination of dermabrasion and grafting of the pigmented skin into the depigmented areas.20,21 Guerra et al22 reported achromic epidermis removed with the erbium:YAG laser and autologous cultured epidermal grafts were applied to the recipient bed in 6 patients. Autologous cultured epidermis, bearing a controlled number of melanocytes, induced repigmentation of all piebald lesions. The mean percentage repigmentation was 95.45%.22

HONOLULU — Although many black men with pseudofolliculitis barbae, otherwise known as "razor bumps," may express horror at the idea of shaving every day, this may be their best option, said Dr. Milton Moore at the annual meeting of the National Medical Association.

"You'd be surprised at how many African American men, when you talk about shaving with razors, [say,] 'Oh no, I can't do that!' " said Dr. Moore, who is in private practice in Houston. "Many of them don't even know that they can shave. They know Dad couldn't, and Dad didn't, and Dad didn't show them how to shave with razors, so they assume that they will have a problem if they use a razor."

As a result, these men may not be getting the best results in managing pseudofolliculitis barbae (PFB), he said. "The razor is the best shave."

The quality of the blade can make a big difference in treatment, he noted. "Some of the lesser expensive blades are very ineffective in shaving for someone with PFB," because they can get dull before the shaving process is finished. "You're already causing a problem by dragging and pulling the hair when trying to cut these hairs."

"The more expensive blades are more expensive because they are coated with different ingredients that harden the blade," he said. They also are made with a better grade of steel.

"I find that you can use a good razor for anywhere between five to seven shaves before you have to discard it," said Dr. Moore. While there are many blades on the market, the brands that have three to five blades with a lubricating strip are the best.

He disclosed that he has a patent for the Moore Technique Shaving System for treatment of PFB.

PFB affects about 60% of young black men, and 10%-15% of white men. In PFB, hair has grown out from the skin, curled over, and then pierced and reentered the skin. In the treatment of this condition, it is important to prevent this reentrance to the skin. Symptoms range widely in severity, from two or three papules in some white men to a great many found in black men. Shaving of the papules can result in bleeding. And because the papules are present, many men start shaving less frequently to avoid discomfort or they grow beards instead.

By lifting the hair before shaving, and by shaving every day, the hair doesn't grow long enough to curl back and pierce and reenter the skin, he explained. "That is why it is essential that a person shave daily, or every other day in someone who has very slow-growing hair."

To help with shaving, an exfoliant may be used, especially one that focuses on the beard area but not to the extent that discoloration and irritation occur.

An antibacterial preparation also may be needed because of infection in PFB. Products commonly used include "sulfur salicylic acid, which causes exfoliation and does have antibacterial activity," he said. Other antibacterials that have been used include clindamycin and benzoyl peroxide. Using a combination of these products in a patient with both PFB and acne can help treat both problems. "But antibacterial agents alone are not sufficient to control PFB," because hair does still grow and is trapped in the skin, he noted.

Dr. Moore has found that the optimal PFB treatment may differ between people, but most individuals can get good results. Helpful agents soften the hair, and cause "some exfoliation around the hair follicle."

Depilatories have been the mainstay of reducing razor bumps, he said. These products dissolve hair. But many people have found this treatment inadequate. Depilatories can irritate the skin and may not allow men to be clean shaven every day. "They may have to shave every 2 or 3 days," he added. Their appearance may not be good between shaves.

As with the use of depilatories, the use of clippers can be "somewhat effective," he said, in reducing the number of hairs that are trapped beneath the skin. But clippers don't cut the hair very short.

Another common technique is to use tweezers to pluck out the hairs that are trapped, but this can make the condition worse because the plucked hair is typically broken off at the core of the follicle. As it grows back, the result can be more papule formation.

Lastly, while laser hair-removal treatments may be helpful, these can be expensive, he concluded.

HONOLULU — Although many black men with pseudofolliculitis barbae, otherwise known as "razor bumps," may express horror at the idea of shaving every day, this may be their best option, said Dr. Milton Moore at the annual meeting of the National Medical Association.

"You'd be surprised at how many African American men, when you talk about shaving with razors, [say,] 'Oh no, I can't do that!' " said Dr. Moore, who is in private practice in Houston. "Many of them don't even know that they can shave. They know Dad couldn't, and Dad didn't, and Dad didn't show them how to shave with razors, so they assume that they will have a problem if they use a razor."

As a result, these men may not be getting the best results in managing pseudofolliculitis barbae (PFB), he said. "The razor is the best shave."

The quality of the blade can make a big difference in treatment, he noted. "Some of the lesser expensive blades are very ineffective in shaving for someone with PFB," because they can get dull before the shaving process is finished. "You're already causing a problem by dragging and pulling the hair when trying to cut these hairs."

"The more expensive blades are more expensive because they are coated with different ingredients that harden the blade," he said. They also are made with a better grade of steel.

"I find that you can use a good razor for anywhere between five to seven shaves before you have to discard it," said Dr. Moore. While there are many blades on the market, the brands that have three to five blades with a lubricating strip are the best.

He disclosed that he has a patent for the Moore Technique Shaving System for treatment of PFB.

PFB affects about 60% of young black men, and 10%-15% of white men. In PFB, hair has grown out from the skin, curled over, and then pierced and reentered the skin. In the treatment of this condition, it is important to prevent this reentrance to the skin. Symptoms range widely in severity, from two or three papules in some white men to a great many found in black men. Shaving of the papules can result in bleeding. And because the papules are present, many men start shaving less frequently to avoid discomfort or they grow beards instead.

By lifting the hair before shaving, and by shaving every day, the hair doesn't grow long enough to curl back and pierce and reenter the skin, he explained. "That is why it is essential that a person shave daily, or every other day in someone who has very slow-growing hair."

To help with shaving, an exfoliant may be used, especially one that focuses on the beard area but not to the extent that discoloration and irritation occur.

An antibacterial preparation also may be needed because of infection in PFB. Products commonly used include "sulfur salicylic acid, which causes exfoliation and does have antibacterial activity," he said. Other antibacterials that have been used include clindamycin and benzoyl peroxide. Using a combination of these products in a patient with both PFB and acne can help treat both problems. "But antibacterial agents alone are not sufficient to control PFB," because hair does still grow and is trapped in the skin, he noted.

Dr. Moore has found that the optimal PFB treatment may differ between people, but most individuals can get good results. Helpful agents soften the hair, and cause "some exfoliation around the hair follicle."

Depilatories have been the mainstay of reducing razor bumps, he said. These products dissolve hair. But many people have found this treatment inadequate. Depilatories can irritate the skin and may not allow men to be clean shaven every day. "They may have to shave every 2 or 3 days," he added. Their appearance may not be good between shaves.

As with the use of depilatories, the use of clippers can be "somewhat effective," he said, in reducing the number of hairs that are trapped beneath the skin. But clippers don't cut the hair very short.

Another common technique is to use tweezers to pluck out the hairs that are trapped, but this can make the condition worse because the plucked hair is typically broken off at the core of the follicle. As it grows back, the result can be more papule formation.

Lastly, while laser hair-removal treatments may be helpful, these can be expensive, he concluded.

HONOLULU — Although many black men with pseudofolliculitis barbae, otherwise known as "razor bumps," may express horror at the idea of shaving every day, this may be their best option, said Dr. Milton Moore at the annual meeting of the National Medical Association.

"You'd be surprised at how many African American men, when you talk about shaving with razors, [say,] 'Oh no, I can't do that!' " said Dr. Moore, who is in private practice in Houston. "Many of them don't even know that they can shave. They know Dad couldn't, and Dad didn't, and Dad didn't show them how to shave with razors, so they assume that they will have a problem if they use a razor."

As a result, these men may not be getting the best results in managing pseudofolliculitis barbae (PFB), he said. "The razor is the best shave."

The quality of the blade can make a big difference in treatment, he noted. "Some of the lesser expensive blades are very ineffective in shaving for someone with PFB," because they can get dull before the shaving process is finished. "You're already causing a problem by dragging and pulling the hair when trying to cut these hairs."

"The more expensive blades are more expensive because they are coated with different ingredients that harden the blade," he said. They also are made with a better grade of steel.

"I find that you can use a good razor for anywhere between five to seven shaves before you have to discard it," said Dr. Moore. While there are many blades on the market, the brands that have three to five blades with a lubricating strip are the best.

He disclosed that he has a patent for the Moore Technique Shaving System for treatment of PFB.

PFB affects about 60% of young black men, and 10%-15% of white men. In PFB, hair has grown out from the skin, curled over, and then pierced and reentered the skin. In the treatment of this condition, it is important to prevent this reentrance to the skin. Symptoms range widely in severity, from two or three papules in some white men to a great many found in black men. Shaving of the papules can result in bleeding. And because the papules are present, many men start shaving less frequently to avoid discomfort or they grow beards instead.

By lifting the hair before shaving, and by shaving every day, the hair doesn't grow long enough to curl back and pierce and reenter the skin, he explained. "That is why it is essential that a person shave daily, or every other day in someone who has very slow-growing hair."

To help with shaving, an exfoliant may be used, especially one that focuses on the beard area but not to the extent that discoloration and irritation occur.

An antibacterial preparation also may be needed because of infection in PFB. Products commonly used include "sulfur salicylic acid, which causes exfoliation and does have antibacterial activity," he said. Other antibacterials that have been used include clindamycin and benzoyl peroxide. Using a combination of these products in a patient with both PFB and acne can help treat both problems. "But antibacterial agents alone are not sufficient to control PFB," because hair does still grow and is trapped in the skin, he noted.

Dr. Moore has found that the optimal PFB treatment may differ between people, but most individuals can get good results. Helpful agents soften the hair, and cause "some exfoliation around the hair follicle."

Depilatories have been the mainstay of reducing razor bumps, he said. These products dissolve hair. But many people have found this treatment inadequate. Depilatories can irritate the skin and may not allow men to be clean shaven every day. "They may have to shave every 2 or 3 days," he added. Their appearance may not be good between shaves.

As with the use of depilatories, the use of clippers can be "somewhat effective," he said, in reducing the number of hairs that are trapped beneath the skin. But clippers don't cut the hair very short.

Another common technique is to use tweezers to pluck out the hairs that are trapped, but this can make the condition worse because the plucked hair is typically broken off at the core of the follicle. As it grows back, the result can be more papule formation.

Lastly, while laser hair-removal treatments may be helpful, these can be expensive, he concluded.

NEW YORK — End-on dermoscopy is an invaluable tool in making an accurate diagnosis in patients who present with dark streaks in the nails of their fingers or toes, Dr. Nathaniel Jellinek said at the American Academy of Dermatology's Academy 2007 meeting.

Because the dorsal nail plate is produced by the proximal nail matrix, and the ventral plate is produced by the distal matrix, an end-on dermoscopic view of the patient's nails can provide something of a map of the nail, indicating the points from which the pigment is emanating (J. Am. Acad. Dermatol. 2006;55:512–3). This can be a helpful guide as to where and when to biopsy, said Dr. Jellinek of the department of dermatology, Brown University, Providence, R.I.

The real value of end-on dermoscopy is not so much that it leads to a definite diagnosis in and of itself, but that it can tell you where you need to look when taking a biopsy, he said. It helps you zero in on the lesion location.

Dorsal pigmentation points to a proximal matrix lesion, whereas pigmentation of the ventral aspect of the nail plate points to distal lesions. "You still have to biopsy if you are not sure what you're looking at," Dr. Jellinek said.

Nail biopsies, however, are tricky. Small biopsies in the setting of a large lesion run the risk of missing something important, but larger full-thickness biopsies (greater than 3 mm) increase the risk of permanent dystrophy, particularly of the proximal matrix. This can lead to permanent split nails.

Dr. Jellinek outlined his published algorithmic approach for assessing and evaluating longitudinal melanonychia. If the lesion seems to be in the distal nail matrix and measures 3 mm or less, a 3-mm punch biopsy is adequate and safe. If the lesion is larger than 3 mm, however, a newer technique—the matrix shave biopsy—may be a better option (J. Amer. Acad. Dermatol. 2007;56:803–10).

Any proximal matrix lesion can be handled elegantly by the matrix shave biopsy. "Done right, there's minimal risk of nail dystrophy," he said of the shave technique. Any lesion of the lateral aspects of the nail unit should be handled by lateral longitudinal excision.

Longitudinal brown or black streaks on a nail present a diagnostic challenge. In most cases, the underlying etiology is benign, but in some, these streaks can signal the presence of nail melanoma.

The first diagnostic step is to consider the patient's age and overall cutaneous appearance, according to Dr. Jellinek. Melanomas are extremely rare in children and younger adolescents; this is reassuring but certainly not an absolute finding, and each patient must be evaluated on a case-by-case basis. Furthermore, "always look at the patient's whole skin. It can provide a lot of clues," Dr. Jellinek added. Then, go to dermoscopy and end-on dermoscopy, preferably using a water-soluble medium.

The observable diagnostic features of melanocytic nevi on dermoscopy include brown, longitudinal pigmentation with smooth, parallel lines and consistent thickness. Brown pigmentation overlaid by longitudinal lines showing irregularity of thickness, spacing, or alignment are suggestive of melanoma (Dermatol. Ther. 2007;20:3–10).

Grayish bands without any brown stripes are suggestive of lentigines or other types of melanocytic activation, and are much less suggestive of melanoma. Round-shaped black spots are generally blood spots under the nail plate, indicative of injury but not neoplasia. It is important to note that the presence of blood does not rule out an underlying neoplasm (J. Am. Acad. Dermatol. 2007;57:176).

Although most physicians notice brown streaks on a patient's nails, and quickly jump into a work-up to rule out malignant melanoma, many overlook cases of erythronychia, or red streaks in the nail plate. "It's underrecognized in our clinics. I'm seeing red bands in the nails at least once a week," Dr. Jellinek said.

These lesions almost always involve the distal nail matrix, and although they are usually innocuous, this is not always the case.

The real worry is squamous cell carcinoma, which is, fortunately, rare in the nail bed, he noted. If the red streak is on only one nail and is long standing, then it is probably stable and not neoplastic.

Dermoscopy of the left great toenail (left) shows a longitudinal band with parallel brown lines. With end-on dermoscopy, the pigment maps to the ventral surface of the nail plate's free edge (arrow). PHOTOS COURTESY DR. NATHANIEL JELLINEK

NEW YORK — End-on dermoscopy is an invaluable tool in making an accurate diagnosis in patients who present with dark streaks in the nails of their fingers or toes, Dr. Nathaniel Jellinek said at the American Academy of Dermatology's Academy 2007 meeting.

Because the dorsal nail plate is produced by the proximal nail matrix, and the ventral plate is produced by the distal matrix, an end-on dermoscopic view of the patient's nails can provide something of a map of the nail, indicating the points from which the pigment is emanating (J. Am. Acad. Dermatol. 2006;55:512–3). This can be a helpful guide as to where and when to biopsy, said Dr. Jellinek of the department of dermatology, Brown University, Providence, R.I.

The real value of end-on dermoscopy is not so much that it leads to a definite diagnosis in and of itself, but that it can tell you where you need to look when taking a biopsy, he said. It helps you zero in on the lesion location.

Dorsal pigmentation points to a proximal matrix lesion, whereas pigmentation of the ventral aspect of the nail plate points to distal lesions. "You still have to biopsy if you are not sure what you're looking at," Dr. Jellinek said.

Nail biopsies, however, are tricky. Small biopsies in the setting of a large lesion run the risk of missing something important, but larger full-thickness biopsies (greater than 3 mm) increase the risk of permanent dystrophy, particularly of the proximal matrix. This can lead to permanent split nails.

Dr. Jellinek outlined his published algorithmic approach for assessing and evaluating longitudinal melanonychia. If the lesion seems to be in the distal nail matrix and measures 3 mm or less, a 3-mm punch biopsy is adequate and safe. If the lesion is larger than 3 mm, however, a newer technique—the matrix shave biopsy—may be a better option (J. Amer. Acad. Dermatol. 2007;56:803–10).

Any proximal matrix lesion can be handled elegantly by the matrix shave biopsy. "Done right, there's minimal risk of nail dystrophy," he said of the shave technique. Any lesion of the lateral aspects of the nail unit should be handled by lateral longitudinal excision.

Longitudinal brown or black streaks on a nail present a diagnostic challenge. In most cases, the underlying etiology is benign, but in some, these streaks can signal the presence of nail melanoma.

The first diagnostic step is to consider the patient's age and overall cutaneous appearance, according to Dr. Jellinek. Melanomas are extremely rare in children and younger adolescents; this is reassuring but certainly not an absolute finding, and each patient must be evaluated on a case-by-case basis. Furthermore, "always look at the patient's whole skin. It can provide a lot of clues," Dr. Jellinek added. Then, go to dermoscopy and end-on dermoscopy, preferably using a water-soluble medium.

The observable diagnostic features of melanocytic nevi on dermoscopy include brown, longitudinal pigmentation with smooth, parallel lines and consistent thickness. Brown pigmentation overlaid by longitudinal lines showing irregularity of thickness, spacing, or alignment are suggestive of melanoma (Dermatol. Ther. 2007;20:3–10).

Grayish bands without any brown stripes are suggestive of lentigines or other types of melanocytic activation, and are much less suggestive of melanoma. Round-shaped black spots are generally blood spots under the nail plate, indicative of injury but not neoplasia. It is important to note that the presence of blood does not rule out an underlying neoplasm (J. Am. Acad. Dermatol. 2007;57:176).

Although most physicians notice brown streaks on a patient's nails, and quickly jump into a work-up to rule out malignant melanoma, many overlook cases of erythronychia, or red streaks in the nail plate. "It's underrecognized in our clinics. I'm seeing red bands in the nails at least once a week," Dr. Jellinek said.

These lesions almost always involve the distal nail matrix, and although they are usually innocuous, this is not always the case.

The real worry is squamous cell carcinoma, which is, fortunately, rare in the nail bed, he noted. If the red streak is on only one nail and is long standing, then it is probably stable and not neoplastic.

Dermoscopy of the left great toenail (left) shows a longitudinal band with parallel brown lines. With end-on dermoscopy, the pigment maps to the ventral surface of the nail plate's free edge (arrow). PHOTOS COURTESY DR. NATHANIEL JELLINEK

NEW YORK — End-on dermoscopy is an invaluable tool in making an accurate diagnosis in patients who present with dark streaks in the nails of their fingers or toes, Dr. Nathaniel Jellinek said at the American Academy of Dermatology's Academy 2007 meeting.

Because the dorsal nail plate is produced by the proximal nail matrix, and the ventral plate is produced by the distal matrix, an end-on dermoscopic view of the patient's nails can provide something of a map of the nail, indicating the points from which the pigment is emanating (J. Am. Acad. Dermatol. 2006;55:512–3). This can be a helpful guide as to where and when to biopsy, said Dr. Jellinek of the department of dermatology, Brown University, Providence, R.I.

The real value of end-on dermoscopy is not so much that it leads to a definite diagnosis in and of itself, but that it can tell you where you need to look when taking a biopsy, he said. It helps you zero in on the lesion location.

Dorsal pigmentation points to a proximal matrix lesion, whereas pigmentation of the ventral aspect of the nail plate points to distal lesions. "You still have to biopsy if you are not sure what you're looking at," Dr. Jellinek said.

Nail biopsies, however, are tricky. Small biopsies in the setting of a large lesion run the risk of missing something important, but larger full-thickness biopsies (greater than 3 mm) increase the risk of permanent dystrophy, particularly of the proximal matrix. This can lead to permanent split nails.

Dr. Jellinek outlined his published algorithmic approach for assessing and evaluating longitudinal melanonychia. If the lesion seems to be in the distal nail matrix and measures 3 mm or less, a 3-mm punch biopsy is adequate and safe. If the lesion is larger than 3 mm, however, a newer technique—the matrix shave biopsy—may be a better option (J. Amer. Acad. Dermatol. 2007;56:803–10).

Any proximal matrix lesion can be handled elegantly by the matrix shave biopsy. "Done right, there's minimal risk of nail dystrophy," he said of the shave technique. Any lesion of the lateral aspects of the nail unit should be handled by lateral longitudinal excision.

Longitudinal brown or black streaks on a nail present a diagnostic challenge. In most cases, the underlying etiology is benign, but in some, these streaks can signal the presence of nail melanoma.

The first diagnostic step is to consider the patient's age and overall cutaneous appearance, according to Dr. Jellinek. Melanomas are extremely rare in children and younger adolescents; this is reassuring but certainly not an absolute finding, and each patient must be evaluated on a case-by-case basis. Furthermore, "always look at the patient's whole skin. It can provide a lot of clues," Dr. Jellinek added. Then, go to dermoscopy and end-on dermoscopy, preferably using a water-soluble medium.

The observable diagnostic features of melanocytic nevi on dermoscopy include brown, longitudinal pigmentation with smooth, parallel lines and consistent thickness. Brown pigmentation overlaid by longitudinal lines showing irregularity of thickness, spacing, or alignment are suggestive of melanoma (Dermatol. Ther. 2007;20:3–10).

Grayish bands without any brown stripes are suggestive of lentigines or other types of melanocytic activation, and are much less suggestive of melanoma. Round-shaped black spots are generally blood spots under the nail plate, indicative of injury but not neoplasia. It is important to note that the presence of blood does not rule out an underlying neoplasm (J. Am. Acad. Dermatol. 2007;57:176).

Although most physicians notice brown streaks on a patient's nails, and quickly jump into a work-up to rule out malignant melanoma, many overlook cases of erythronychia, or red streaks in the nail plate. "It's underrecognized in our clinics. I'm seeing red bands in the nails at least once a week," Dr. Jellinek said.

These lesions almost always involve the distal nail matrix, and although they are usually innocuous, this is not always the case.

The real worry is squamous cell carcinoma, which is, fortunately, rare in the nail bed, he noted. If the red streak is on only one nail and is long standing, then it is probably stable and not neoplastic.

Dermoscopy of the left great toenail (left) shows a longitudinal band with parallel brown lines. With end-on dermoscopy, the pigment maps to the ventral surface of the nail plate's free edge (arrow). PHOTOS COURTESY DR. NATHANIEL JELLINEK

CORONADO, CALIF. — A patient who has abnormal-looking nails with a normal plantar and web surface is unlikely to have onychomycosis, Dr. Boni E. Elewski said at the annual meeting of the Pacific Dermatologic Association.

The presence of tinea pedis on the plantar surface or web space confirms that clinical suspicion.

"There are several exceptions, one of which is someone who has obtained an infection from a pedicure," said Dr. Elewski, professor of dermatology at the University of Alabama, Birmingham.

"You can't eliminate that. So if you have a patient with pristine feet and they have no [previous] history of tinea pedis, ask if they get regular pedicures, because you can get a direct infection of the nail plate from a pedicure," she explained.

The other exceptions are white superficial onychomycosis and proximal white subungual onychomycosis, two subtypes in which the fungus directly attacks the nail plate rather than the skin first.

Dr. Elewski provided several other clinical pearls regarding onychomycosis:

▸ A patient with abnormal fingernails and normal toenails is unlikely to have onychomycosis. The exception is Candida onycholysis. "This occurs commonly in women who have Raynaud's syndrome and other patients who have collagen vascular disease, but that's a very small minority of patients," she said.

▸ Fluconazole 200–400 mg once a week is effective for Candida onychomycosis or paronychia. "We underuse this drug in dermatology," she said. "It is a good antifungal and it's very cheap, about 25 cents per tablet. You only need to treat for 6–8 weeks in most patients."

She usually instructs her patients to take fluconazole on Fridays and uses the term "fungal Fridays" as a catchy reminder. Some of her dermatology residents prefer Tuesdays or, as they call it, "Toesdays."

▸ Know the bad prognostic factors of onychomycosis. These include dermatophytoma, thick nail, a total dystrophic nail, predominantly lateral nail involvement, and immunocompromised and/or diabetic patients.

Physicians can improve the prognosis in patients with dermatophytoma by debriding the area as much as possible. "You can give patients antifungal cream, lotion, or gel to smear under it, and then treat it with an oral antifungal," said Dr. Elewski, a past president of the American Academy of Dermatology.

She also noted that patients with thick nails require careful evaluation because not all of them will have onychomycosis. "Thick nails could come from trauma, from running or skiing, or from runner's toe," she explained.

In patients with lateral nail involvement, she clips away at the lateral edge, smears in antifungal cream, and continues treatment with oral antifungals.

Most patients with a bad prognostic factor will require treatment with oral terbinafine 250 mg daily or itraconazole 400 mg daily for 1 week per month for 4 months or longer.

▸ Itraconazole is the choice in nondermatophyte mold infections of the nail. There are two other drugs on the horizon "that may supersede itraconazole in this situation," Dr. Elewski said. These are posaconazole (Noxafil), which is not approved for this indication but is under investigation, and a drug in development called albaconazole.

▸ Topical antimycotic agents may be sufficient to treat onychomycosis in certain situations. The only topical agent that is approved by the Food and Drug Administration for onychomycosis is 8% ciclopirox olamine lacquer. Dr. Elewski said that she also finds it useful in white superficial onychomycosis and in minimal nail disease.

▸ The nail can provide clues to skin disease. To illustrate, she discussed the case of a patient who presented with a scaly dermatosis on the pretibial area. "Is this eczema? Stasis dermatitis?" she asked. "If the toes are abnormal and the patient has onychomycosis, there is a high likelihood that a scaly rash on the lower legs could be a dermatophyte infection. If the toes are normal, the patient probably does not have a dermatophyte infection on the lower legs."

Dr. Elewski disclosed that she has conducted clinical research for Novartis, Barrier Therapeutics, and Stiefel Laboratories.

Bad prognostic factors for onychomycosis include dermatophytoma, thick nail, and a total dystrophic nail. COURTESY DR. BONI E. ELEWSKI

CORONADO, CALIF. — A patient who has abnormal-looking nails with a normal plantar and web surface is unlikely to have onychomycosis, Dr. Boni E. Elewski said at the annual meeting of the Pacific Dermatologic Association.

The presence of tinea pedis on the plantar surface or web space confirms that clinical suspicion.

"There are several exceptions, one of which is someone who has obtained an infection from a pedicure," said Dr. Elewski, professor of dermatology at the University of Alabama, Birmingham.

"You can't eliminate that. So if you have a patient with pristine feet and they have no [previous] history of tinea pedis, ask if they get regular pedicures, because you can get a direct infection of the nail plate from a pedicure," she explained.

The other exceptions are white superficial onychomycosis and proximal white subungual onychomycosis, two subtypes in which the fungus directly attacks the nail plate rather than the skin first.

Dr. Elewski provided several other clinical pearls regarding onychomycosis:

▸ A patient with abnormal fingernails and normal toenails is unlikely to have onychomycosis. The exception is Candida onycholysis. "This occurs commonly in women who have Raynaud's syndrome and other patients who have collagen vascular disease, but that's a very small minority of patients," she said.

▸ Fluconazole 200–400 mg once a week is effective for Candida onychomycosis or paronychia. "We underuse this drug in dermatology," she said. "It is a good antifungal and it's very cheap, about 25 cents per tablet. You only need to treat for 6–8 weeks in most patients."

She usually instructs her patients to take fluconazole on Fridays and uses the term "fungal Fridays" as a catchy reminder. Some of her dermatology residents prefer Tuesdays or, as they call it, "Toesdays."

▸ Know the bad prognostic factors of onychomycosis. These include dermatophytoma, thick nail, a total dystrophic nail, predominantly lateral nail involvement, and immunocompromised and/or diabetic patients.

Physicians can improve the prognosis in patients with dermatophytoma by debriding the area as much as possible. "You can give patients antifungal cream, lotion, or gel to smear under it, and then treat it with an oral antifungal," said Dr. Elewski, a past president of the American Academy of Dermatology.

She also noted that patients with thick nails require careful evaluation because not all of them will have onychomycosis. "Thick nails could come from trauma, from running or skiing, or from runner's toe," she explained.

In patients with lateral nail involvement, she clips away at the lateral edge, smears in antifungal cream, and continues treatment with oral antifungals.

Most patients with a bad prognostic factor will require treatment with oral terbinafine 250 mg daily or itraconazole 400 mg daily for 1 week per month for 4 months or longer.

▸ Itraconazole is the choice in nondermatophyte mold infections of the nail. There are two other drugs on the horizon "that may supersede itraconazole in this situation," Dr. Elewski said. These are posaconazole (Noxafil), which is not approved for this indication but is under investigation, and a drug in development called albaconazole.

▸ Topical antimycotic agents may be sufficient to treat onychomycosis in certain situations. The only topical agent that is approved by the Food and Drug Administration for onychomycosis is 8% ciclopirox olamine lacquer. Dr. Elewski said that she also finds it useful in white superficial onychomycosis and in minimal nail disease.

▸ The nail can provide clues to skin disease. To illustrate, she discussed the case of a patient who presented with a scaly dermatosis on the pretibial area. "Is this eczema? Stasis dermatitis?" she asked. "If the toes are abnormal and the patient has onychomycosis, there is a high likelihood that a scaly rash on the lower legs could be a dermatophyte infection. If the toes are normal, the patient probably does not have a dermatophyte infection on the lower legs."

Dr. Elewski disclosed that she has conducted clinical research for Novartis, Barrier Therapeutics, and Stiefel Laboratories.

Bad prognostic factors for onychomycosis include dermatophytoma, thick nail, and a total dystrophic nail. COURTESY DR. BONI E. ELEWSKI

CORONADO, CALIF. — A patient who has abnormal-looking nails with a normal plantar and web surface is unlikely to have onychomycosis, Dr. Boni E. Elewski said at the annual meeting of the Pacific Dermatologic Association.

The presence of tinea pedis on the plantar surface or web space confirms that clinical suspicion.

"There are several exceptions, one of which is someone who has obtained an infection from a pedicure," said Dr. Elewski, professor of dermatology at the University of Alabama, Birmingham.

"You can't eliminate that. So if you have a patient with pristine feet and they have no [previous] history of tinea pedis, ask if they get regular pedicures, because you can get a direct infection of the nail plate from a pedicure," she explained.

The other exceptions are white superficial onychomycosis and proximal white subungual onychomycosis, two subtypes in which the fungus directly attacks the nail plate rather than the skin first.

Dr. Elewski provided several other clinical pearls regarding onychomycosis:

▸ A patient with abnormal fingernails and normal toenails is unlikely to have onychomycosis. The exception is Candida onycholysis. "This occurs commonly in women who have Raynaud's syndrome and other patients who have collagen vascular disease, but that's a very small minority of patients," she said.

▸ Fluconazole 200–400 mg once a week is effective for Candida onychomycosis or paronychia. "We underuse this drug in dermatology," she said. "It is a good antifungal and it's very cheap, about 25 cents per tablet. You only need to treat for 6–8 weeks in most patients."

She usually instructs her patients to take fluconazole on Fridays and uses the term "fungal Fridays" as a catchy reminder. Some of her dermatology residents prefer Tuesdays or, as they call it, "Toesdays."

▸ Know the bad prognostic factors of onychomycosis. These include dermatophytoma, thick nail, a total dystrophic nail, predominantly lateral nail involvement, and immunocompromised and/or diabetic patients.

Physicians can improve the prognosis in patients with dermatophytoma by debriding the area as much as possible. "You can give patients antifungal cream, lotion, or gel to smear under it, and then treat it with an oral antifungal," said Dr. Elewski, a past president of the American Academy of Dermatology.

She also noted that patients with thick nails require careful evaluation because not all of them will have onychomycosis. "Thick nails could come from trauma, from running or skiing, or from runner's toe," she explained.

In patients with lateral nail involvement, she clips away at the lateral edge, smears in antifungal cream, and continues treatment with oral antifungals.

Most patients with a bad prognostic factor will require treatment with oral terbinafine 250 mg daily or itraconazole 400 mg daily for 1 week per month for 4 months or longer.

▸ Itraconazole is the choice in nondermatophyte mold infections of the nail. There are two other drugs on the horizon "that may supersede itraconazole in this situation," Dr. Elewski said. These are posaconazole (Noxafil), which is not approved for this indication but is under investigation, and a drug in development called albaconazole.

▸ Topical antimycotic agents may be sufficient to treat onychomycosis in certain situations. The only topical agent that is approved by the Food and Drug Administration for onychomycosis is 8% ciclopirox olamine lacquer. Dr. Elewski said that she also finds it useful in white superficial onychomycosis and in minimal nail disease.

▸ The nail can provide clues to skin disease. To illustrate, she discussed the case of a patient who presented with a scaly dermatosis on the pretibial area. "Is this eczema? Stasis dermatitis?" she asked. "If the toes are abnormal and the patient has onychomycosis, there is a high likelihood that a scaly rash on the lower legs could be a dermatophyte infection. If the toes are normal, the patient probably does not have a dermatophyte infection on the lower legs."

Dr. Elewski disclosed that she has conducted clinical research for Novartis, Barrier Therapeutics, and Stiefel Laboratories.

Bad prognostic factors for onychomycosis include dermatophytoma, thick nail, and a total dystrophic nail. COURTESY DR. BONI E. ELEWSKI