Hair & Nails

Folliculitis is a common complaint seen in dermatology practice. The differential diagnosis of folliculitis is broad and includes Demodex folliculitis. In humans, the Demodex mite species Demodex folliculorum and Demodex brevis have been found to inhabit the pilosebaceous unit. D folliculorum typically is found in the follicular infundibulum; D brevis exists in the sebaceous and meibomian glands.¹ Although the prevalence of Demodex approaches 100% in middle-aged and elderly adults,¹ mite density normally is low in healthy skin.²Demodex mites are considered pathogenic only when they are found in large numbers or in an intradermal location³; therefore, it has been suggested that D folliculorum may play a role in various papular and pustular eruptions of the head and neck, such as demodicosis and rosacea.³ We examine a case of scalp folliculitis secondary to Demodex infection and the role that this organism plays in the pathogenesis of folliculitis, as well as the available treatment options. 

Case Report

A 57-year-old white man presented to our department in June 2004 with an "infected scalp" and scalp irritation for 2 months. The patient was diagnosed with bacterial folliculitis and treated with clindamycin 1% gel twice daily for 1 month. He presented for follow-up in July 2004 with continued complaint of scalp pruritus and rash (Figure 1). Results of an examination showed a deep pink 10X7-cm plaque on the scalp with hyperkeratosis and pustules. An ectoparasite wet mount prepared from one of the pustules revealed the presence of several Demodex mites (Figure 2). The patient was treated with sulfacetamide 10% plus sulfur 5% cream twice daily, in addition to a 2-week course of selenium sulfide 2.5% shampoo once daily. When the patient was seen for follow-up in September 2004, his entire scalp had cleared (Figure 3). He was instructed to continue the selenium sulfide 2.5% shampoo twice weekly for 6 months to prevent recurrence.

Please refer to the PDF to view the figures

Comment

The Demodex mite is a ubiquitous arthropod measuring approximately 0.1 to 0.4 mm in length. Typically, it infests areas around the eyelids, nose, and ear canals in human hosts.⁴ The life cycle of the mite is 18 to 24 days. The female mite lays 20 to 24 eggs in a hair follicle where the eggs are nourished by the surrounding pilosebaceous unit. The eggs hatch and the nymphs continue to live in the follicle where their main source of food is human glandular secretions.⁵ The mite primarily is an asymptomatic inhabitant of human pilosebaceous follicles and poses no harm to the host.¹

The role of D folliculorum in cutaneous disease in humans remains controversial. The pathogenicity is difficult to establish secondary to the localization of the disease, the widespread prevalence of infection with the D folliculorum mite, and the obligate nature of the parasite; therefore, the detection of the presence of the mite is not, in and of itself, enough evidence to establish pathogenicity.⁶ Results of immunohistochemical staining have shown that helper T lymphocytes predominate in the dermal infiltrate of demodicosis suggesting a possible role of cell-mediated immune response and delayed hypersensitivity.⁷ There also is evidence for a humoral immune response component with increased macrophages and Langerhans cells in the presence of infestation with Demodex.⁷

Demodex mites have been implicated as a causative agent in rosacea and pustular folliculitis.⁶ It is important to consider the possibility that the vascular changes of rosacea create an environment that is favorable to the multiplication of Demodex mites and their penetration into the dermis.⁸ Forton and Seys⁶ reported that Demodex mites are associated with the inflammatory symptoms of rosacea and that the mites are present in greater numbers and higher frequencies in patients with rosacea. Additionally, a study by Georgala et al⁷ evaluated the importance of D folliculorum in the etiology and course of rosacea and showed that D folliculorum was found in 83 (90.2%) of 92 rosacea subjects studied but in only 11 (11.9%) of the 92 controls, thereby concluding that although Demodex mites may not be the cause of rosacea, they may represent an important cofactor. Finally, Vollmer⁹ examined 388 follicles in 24 resections of skin for the presence of histologic folliculitis and Demodex mites. Results showed that Demodex mites were found in 87 (42%) of 208 follicles with inflammation but in just 18 (10%) of 180 follicles without inflammation. Furthermore, 87 (83%) of 105 follicles with Demodex showed inflammation, which demonstrated a nonrandom association between these 2 entities.⁹ A study by Meinking et al¹⁰ supported the rapid clearing of papulopustular dermatosis of the scalp and granulomatous rosacea when treated with scabicidal preparations such as permethrin or ivermectin, thereby supporting the pathogenic role of Demodex in papulopustular eruptions.

On the other hand, a review by Aylesworth and Vance¹¹ found that 117 (10%) of 1124 skin biopsies and 198 (12%) of 1692 follicles incidentally revealed that follicular mites were found in patients with various unrelated skin disorders, thereby suggesting that Demodex is a normal inhabitant of the hair follicle and is not pathogenic.¹¹ Other histologic evidence that failed to show a correlation between Demodex presence and skin disease was an examination of the results of 108 biopsy specimens of rosacea, of which only 20 (19%) contained Demodex.¹² There was no correlation between Demodex mites and skin disease in a study of 29 biopsy samples of the head and neck by Nutting and Green.¹³ We must note that the reported prevalence of Demodex presence is partially determined by the preciseness of the detection method used.

There are several treatment options available for demodicosis. In our case, the patient cleared with a combination of sulfacetamide 10% plus sulfur 5% cream, in addition to selenium sulfide 2.5% shampoo. Other commonly used treatment options include ivermectin,¹⁰ topical antibiotics, and topical retinoids.

The persistence of the patient's folliculitis despite treatment with clindamycin 1% gel; rapid clearance after therapy with sulfacetamide 10% plus sulfur 5% cream twice daily and selenium sulfide 2.5% shampoo once daily is initiated; and positive results of the ectoparasite wet mount suggest a pathogenic role of Demodex in causing the patient's symptoms. Although the link between folliculitis and Demodex infection remains controversial, this case demonstrates the importance of considering the possible role of Demodex in the differential diagnosis of rosacea and papulopustular eruptions of the head and neck. 

Folliculitis is a common complaint seen in dermatology practice. The differential diagnosis of folliculitis is broad and includes Demodex folliculitis. In humans, the Demodex mite species Demodex folliculorum and Demodex brevis have been found to inhabit the pilosebaceous unit. D folliculorum typically is found in the follicular infundibulum; D brevis exists in the sebaceous and meibomian glands.¹ Although the prevalence of Demodex approaches 100% in middle-aged and elderly adults,¹ mite density normally is low in healthy skin.²Demodex mites are considered pathogenic only when they are found in large numbers or in an intradermal location³; therefore, it has been suggested that D folliculorum may play a role in various papular and pustular eruptions of the head and neck, such as demodicosis and rosacea.³ We examine a case of scalp folliculitis secondary to Demodex infection and the role that this organism plays in the pathogenesis of folliculitis, as well as the available treatment options. 

Case Report

A 57-year-old white man presented to our department in June 2004 with an "infected scalp" and scalp irritation for 2 months. The patient was diagnosed with bacterial folliculitis and treated with clindamycin 1% gel twice daily for 1 month. He presented for follow-up in July 2004 with continued complaint of scalp pruritus and rash (Figure 1). Results of an examination showed a deep pink 10X7-cm plaque on the scalp with hyperkeratosis and pustules. An ectoparasite wet mount prepared from one of the pustules revealed the presence of several Demodex mites (Figure 2). The patient was treated with sulfacetamide 10% plus sulfur 5% cream twice daily, in addition to a 2-week course of selenium sulfide 2.5% shampoo once daily. When the patient was seen for follow-up in September 2004, his entire scalp had cleared (Figure 3). He was instructed to continue the selenium sulfide 2.5% shampoo twice weekly for 6 months to prevent recurrence.

Please refer to the PDF to view the figures

Comment

The Demodex mite is a ubiquitous arthropod measuring approximately 0.1 to 0.4 mm in length. Typically, it infests areas around the eyelids, nose, and ear canals in human hosts.⁴ The life cycle of the mite is 18 to 24 days. The female mite lays 20 to 24 eggs in a hair follicle where the eggs are nourished by the surrounding pilosebaceous unit. The eggs hatch and the nymphs continue to live in the follicle where their main source of food is human glandular secretions.⁵ The mite primarily is an asymptomatic inhabitant of human pilosebaceous follicles and poses no harm to the host.¹

The role of D folliculorum in cutaneous disease in humans remains controversial. The pathogenicity is difficult to establish secondary to the localization of the disease, the widespread prevalence of infection with the D folliculorum mite, and the obligate nature of the parasite; therefore, the detection of the presence of the mite is not, in and of itself, enough evidence to establish pathogenicity.⁶ Results of immunohistochemical staining have shown that helper T lymphocytes predominate in the dermal infiltrate of demodicosis suggesting a possible role of cell-mediated immune response and delayed hypersensitivity.⁷ There also is evidence for a humoral immune response component with increased macrophages and Langerhans cells in the presence of infestation with Demodex.⁷

Demodex mites have been implicated as a causative agent in rosacea and pustular folliculitis.⁶ It is important to consider the possibility that the vascular changes of rosacea create an environment that is favorable to the multiplication of Demodex mites and their penetration into the dermis.⁸ Forton and Seys⁶ reported that Demodex mites are associated with the inflammatory symptoms of rosacea and that the mites are present in greater numbers and higher frequencies in patients with rosacea. Additionally, a study by Georgala et al⁷ evaluated the importance of D folliculorum in the etiology and course of rosacea and showed that D folliculorum was found in 83 (90.2%) of 92 rosacea subjects studied but in only 11 (11.9%) of the 92 controls, thereby concluding that although Demodex mites may not be the cause of rosacea, they may represent an important cofactor. Finally, Vollmer⁹ examined 388 follicles in 24 resections of skin for the presence of histologic folliculitis and Demodex mites. Results showed that Demodex mites were found in 87 (42%) of 208 follicles with inflammation but in just 18 (10%) of 180 follicles without inflammation. Furthermore, 87 (83%) of 105 follicles with Demodex showed inflammation, which demonstrated a nonrandom association between these 2 entities.⁹ A study by Meinking et al¹⁰ supported the rapid clearing of papulopustular dermatosis of the scalp and granulomatous rosacea when treated with scabicidal preparations such as permethrin or ivermectin, thereby supporting the pathogenic role of Demodex in papulopustular eruptions.

On the other hand, a review by Aylesworth and Vance¹¹ found that 117 (10%) of 1124 skin biopsies and 198 (12%) of 1692 follicles incidentally revealed that follicular mites were found in patients with various unrelated skin disorders, thereby suggesting that Demodex is a normal inhabitant of the hair follicle and is not pathogenic.¹¹ Other histologic evidence that failed to show a correlation between Demodex presence and skin disease was an examination of the results of 108 biopsy specimens of rosacea, of which only 20 (19%) contained Demodex.¹² There was no correlation between Demodex mites and skin disease in a study of 29 biopsy samples of the head and neck by Nutting and Green.¹³ We must note that the reported prevalence of Demodex presence is partially determined by the preciseness of the detection method used.

There are several treatment options available for demodicosis. In our case, the patient cleared with a combination of sulfacetamide 10% plus sulfur 5% cream, in addition to selenium sulfide 2.5% shampoo. Other commonly used treatment options include ivermectin,¹⁰ topical antibiotics, and topical retinoids.

The persistence of the patient's folliculitis despite treatment with clindamycin 1% gel; rapid clearance after therapy with sulfacetamide 10% plus sulfur 5% cream twice daily and selenium sulfide 2.5% shampoo once daily is initiated; and positive results of the ectoparasite wet mount suggest a pathogenic role of Demodex in causing the patient's symptoms. Although the link between folliculitis and Demodex infection remains controversial, this case demonstrates the importance of considering the possible role of Demodex in the differential diagnosis of rosacea and papulopustular eruptions of the head and neck. 

Folliculitis is a common complaint seen in dermatology practice. The differential diagnosis of folliculitis is broad and includes Demodex folliculitis. In humans, the Demodex mite species Demodex folliculorum and Demodex brevis have been found to inhabit the pilosebaceous unit. D folliculorum typically is found in the follicular infundibulum; D brevis exists in the sebaceous and meibomian glands.¹ Although the prevalence of Demodex approaches 100% in middle-aged and elderly adults,¹ mite density normally is low in healthy skin.²Demodex mites are considered pathogenic only when they are found in large numbers or in an intradermal location³; therefore, it has been suggested that D folliculorum may play a role in various papular and pustular eruptions of the head and neck, such as demodicosis and rosacea.³ We examine a case of scalp folliculitis secondary to Demodex infection and the role that this organism plays in the pathogenesis of folliculitis, as well as the available treatment options. 

Case Report

A 57-year-old white man presented to our department in June 2004 with an "infected scalp" and scalp irritation for 2 months. The patient was diagnosed with bacterial folliculitis and treated with clindamycin 1% gel twice daily for 1 month. He presented for follow-up in July 2004 with continued complaint of scalp pruritus and rash (Figure 1). Results of an examination showed a deep pink 10X7-cm plaque on the scalp with hyperkeratosis and pustules. An ectoparasite wet mount prepared from one of the pustules revealed the presence of several Demodex mites (Figure 2). The patient was treated with sulfacetamide 10% plus sulfur 5% cream twice daily, in addition to a 2-week course of selenium sulfide 2.5% shampoo once daily. When the patient was seen for follow-up in September 2004, his entire scalp had cleared (Figure 3). He was instructed to continue the selenium sulfide 2.5% shampoo twice weekly for 6 months to prevent recurrence.

Please refer to the PDF to view the figures

Comment

The Demodex mite is a ubiquitous arthropod measuring approximately 0.1 to 0.4 mm in length. Typically, it infests areas around the eyelids, nose, and ear canals in human hosts.⁴ The life cycle of the mite is 18 to 24 days. The female mite lays 20 to 24 eggs in a hair follicle where the eggs are nourished by the surrounding pilosebaceous unit. The eggs hatch and the nymphs continue to live in the follicle where their main source of food is human glandular secretions.⁵ The mite primarily is an asymptomatic inhabitant of human pilosebaceous follicles and poses no harm to the host.¹

The role of D folliculorum in cutaneous disease in humans remains controversial. The pathogenicity is difficult to establish secondary to the localization of the disease, the widespread prevalence of infection with the D folliculorum mite, and the obligate nature of the parasite; therefore, the detection of the presence of the mite is not, in and of itself, enough evidence to establish pathogenicity.⁶ Results of immunohistochemical staining have shown that helper T lymphocytes predominate in the dermal infiltrate of demodicosis suggesting a possible role of cell-mediated immune response and delayed hypersensitivity.⁷ There also is evidence for a humoral immune response component with increased macrophages and Langerhans cells in the presence of infestation with Demodex.⁷

Demodex mites have been implicated as a causative agent in rosacea and pustular folliculitis.⁶ It is important to consider the possibility that the vascular changes of rosacea create an environment that is favorable to the multiplication of Demodex mites and their penetration into the dermis.⁸ Forton and Seys⁶ reported that Demodex mites are associated with the inflammatory symptoms of rosacea and that the mites are present in greater numbers and higher frequencies in patients with rosacea. Additionally, a study by Georgala et al⁷ evaluated the importance of D folliculorum in the etiology and course of rosacea and showed that D folliculorum was found in 83 (90.2%) of 92 rosacea subjects studied but in only 11 (11.9%) of the 92 controls, thereby concluding that although Demodex mites may not be the cause of rosacea, they may represent an important cofactor. Finally, Vollmer⁹ examined 388 follicles in 24 resections of skin for the presence of histologic folliculitis and Demodex mites. Results showed that Demodex mites were found in 87 (42%) of 208 follicles with inflammation but in just 18 (10%) of 180 follicles without inflammation. Furthermore, 87 (83%) of 105 follicles with Demodex showed inflammation, which demonstrated a nonrandom association between these 2 entities.⁹ A study by Meinking et al¹⁰ supported the rapid clearing of papulopustular dermatosis of the scalp and granulomatous rosacea when treated with scabicidal preparations such as permethrin or ivermectin, thereby supporting the pathogenic role of Demodex in papulopustular eruptions.

On the other hand, a review by Aylesworth and Vance¹¹ found that 117 (10%) of 1124 skin biopsies and 198 (12%) of 1692 follicles incidentally revealed that follicular mites were found in patients with various unrelated skin disorders, thereby suggesting that Demodex is a normal inhabitant of the hair follicle and is not pathogenic.¹¹ Other histologic evidence that failed to show a correlation between Demodex presence and skin disease was an examination of the results of 108 biopsy specimens of rosacea, of which only 20 (19%) contained Demodex.¹² There was no correlation between Demodex mites and skin disease in a study of 29 biopsy samples of the head and neck by Nutting and Green.¹³ We must note that the reported prevalence of Demodex presence is partially determined by the preciseness of the detection method used.

There are several treatment options available for demodicosis. In our case, the patient cleared with a combination of sulfacetamide 10% plus sulfur 5% cream, in addition to selenium sulfide 2.5% shampoo. Other commonly used treatment options include ivermectin,¹⁰ topical antibiotics, and topical retinoids.

The persistence of the patient's folliculitis despite treatment with clindamycin 1% gel; rapid clearance after therapy with sulfacetamide 10% plus sulfur 5% cream twice daily and selenium sulfide 2.5% shampoo once daily is initiated; and positive results of the ectoparasite wet mount suggest a pathogenic role of Demodex in causing the patient's symptoms. Although the link between folliculitis and Demodex infection remains controversial, this case demonstrates the importance of considering the possible role of Demodex in the differential diagnosis of rosacea and papulopustular eruptions of the head and neck. 

Median canaliform nail dystrophy is a nail abnormality that typically involves one or both thumbnails. The first case of this disorder was recorded by Heller¹ in 1928. Median canaliform nail dystrophy presents as a central longitudinal groove of the nail plate, extending proximally from the end of the nail.² This condition is usually not inherited. However, it may be acquired following trauma to the nail. We describe a man with familial median canaliform nail dystrophy and discuss the differential diagnosis.

Case Report

A 68-year-old man presented with bilateral dystrophy of his thumbnails. The nail abnormality initially appeared at 34 years of age with no preceding trauma to the digits. His older brother and his mother also had developed the same nail changes as young adults. Neither the patient nor his brother or mother rubbed their proximal thumbnail fold with the tip of their second finger; the absence of this behavioral activity was repeatedly confirmed by both the patient and his wife during several subsequent office visits.

Examination of both thumbnails showed an asymptomatic distal fissure with a fir tree–like pattern (Figure). Proximally, the nail plates showed transverse grooves. In addition, the lunula was red and enlarged.

Please refer to the PDF to view the figure

Comment

Median canaliform nail dystrophy appears as a long longitudinal groove extending from either the proximal nail fold or a more distal portion of the nail plate to the end of the nail. Lateral extensions of this fissure create a conspicuous inverted fir tree–like pattern. In severe cases, the nail can split along the groove.³ Thickening of the proximal nail fold, enlargement of the lunula, and redness of the lunula also may occur.^4-9

The diagnosis of this condition is usually established based on clinical features because pathologic correlation is rarely available. However, specimens for microscopic evaluation have occasionally been provided. Parakeratosis, as well as an accumulation of melanin within and between the nail bed keratinocytes, was demonstrated in the evaluation of an affected nail by Heller¹⁰ in 1927. Subsequently, parakeratosis and intranuclear pigmentation were found within the longitudinal canal of the affected nail plate of a 12-year-old girl with median canaliform nail dystrophy who was described by Robinson and Weidman¹¹ in 1948.

Median canaliform nail dystrophy may present following trauma to the nail plate or nail matrix.^3-7,12-15 In addition, coexisting conditions such as either soft tissue in the nail defect or dental caries have been observed in some patients with median canaliform nail dystrophy. In one case, a 19-year-old woman presented with a flabby filament of fleshy tissue that was observed within the dystrophic nail canal.¹⁴ The tissue was extracted, and the nail abnormality resolved. Subsequently, the nail dystrophy, including the associated tissue, reappeared.¹⁴ Tooth decay associated with median canaliform nail dystrophy was reported in a 23-year-old woman with a deformity that involved many of the nails on both of her hands. Her nail condition spontaneously cleared after 3 carious teeth were extracted.¹⁶

Medication was postulated as the causative factor for the development of median canaliform nail dystrophy in 3 patients who were receiving isotretinoin. The first, reported by Bottomley and Cunliffe¹⁷ in 1992, was a 38-year-old woman who developed median canaliform nail dystrophy 6 weeks after beginning treatment with isotretinoin. Her thumbnail returned to normal 4 weeks after she discontinued the drug.¹⁷ The second patient, described by Griego et al⁴ in 1995, was an 18-year-old man who developed median canaliform nail dystrophy of both thumbnails after starting therapy with isotretinoin for his acne. The nail disfigurement became distinct after 4 months of treatment; his new thumbnail dystrophy resolved 5 months after he discontinued the medication.⁴ A third patient was reported by Dharmagunawardena and Charles-Holmes¹² in 1997. They described a 19-year-old man who developed median canaliform nail dystrophy in both thumbnails within 4 weeks after starting treatment with isotretinoin for his acne. His nails returned to normal 3 months after completing a 5-month course of isotretinoin therapy.¹²

Familial median canaliform nail dystrophy has not been associated with any systemic syndromes. In our patient and his family, the nail dystrophy was not congenital but rather appeared as an acquired abnormality of the nails in adulthood.

The etiology of median canaliform nail dystrophy is unknown.^5,7,13,16-18 It usually is an acquired condition. Nail matrix trauma may precede the onset; however, an associated nail injury has often not occurred.^{3-7,12-16,19-21} This nail dystrophy is not considered to be inherited. The familial occurrence of median canaliform nail dystrophy has rarely been described. Indeed, to the best of our knowledge, in addition to our patient, only 3 families with median canaliform nail dystrophy have been described.^20,22,23 In the first such family, a 16-year-old girl with bilateral median canaliform nail dystrophy of her thumbnails since the age of 13 years had a mother with similar-appearing thumbnails.²⁰ A second such family also included a mother and daughter.²² Long longitudinal grooves were present in the daughter's left thumbnail since the age of 11 years; her mother had a similar dystrophy involving her right thumbnail that began when she was 12 years old. Her mother, currently 34 years old, still has recurrent episodes of spontaneously resolving median canaliform nail dystrophy. The family had no history of other hereditary diseases.²² The third family in which median canaliform nail dystrophy occurred was reported by Bossi²³ in the Italian literature in 1965. Our patient and his brother and mother represent the fourth such family.

The differential diagnosis of median canaliform nail dystrophy includes habit tic deformity (Table). It also includes other causes of longitudinal splits in the nail plate such as direct trauma to the nail unit. In addition, digital mucous cyst (synovial cyst), lichen striatus, nail-patella syndrome, pterygium, Raynaud disease, and trachyonychia are other conditions in which a longitudinal nail defect has been described.^5,7,30,31

Please refer to the PDF to view the table

Habit tic deformity is usually present in one or both thumbnails and results in alteration of the normal nail growth. It is caused by the constant or habitual rubbing of the thumb's proximal nail fold by the tip of the second digit. The subsequent damage to the nail matrix causes clinical changes in the nail plate that appear different than those of median canaliform nail dystrophy. The habit tic deformity produces transverse ridges along the central nail plate depression instead of a longitudinal groove with lateral projections. The depth of the central nail plate canal depends on the intensity of the inflicted trauma by the index finger to the matrix of the thumbnail. In addition, the lunula may appear red and enlarged.^9,29 Also, the proximal nail fold may be swollen.^5,13

Median canaliform nail dystrophy has occasionally been described to periodically disappear; often, the nail defect reappears in these individuals.^{4-7,13,15,17,24} In some patients, the central nail defect is replaced by a longitudinal ridge^5,6; however, in most patients, such as ours, the condition does not resolve spontaneously. Keeping the nail length short and buffing the surface of the nail can prevent the edge of the nail plate from catching on clothing and other objects.⁵ Covering the nail plate with tape or a nail wrap also can aid in ensuring that jagged edges are not present.^4,7 

Conclusion

Familial median canaliform nail dystrophy has rarely been described. Our patient had adult onset of his condition involving both thumbnails with associated red macrolunula. His brother and his mother also experienced the same nail dystrophy. Including our patient and his family, median canaliform nail dystrophy has only been reported in 4 families. The mode of inheritance for median canaliform nail dystrophy in these families remains to be determined. 

Median canaliform nail dystrophy is a nail abnormality that typically involves one or both thumbnails. The first case of this disorder was recorded by Heller¹ in 1928. Median canaliform nail dystrophy presents as a central longitudinal groove of the nail plate, extending proximally from the end of the nail.² This condition is usually not inherited. However, it may be acquired following trauma to the nail. We describe a man with familial median canaliform nail dystrophy and discuss the differential diagnosis.

Case Report

A 68-year-old man presented with bilateral dystrophy of his thumbnails. The nail abnormality initially appeared at 34 years of age with no preceding trauma to the digits. His older brother and his mother also had developed the same nail changes as young adults. Neither the patient nor his brother or mother rubbed their proximal thumbnail fold with the tip of their second finger; the absence of this behavioral activity was repeatedly confirmed by both the patient and his wife during several subsequent office visits.

Examination of both thumbnails showed an asymptomatic distal fissure with a fir tree–like pattern (Figure). Proximally, the nail plates showed transverse grooves. In addition, the lunula was red and enlarged.

Please refer to the PDF to view the figure

Comment

Median canaliform nail dystrophy appears as a long longitudinal groove extending from either the proximal nail fold or a more distal portion of the nail plate to the end of the nail. Lateral extensions of this fissure create a conspicuous inverted fir tree–like pattern. In severe cases, the nail can split along the groove.³ Thickening of the proximal nail fold, enlargement of the lunula, and redness of the lunula also may occur.^4-9

The diagnosis of this condition is usually established based on clinical features because pathologic correlation is rarely available. However, specimens for microscopic evaluation have occasionally been provided. Parakeratosis, as well as an accumulation of melanin within and between the nail bed keratinocytes, was demonstrated in the evaluation of an affected nail by Heller¹⁰ in 1927. Subsequently, parakeratosis and intranuclear pigmentation were found within the longitudinal canal of the affected nail plate of a 12-year-old girl with median canaliform nail dystrophy who was described by Robinson and Weidman¹¹ in 1948.

Median canaliform nail dystrophy may present following trauma to the nail plate or nail matrix.^3-7,12-15 In addition, coexisting conditions such as either soft tissue in the nail defect or dental caries have been observed in some patients with median canaliform nail dystrophy. In one case, a 19-year-old woman presented with a flabby filament of fleshy tissue that was observed within the dystrophic nail canal.¹⁴ The tissue was extracted, and the nail abnormality resolved. Subsequently, the nail dystrophy, including the associated tissue, reappeared.¹⁴ Tooth decay associated with median canaliform nail dystrophy was reported in a 23-year-old woman with a deformity that involved many of the nails on both of her hands. Her nail condition spontaneously cleared after 3 carious teeth were extracted.¹⁶

Medication was postulated as the causative factor for the development of median canaliform nail dystrophy in 3 patients who were receiving isotretinoin. The first, reported by Bottomley and Cunliffe¹⁷ in 1992, was a 38-year-old woman who developed median canaliform nail dystrophy 6 weeks after beginning treatment with isotretinoin. Her thumbnail returned to normal 4 weeks after she discontinued the drug.¹⁷ The second patient, described by Griego et al⁴ in 1995, was an 18-year-old man who developed median canaliform nail dystrophy of both thumbnails after starting therapy with isotretinoin for his acne. The nail disfigurement became distinct after 4 months of treatment; his new thumbnail dystrophy resolved 5 months after he discontinued the medication.⁴ A third patient was reported by Dharmagunawardena and Charles-Holmes¹² in 1997. They described a 19-year-old man who developed median canaliform nail dystrophy in both thumbnails within 4 weeks after starting treatment with isotretinoin for his acne. His nails returned to normal 3 months after completing a 5-month course of isotretinoin therapy.¹²

Familial median canaliform nail dystrophy has not been associated with any systemic syndromes. In our patient and his family, the nail dystrophy was not congenital but rather appeared as an acquired abnormality of the nails in adulthood.

The etiology of median canaliform nail dystrophy is unknown.^5,7,13,16-18 It usually is an acquired condition. Nail matrix trauma may precede the onset; however, an associated nail injury has often not occurred.^{3-7,12-16,19-21} This nail dystrophy is not considered to be inherited. The familial occurrence of median canaliform nail dystrophy has rarely been described. Indeed, to the best of our knowledge, in addition to our patient, only 3 families with median canaliform nail dystrophy have been described.^20,22,23 In the first such family, a 16-year-old girl with bilateral median canaliform nail dystrophy of her thumbnails since the age of 13 years had a mother with similar-appearing thumbnails.²⁰ A second such family also included a mother and daughter.²² Long longitudinal grooves were present in the daughter's left thumbnail since the age of 11 years; her mother had a similar dystrophy involving her right thumbnail that began when she was 12 years old. Her mother, currently 34 years old, still has recurrent episodes of spontaneously resolving median canaliform nail dystrophy. The family had no history of other hereditary diseases.²² The third family in which median canaliform nail dystrophy occurred was reported by Bossi²³ in the Italian literature in 1965. Our patient and his brother and mother represent the fourth such family.

The differential diagnosis of median canaliform nail dystrophy includes habit tic deformity (Table). It also includes other causes of longitudinal splits in the nail plate such as direct trauma to the nail unit. In addition, digital mucous cyst (synovial cyst), lichen striatus, nail-patella syndrome, pterygium, Raynaud disease, and trachyonychia are other conditions in which a longitudinal nail defect has been described.^5,7,30,31

Please refer to the PDF to view the table

Habit tic deformity is usually present in one or both thumbnails and results in alteration of the normal nail growth. It is caused by the constant or habitual rubbing of the thumb's proximal nail fold by the tip of the second digit. The subsequent damage to the nail matrix causes clinical changes in the nail plate that appear different than those of median canaliform nail dystrophy. The habit tic deformity produces transverse ridges along the central nail plate depression instead of a longitudinal groove with lateral projections. The depth of the central nail plate canal depends on the intensity of the inflicted trauma by the index finger to the matrix of the thumbnail. In addition, the lunula may appear red and enlarged.^9,29 Also, the proximal nail fold may be swollen.^5,13

Median canaliform nail dystrophy has occasionally been described to periodically disappear; often, the nail defect reappears in these individuals.^{4-7,13,15,17,24} In some patients, the central nail defect is replaced by a longitudinal ridge^5,6; however, in most patients, such as ours, the condition does not resolve spontaneously. Keeping the nail length short and buffing the surface of the nail can prevent the edge of the nail plate from catching on clothing and other objects.⁵ Covering the nail plate with tape or a nail wrap also can aid in ensuring that jagged edges are not present.^4,7 

Conclusion

Familial median canaliform nail dystrophy has rarely been described. Our patient had adult onset of his condition involving both thumbnails with associated red macrolunula. His brother and his mother also experienced the same nail dystrophy. Including our patient and his family, median canaliform nail dystrophy has only been reported in 4 families. The mode of inheritance for median canaliform nail dystrophy in these families remains to be determined. 

Median canaliform nail dystrophy is a nail abnormality that typically involves one or both thumbnails. The first case of this disorder was recorded by Heller¹ in 1928. Median canaliform nail dystrophy presents as a central longitudinal groove of the nail plate, extending proximally from the end of the nail.² This condition is usually not inherited. However, it may be acquired following trauma to the nail. We describe a man with familial median canaliform nail dystrophy and discuss the differential diagnosis.

Case Report

A 68-year-old man presented with bilateral dystrophy of his thumbnails. The nail abnormality initially appeared at 34 years of age with no preceding trauma to the digits. His older brother and his mother also had developed the same nail changes as young adults. Neither the patient nor his brother or mother rubbed their proximal thumbnail fold with the tip of their second finger; the absence of this behavioral activity was repeatedly confirmed by both the patient and his wife during several subsequent office visits.

Examination of both thumbnails showed an asymptomatic distal fissure with a fir tree–like pattern (Figure). Proximally, the nail plates showed transverse grooves. In addition, the lunula was red and enlarged.

Please refer to the PDF to view the figure

Comment

Median canaliform nail dystrophy appears as a long longitudinal groove extending from either the proximal nail fold or a more distal portion of the nail plate to the end of the nail. Lateral extensions of this fissure create a conspicuous inverted fir tree–like pattern. In severe cases, the nail can split along the groove.³ Thickening of the proximal nail fold, enlargement of the lunula, and redness of the lunula also may occur.^4-9

The diagnosis of this condition is usually established based on clinical features because pathologic correlation is rarely available. However, specimens for microscopic evaluation have occasionally been provided. Parakeratosis, as well as an accumulation of melanin within and between the nail bed keratinocytes, was demonstrated in the evaluation of an affected nail by Heller¹⁰ in 1927. Subsequently, parakeratosis and intranuclear pigmentation were found within the longitudinal canal of the affected nail plate of a 12-year-old girl with median canaliform nail dystrophy who was described by Robinson and Weidman¹¹ in 1948.

Median canaliform nail dystrophy may present following trauma to the nail plate or nail matrix.^3-7,12-15 In addition, coexisting conditions such as either soft tissue in the nail defect or dental caries have been observed in some patients with median canaliform nail dystrophy. In one case, a 19-year-old woman presented with a flabby filament of fleshy tissue that was observed within the dystrophic nail canal.¹⁴ The tissue was extracted, and the nail abnormality resolved. Subsequently, the nail dystrophy, including the associated tissue, reappeared.¹⁴ Tooth decay associated with median canaliform nail dystrophy was reported in a 23-year-old woman with a deformity that involved many of the nails on both of her hands. Her nail condition spontaneously cleared after 3 carious teeth were extracted.¹⁶

Medication was postulated as the causative factor for the development of median canaliform nail dystrophy in 3 patients who were receiving isotretinoin. The first, reported by Bottomley and Cunliffe¹⁷ in 1992, was a 38-year-old woman who developed median canaliform nail dystrophy 6 weeks after beginning treatment with isotretinoin. Her thumbnail returned to normal 4 weeks after she discontinued the drug.¹⁷ The second patient, described by Griego et al⁴ in 1995, was an 18-year-old man who developed median canaliform nail dystrophy of both thumbnails after starting therapy with isotretinoin for his acne. The nail disfigurement became distinct after 4 months of treatment; his new thumbnail dystrophy resolved 5 months after he discontinued the medication.⁴ A third patient was reported by Dharmagunawardena and Charles-Holmes¹² in 1997. They described a 19-year-old man who developed median canaliform nail dystrophy in both thumbnails within 4 weeks after starting treatment with isotretinoin for his acne. His nails returned to normal 3 months after completing a 5-month course of isotretinoin therapy.¹²

Familial median canaliform nail dystrophy has not been associated with any systemic syndromes. In our patient and his family, the nail dystrophy was not congenital but rather appeared as an acquired abnormality of the nails in adulthood.

The etiology of median canaliform nail dystrophy is unknown.^5,7,13,16-18 It usually is an acquired condition. Nail matrix trauma may precede the onset; however, an associated nail injury has often not occurred.^{3-7,12-16,19-21} This nail dystrophy is not considered to be inherited. The familial occurrence of median canaliform nail dystrophy has rarely been described. Indeed, to the best of our knowledge, in addition to our patient, only 3 families with median canaliform nail dystrophy have been described.^20,22,23 In the first such family, a 16-year-old girl with bilateral median canaliform nail dystrophy of her thumbnails since the age of 13 years had a mother with similar-appearing thumbnails.²⁰ A second such family also included a mother and daughter.²² Long longitudinal grooves were present in the daughter's left thumbnail since the age of 11 years; her mother had a similar dystrophy involving her right thumbnail that began when she was 12 years old. Her mother, currently 34 years old, still has recurrent episodes of spontaneously resolving median canaliform nail dystrophy. The family had no history of other hereditary diseases.²² The third family in which median canaliform nail dystrophy occurred was reported by Bossi²³ in the Italian literature in 1965. Our patient and his brother and mother represent the fourth such family.

The differential diagnosis of median canaliform nail dystrophy includes habit tic deformity (Table). It also includes other causes of longitudinal splits in the nail plate such as direct trauma to the nail unit. In addition, digital mucous cyst (synovial cyst), lichen striatus, nail-patella syndrome, pterygium, Raynaud disease, and trachyonychia are other conditions in which a longitudinal nail defect has been described.^5,7,30,31

Please refer to the PDF to view the table

Habit tic deformity is usually present in one or both thumbnails and results in alteration of the normal nail growth. It is caused by the constant or habitual rubbing of the thumb's proximal nail fold by the tip of the second digit. The subsequent damage to the nail matrix causes clinical changes in the nail plate that appear different than those of median canaliform nail dystrophy. The habit tic deformity produces transverse ridges along the central nail plate depression instead of a longitudinal groove with lateral projections. The depth of the central nail plate canal depends on the intensity of the inflicted trauma by the index finger to the matrix of the thumbnail. In addition, the lunula may appear red and enlarged.^9,29 Also, the proximal nail fold may be swollen.^5,13

Median canaliform nail dystrophy has occasionally been described to periodically disappear; often, the nail defect reappears in these individuals.^{4-7,13,15,17,24} In some patients, the central nail defect is replaced by a longitudinal ridge^5,6; however, in most patients, such as ours, the condition does not resolve spontaneously. Keeping the nail length short and buffing the surface of the nail can prevent the edge of the nail plate from catching on clothing and other objects.⁵ Covering the nail plate with tape or a nail wrap also can aid in ensuring that jagged edges are not present.^4,7 

Conclusion

Familial median canaliform nail dystrophy has rarely been described. Our patient had adult onset of his condition involving both thumbnails with associated red macrolunula. His brother and his mother also experienced the same nail dystrophy. Including our patient and his family, median canaliform nail dystrophy has only been reported in 4 families. The mode of inheritance for median canaliform nail dystrophy in these families remains to be determined. 

Onychotillomania is an uncommon condition characterized by self-destruction of the fingernails and/or toenails by compulsive manipulation. We report 2 cases of onychotillomania with differing presentations in a young man and in an older man. Onychotillomania may be a form of obsessive-compulsive disorder (OCD), and we discuss the psychologic factors and current treatments for this condition.

Emotional and psychologic factors have the ability to influence the underlying disease process in at least 33% of patients with a dermatologic condition.1 In some cases, such as onychotillomania, a psychiatric condition can be the underlining cause. Onychotillomania, a condition whose true incidence is unknown, is characterized by the compulsive or irresistible urge in patients to pick at, pull off, or harmfully bite or chew their nails. This urge may be conscious or unconscious. The word onychotillomania is derived from the Greek onycho, nail; tillo, to pull; and mania, madness or frenzy. In psychiatry, onychotillomania has been classified as an impulse control disorder that includes conditions such as compulsive gambling, kleptomania, pyromania, habit-tic deformity, and obsessive-compulsive disorder (OCD). The more well-documented trichotillomania, or pulling of the hair, is estimated to occur in up to 1 in 200 individuals.2 The incidence of onychotillomania is thought to be much lower and widely underreported. However, the incidence may surpass that of trichotillomania when nail biting, nail chewing, or habit-tic deformity is included, though this thought is controversial. In this report, we document 2 patients with slightly different presentations of onychotillomania and the approaches to their therapy.

Case Reports

Patient 1—A 72-year-old white man was referred to the dermatology clinic with an 8-month history of fingernail loss and pain. On physical examination, he was missing 2 nails on the left hand. Prominent longitudinal ridging was observed on the remaining nails, which were thick and yellow and showed some loss of the distal nail plate. All nails on the right hand were normal. Results of a biopsy showed epithelial necrosis with no evidence of lichen planus or inflammation. Fungal culture results were negative.

The patient was confrontational during the visit, protesting the nail examination. He continually drew back in protest, not wanting his nails examined. His wife reported the same, stating that he would slap her hands away anytime she tried to look at his nails. He also reported that there was a "clear goo" under his nails that he thought was necessary to remove by picking. Past medical history was significant for essential tremors, chronic obstructive pulmonary disease, and congestive heart failure. Medications included primidone and gabapentin for essential tremor and alprazolam at night for insomnia.

Based on examination findings and the patient's own admission, the diagnosis of onychotillomania was made. Results of plain film radiographs that were obtained to rule out osteomyelitis were negative. Attempts to use occlusive dressings were made, but the patient refused to keep the nails covered because he was unable to manipulate the remaining nails or nail beds. Also, referral for psychiatric evaluation was vehemently refused. The patient did not return for follow-up.

Patient 2—A 22-year-old white man presented to the dermatology clinic with a several-month history of pain in his toenails. On physical examination, he was missing all nails on his right foot. He had blood on and under all the remaining toenails, blood on all nail beds, and blood under most of his fingernails and on his fingertips. On questioning, the patient adamantly denied pulling his nails, even after confronted with the blood evidence on his fingers and fingernails. His mother reported that he constantly picked at his toenails.

Due to our suspicion of onychotillomania with secondary infection, the patient was treated initially with oral cephalexin followed by placement of an Unna boot on the involved foot with modifications to cover the entire foot and digits. This was changed once weekly. After one month, new healthy nail was noted, but the patient refused our recommendation for psychiatric evaluation and did not follow-up with us as recommended.

Comment

In both of our cases, the diagnosis of onychotillomania was made by the obvious physical signs on examination, as well as by self-admission in patient 1. Although we believed a psychiatric evaluation was necessary for proper treatment, it was refused by both patients.

Psychodermatologic problems can be grouped into 3 categories. Psychophysiologic disorders are exacerbated by emotional stress and include atopic dermatitis and psoriasis.3 Primary psychiatric disorders (anxiety, depression, delusion, and OCD) may present as delusions of parasitosis, neurotic excoriations, trichotillomania, and onychotillomania. In secondary psychiatric disorders, patients endure psychologic or emotional distress as a result of physical or visual deformity caused by primary skin disorders such as acne, leprosy, psoriasis, and vitiligo.4

The term onychotillomania previously has been used to include nail biting in addition to physical deformities caused by self-induced damage to the nails or periungual tissues by picking or pulling. However, it is generally reserved for the manual removal of the nail plate. Examination of individuals with onychotillomania may show periungual erosions and crusts associated with nail-plate surface abnormalities.5 The damage simply may be diminished or missing nails. The matrix melanocytes can be stimulated by chronic trauma, which may result in longitudinal melanonychia.6

Onychotillomania has been classified as a habit-tic deformity that may occur after psychological and emotional stress or as a form of OCD.7 However, the habit-tic deformity may not fit the true definition of onychotillomania, though pharmacologic treatment is similar. Paranoid delusions and psychoses also have been associated with onychotillomania,8 as has Smith-Magenis syndrome. This congenital anomaly associated with mental retardation is estimated to occur in 1 in 25,000 individuals. Self-mutilatory behavior is seen in 70% of patients and includes onychotillomania.9 The differential diagnosis also should include Lesch-Nyhan syndrome.

Treatment of the underlying psychologic disorders should be considered in those with onychotillomania. In addition to onychotillomania, the more common manifestations of OCD in dermatology include trichotillomania, onychophagia, acne excoriee, and neurotic excoriations.10 OCD most frequently is manifested in childhood, though behavior such as obsessive hand washing, AIDS phobia, and other psychosomatic dermatoses can be observed in all age groups.

However, not every patient with onychotillomania has OCD as the underlying psychopathology. Before coming to a conclusion that a patient with onychotillomania has OCD, one must rule out other psychiatric diagnostic possibilities, mainly delusion and simple habit disorder (habit-tic deformity). The key distinction between obsession and delusion is the presence or absence of insight on the part of the patient. Obsessive patients have more insight than delusional patients do. Often, patients with OCD are apologetic for their behavior.10 Patients with habit-tic deformity may be differentiated from true onychotillomania in that they may only rub their nails unconsciously and not actually pick off their nails.

It is important for the underlying psychiatric disorder to be defined by psychiatric evaluation and subsequent treatment with psychoactive medications.11 Common treatments for OCD include individual psychotherapy and behavioral therapy. In addition, there are 3 oral medications commonly used for their anti–obsessive-compulsive effect, namely, clomipramine, fluoxetine, and fluvoxamine.9 Paroxetine, sertraline, the mixed uptake inhibitor venlafaxine, and citalopram are the latest additions for the treatment of OCD.12 Fluoxetine hydrochloride also has been found helpful, specifically in the treatment of onychotillomania.12 In addition, pimozide has been used specifically to treat onychotillomania.8 Topical treatments also have been approached using distasteful preparations applied to the nails to discourage nail biting and chewing.5 The physical barrier method appeared to work quite well in our younger patient, though it was not effective in the treatment of our older patient.

Onychotillomania has been cited in the literature to include both nail pulling and nail biting, but our 2 patients exhibited the most classic form of onychotillomania of picking and pulling of the nails, as the term was originally coined. Neither of our patients had what would be classified as habit-tic deformity. We speculate that onychotillomania can be divided into a nail-pulling/picking group, a nail-biting group, and a combination of the 2. In any case, it is advisable to explore etiologies other than self-inflicted trauma, such as mechanical or friction trauma, fungal infection, or another form of nail dystrophy. However, when the diagnosis of onychotillomania is reached, in addition to occlusion to prevent the self-induced damage, referral to and treatment by a psychiatrist is warranted because of the strong association with underlying psychiatric conditions, namely, OCD. 

Onychotillomania is an uncommon condition characterized by self-destruction of the fingernails and/or toenails by compulsive manipulation. We report 2 cases of onychotillomania with differing presentations in a young man and in an older man. Onychotillomania may be a form of obsessive-compulsive disorder (OCD), and we discuss the psychologic factors and current treatments for this condition.

Emotional and psychologic factors have the ability to influence the underlying disease process in at least 33% of patients with a dermatologic condition.1 In some cases, such as onychotillomania, a psychiatric condition can be the underlining cause. Onychotillomania, a condition whose true incidence is unknown, is characterized by the compulsive or irresistible urge in patients to pick at, pull off, or harmfully bite or chew their nails. This urge may be conscious or unconscious. The word onychotillomania is derived from the Greek onycho, nail; tillo, to pull; and mania, madness or frenzy. In psychiatry, onychotillomania has been classified as an impulse control disorder that includes conditions such as compulsive gambling, kleptomania, pyromania, habit-tic deformity, and obsessive-compulsive disorder (OCD). The more well-documented trichotillomania, or pulling of the hair, is estimated to occur in up to 1 in 200 individuals.2 The incidence of onychotillomania is thought to be much lower and widely underreported. However, the incidence may surpass that of trichotillomania when nail biting, nail chewing, or habit-tic deformity is included, though this thought is controversial. In this report, we document 2 patients with slightly different presentations of onychotillomania and the approaches to their therapy.

Case Reports

Patient 1—A 72-year-old white man was referred to the dermatology clinic with an 8-month history of fingernail loss and pain. On physical examination, he was missing 2 nails on the left hand. Prominent longitudinal ridging was observed on the remaining nails, which were thick and yellow and showed some loss of the distal nail plate. All nails on the right hand were normal. Results of a biopsy showed epithelial necrosis with no evidence of lichen planus or inflammation. Fungal culture results were negative.

The patient was confrontational during the visit, protesting the nail examination. He continually drew back in protest, not wanting his nails examined. His wife reported the same, stating that he would slap her hands away anytime she tried to look at his nails. He also reported that there was a "clear goo" under his nails that he thought was necessary to remove by picking. Past medical history was significant for essential tremors, chronic obstructive pulmonary disease, and congestive heart failure. Medications included primidone and gabapentin for essential tremor and alprazolam at night for insomnia.

Based on examination findings and the patient's own admission, the diagnosis of onychotillomania was made. Results of plain film radiographs that were obtained to rule out osteomyelitis were negative. Attempts to use occlusive dressings were made, but the patient refused to keep the nails covered because he was unable to manipulate the remaining nails or nail beds. Also, referral for psychiatric evaluation was vehemently refused. The patient did not return for follow-up.

Patient 2—A 22-year-old white man presented to the dermatology clinic with a several-month history of pain in his toenails. On physical examination, he was missing all nails on his right foot. He had blood on and under all the remaining toenails, blood on all nail beds, and blood under most of his fingernails and on his fingertips. On questioning, the patient adamantly denied pulling his nails, even after confronted with the blood evidence on his fingers and fingernails. His mother reported that he constantly picked at his toenails.

Due to our suspicion of onychotillomania with secondary infection, the patient was treated initially with oral cephalexin followed by placement of an Unna boot on the involved foot with modifications to cover the entire foot and digits. This was changed once weekly. After one month, new healthy nail was noted, but the patient refused our recommendation for psychiatric evaluation and did not follow-up with us as recommended.

Comment

In both of our cases, the diagnosis of onychotillomania was made by the obvious physical signs on examination, as well as by self-admission in patient 1. Although we believed a psychiatric evaluation was necessary for proper treatment, it was refused by both patients.

Psychodermatologic problems can be grouped into 3 categories. Psychophysiologic disorders are exacerbated by emotional stress and include atopic dermatitis and psoriasis.3 Primary psychiatric disorders (anxiety, depression, delusion, and OCD) may present as delusions of parasitosis, neurotic excoriations, trichotillomania, and onychotillomania. In secondary psychiatric disorders, patients endure psychologic or emotional distress as a result of physical or visual deformity caused by primary skin disorders such as acne, leprosy, psoriasis, and vitiligo.4

The term onychotillomania previously has been used to include nail biting in addition to physical deformities caused by self-induced damage to the nails or periungual tissues by picking or pulling. However, it is generally reserved for the manual removal of the nail plate. Examination of individuals with onychotillomania may show periungual erosions and crusts associated with nail-plate surface abnormalities.5 The damage simply may be diminished or missing nails. The matrix melanocytes can be stimulated by chronic trauma, which may result in longitudinal melanonychia.6

Onychotillomania has been classified as a habit-tic deformity that may occur after psychological and emotional stress or as a form of OCD.7 However, the habit-tic deformity may not fit the true definition of onychotillomania, though pharmacologic treatment is similar. Paranoid delusions and psychoses also have been associated with onychotillomania,8 as has Smith-Magenis syndrome. This congenital anomaly associated with mental retardation is estimated to occur in 1 in 25,000 individuals. Self-mutilatory behavior is seen in 70% of patients and includes onychotillomania.9 The differential diagnosis also should include Lesch-Nyhan syndrome.

Treatment of the underlying psychologic disorders should be considered in those with onychotillomania. In addition to onychotillomania, the more common manifestations of OCD in dermatology include trichotillomania, onychophagia, acne excoriee, and neurotic excoriations.10 OCD most frequently is manifested in childhood, though behavior such as obsessive hand washing, AIDS phobia, and other psychosomatic dermatoses can be observed in all age groups.

However, not every patient with onychotillomania has OCD as the underlying psychopathology. Before coming to a conclusion that a patient with onychotillomania has OCD, one must rule out other psychiatric diagnostic possibilities, mainly delusion and simple habit disorder (habit-tic deformity). The key distinction between obsession and delusion is the presence or absence of insight on the part of the patient. Obsessive patients have more insight than delusional patients do. Often, patients with OCD are apologetic for their behavior.10 Patients with habit-tic deformity may be differentiated from true onychotillomania in that they may only rub their nails unconsciously and not actually pick off their nails.

It is important for the underlying psychiatric disorder to be defined by psychiatric evaluation and subsequent treatment with psychoactive medications.11 Common treatments for OCD include individual psychotherapy and behavioral therapy. In addition, there are 3 oral medications commonly used for their anti–obsessive-compulsive effect, namely, clomipramine, fluoxetine, and fluvoxamine.9 Paroxetine, sertraline, the mixed uptake inhibitor venlafaxine, and citalopram are the latest additions for the treatment of OCD.12 Fluoxetine hydrochloride also has been found helpful, specifically in the treatment of onychotillomania.12 In addition, pimozide has been used specifically to treat onychotillomania.8 Topical treatments also have been approached using distasteful preparations applied to the nails to discourage nail biting and chewing.5 The physical barrier method appeared to work quite well in our younger patient, though it was not effective in the treatment of our older patient.

Onychotillomania has been cited in the literature to include both nail pulling and nail biting, but our 2 patients exhibited the most classic form of onychotillomania of picking and pulling of the nails, as the term was originally coined. Neither of our patients had what would be classified as habit-tic deformity. We speculate that onychotillomania can be divided into a nail-pulling/picking group, a nail-biting group, and a combination of the 2. In any case, it is advisable to explore etiologies other than self-inflicted trauma, such as mechanical or friction trauma, fungal infection, or another form of nail dystrophy. However, when the diagnosis of onychotillomania is reached, in addition to occlusion to prevent the self-induced damage, referral to and treatment by a psychiatrist is warranted because of the strong association with underlying psychiatric conditions, namely, OCD. 

Onychotillomania is an uncommon condition characterized by self-destruction of the fingernails and/or toenails by compulsive manipulation. We report 2 cases of onychotillomania with differing presentations in a young man and in an older man. Onychotillomania may be a form of obsessive-compulsive disorder (OCD), and we discuss the psychologic factors and current treatments for this condition.

Emotional and psychologic factors have the ability to influence the underlying disease process in at least 33% of patients with a dermatologic condition.1 In some cases, such as onychotillomania, a psychiatric condition can be the underlining cause. Onychotillomania, a condition whose true incidence is unknown, is characterized by the compulsive or irresistible urge in patients to pick at, pull off, or harmfully bite or chew their nails. This urge may be conscious or unconscious. The word onychotillomania is derived from the Greek onycho, nail; tillo, to pull; and mania, madness or frenzy. In psychiatry, onychotillomania has been classified as an impulse control disorder that includes conditions such as compulsive gambling, kleptomania, pyromania, habit-tic deformity, and obsessive-compulsive disorder (OCD). The more well-documented trichotillomania, or pulling of the hair, is estimated to occur in up to 1 in 200 individuals.2 The incidence of onychotillomania is thought to be much lower and widely underreported. However, the incidence may surpass that of trichotillomania when nail biting, nail chewing, or habit-tic deformity is included, though this thought is controversial. In this report, we document 2 patients with slightly different presentations of onychotillomania and the approaches to their therapy.

Case Reports

Patient 1—A 72-year-old white man was referred to the dermatology clinic with an 8-month history of fingernail loss and pain. On physical examination, he was missing 2 nails on the left hand. Prominent longitudinal ridging was observed on the remaining nails, which were thick and yellow and showed some loss of the distal nail plate. All nails on the right hand were normal. Results of a biopsy showed epithelial necrosis with no evidence of lichen planus or inflammation. Fungal culture results were negative.

The patient was confrontational during the visit, protesting the nail examination. He continually drew back in protest, not wanting his nails examined. His wife reported the same, stating that he would slap her hands away anytime she tried to look at his nails. He also reported that there was a "clear goo" under his nails that he thought was necessary to remove by picking. Past medical history was significant for essential tremors, chronic obstructive pulmonary disease, and congestive heart failure. Medications included primidone and gabapentin for essential tremor and alprazolam at night for insomnia.

Based on examination findings and the patient's own admission, the diagnosis of onychotillomania was made. Results of plain film radiographs that were obtained to rule out osteomyelitis were negative. Attempts to use occlusive dressings were made, but the patient refused to keep the nails covered because he was unable to manipulate the remaining nails or nail beds. Also, referral for psychiatric evaluation was vehemently refused. The patient did not return for follow-up.

Patient 2—A 22-year-old white man presented to the dermatology clinic with a several-month history of pain in his toenails. On physical examination, he was missing all nails on his right foot. He had blood on and under all the remaining toenails, blood on all nail beds, and blood under most of his fingernails and on his fingertips. On questioning, the patient adamantly denied pulling his nails, even after confronted with the blood evidence on his fingers and fingernails. His mother reported that he constantly picked at his toenails.

Due to our suspicion of onychotillomania with secondary infection, the patient was treated initially with oral cephalexin followed by placement of an Unna boot on the involved foot with modifications to cover the entire foot and digits. This was changed once weekly. After one month, new healthy nail was noted, but the patient refused our recommendation for psychiatric evaluation and did not follow-up with us as recommended.

Comment

In both of our cases, the diagnosis of onychotillomania was made by the obvious physical signs on examination, as well as by self-admission in patient 1. Although we believed a psychiatric evaluation was necessary for proper treatment, it was refused by both patients.

Psychodermatologic problems can be grouped into 3 categories. Psychophysiologic disorders are exacerbated by emotional stress and include atopic dermatitis and psoriasis.3 Primary psychiatric disorders (anxiety, depression, delusion, and OCD) may present as delusions of parasitosis, neurotic excoriations, trichotillomania, and onychotillomania. In secondary psychiatric disorders, patients endure psychologic or emotional distress as a result of physical or visual deformity caused by primary skin disorders such as acne, leprosy, psoriasis, and vitiligo.4

The term onychotillomania previously has been used to include nail biting in addition to physical deformities caused by self-induced damage to the nails or periungual tissues by picking or pulling. However, it is generally reserved for the manual removal of the nail plate. Examination of individuals with onychotillomania may show periungual erosions and crusts associated with nail-plate surface abnormalities.5 The damage simply may be diminished or missing nails. The matrix melanocytes can be stimulated by chronic trauma, which may result in longitudinal melanonychia.6

Onychotillomania has been classified as a habit-tic deformity that may occur after psychological and emotional stress or as a form of OCD.7 However, the habit-tic deformity may not fit the true definition of onychotillomania, though pharmacologic treatment is similar. Paranoid delusions and psychoses also have been associated with onychotillomania,8 as has Smith-Magenis syndrome. This congenital anomaly associated with mental retardation is estimated to occur in 1 in 25,000 individuals. Self-mutilatory behavior is seen in 70% of patients and includes onychotillomania.9 The differential diagnosis also should include Lesch-Nyhan syndrome.

Treatment of the underlying psychologic disorders should be considered in those with onychotillomania. In addition to onychotillomania, the more common manifestations of OCD in dermatology include trichotillomania, onychophagia, acne excoriee, and neurotic excoriations.10 OCD most frequently is manifested in childhood, though behavior such as obsessive hand washing, AIDS phobia, and other psychosomatic dermatoses can be observed in all age groups.

However, not every patient with onychotillomania has OCD as the underlying psychopathology. Before coming to a conclusion that a patient with onychotillomania has OCD, one must rule out other psychiatric diagnostic possibilities, mainly delusion and simple habit disorder (habit-tic deformity). The key distinction between obsession and delusion is the presence or absence of insight on the part of the patient. Obsessive patients have more insight than delusional patients do. Often, patients with OCD are apologetic for their behavior.10 Patients with habit-tic deformity may be differentiated from true onychotillomania in that they may only rub their nails unconsciously and not actually pick off their nails.

It is important for the underlying psychiatric disorder to be defined by psychiatric evaluation and subsequent treatment with psychoactive medications.11 Common treatments for OCD include individual psychotherapy and behavioral therapy. In addition, there are 3 oral medications commonly used for their anti–obsessive-compulsive effect, namely, clomipramine, fluoxetine, and fluvoxamine.9 Paroxetine, sertraline, the mixed uptake inhibitor venlafaxine, and citalopram are the latest additions for the treatment of OCD.12 Fluoxetine hydrochloride also has been found helpful, specifically in the treatment of onychotillomania.12 In addition, pimozide has been used specifically to treat onychotillomania.8 Topical treatments also have been approached using distasteful preparations applied to the nails to discourage nail biting and chewing.5 The physical barrier method appeared to work quite well in our younger patient, though it was not effective in the treatment of our older patient.

Onychotillomania has been cited in the literature to include both nail pulling and nail biting, but our 2 patients exhibited the most classic form of onychotillomania of picking and pulling of the nails, as the term was originally coined. Neither of our patients had what would be classified as habit-tic deformity. We speculate that onychotillomania can be divided into a nail-pulling/picking group, a nail-biting group, and a combination of the 2. In any case, it is advisable to explore etiologies other than self-inflicted trauma, such as mechanical or friction trauma, fungal infection, or another form of nail dystrophy. However, when the diagnosis of onychotillomania is reached, in addition to occlusion to prevent the self-induced damage, referral to and treatment by a psychiatrist is warranted because of the strong association with underlying psychiatric conditions, namely, OCD. 

Androgenetic alopecia (AGA) is a common patient complaint, affecting approximately half of all men and women by the age of 50 years.1 Hair loss often can have significant negative effects on self-esteem and body image.2 Clinicians may be bombarded by questions from patients who have information about hair loss remedies from the Internet or testimonials from friends. However, it may be difficult or time-consuming for doctors to learn about the dozens of products claiming to promote hair growth and to then appropriately counsel their patients. In this article, we have interposed information obtained from the Internet with that obtained from peer-reviewed journals, when available, to support or refute claims made by the manufacturers or marketers of various products. We intend for this information to serve as a "consumer report" for healthcare providers and patients and help to separate some of the valid claims for hair regrowth from those that are purely fiction.

FDA-Approved Hair Loss Remedies Minoxidil—In 1988, the US Food and Drug Administration (FDA) approved minoxidil 2% topical solution for use in treating AGA in men. A 2% solution marketed toward women became available in 1991, and a 5% solution for use in men became available over-the-counter in 1997.3 Since that time, generic formulations of minoxidil topical solution also have become available. Minoxidil is a vasodilator and a potassium channel opener,3 but its mechanism of action in promoting hair regrowth is unknown and appears to be independent of its vasodilatation properties.3-7 The most common adverse side effects of minoxidil topical solution include scalp irritation, which occurs in about 7% of patients using the 2% solution, and hypertrichosis, which is noted in women.3 Because there are both generic and brand-name formulations of minoxidil topical solution, the cost of this therapy varies depending on which solution patients choose. However, most consumers pay between $10 and $20 for a 1-month supply.8

Minoxidil 2% topical solution has been proven to be effective both in stimulating new hair growth and in helping to prevent continued hair loss in both sexes.3 A recent study comparing minoxidil 2% and 5% topical solution in men showed that the men using the extra-strength formulation had 45% more hair regrowth after 48 weeks and an earlier response to the drug.9 A study published in 1992 showed that a year's treatment with minoxidil 5% was effective in improving hair density in 9 women,10 though the company has not yet obtained FDA approval for the use of this concentration in women. Minoxidil topical solution has even been found to be effective and safe in adolescents, which is an important finding because AGA can occur in older children or teenagers and can cause significant psychological distress.11

Some Web sites are claiming that products used in combination with minoxidil can increase the drug's efficacy. For example, the Hair Loss Control Clinic Web site claims that sebum on the hair follicle at the level of the scalp prevents minoxidil's penetration into the hair follicle, causing it to be absorbed ineffectively.12 The site also claims that the high alcohol content of over-the-counter minoxidil can cause hair damage. The clinic is promoting a product called HLCC Scalp Therapy Dexpanthenol 12% to be used prior to shampooing to dissolve sebum, theoretically allowing the minoxidil solution to better penetrate the hair follicle.12 Another product advertised on this site is Carrier Enhancement Agent, which supposedly neutralizes the alcohol in minoxidil to prevent scalp irritation.12 There are no peer-reviewed studies supporting these claims. Because it is unclear how minoxidil topical solution works, it also is unclear why such additives would increase its effectiveness.

Patients also may see Web sites promoting the use of retinoids with minoxidil to enhance minoxidil's effectiveness. To date, one nonblinded study tested tretinoin 0.025% combined with minoxidil 0.5% topical solution in 36 patients and showed that the tretinoin increased the percutaneous absorption of the minoxidil. The combination of the 2 drugs led to visible hair growth in 66% of the patients tested.13 Therefore, the application of both topical minoxidil solution and tretinoin may give some patients better results than application of topical minoxidil alone. Patients may want to try minoxidil by itself at first and then add the tretinoin only if they are not satisfied with their initial results.

Finasteride—In 1997, finasteride was approved by the FDA for treatment of male AGA at a dose of 1 mg/d.3 This medication is a competitive inhibitor of type-2 5α-reductase, which inhibits testosterone's conversion to dihydrotestosterone (DHT).14-17 Finasteride is able to decrease serum DHT by about 70%.18 Due to the potential for teratogenic effects in male fetuses, finasteride is not FDA approved for use in women.3 The main side effects of finasteride therapy are sexual side effects such as decreased libido and erectile/ejaculatory dysfunction, which occurred in fewer than 2% of men in one trial. In one study, these negative side effects were reversed with cessation of the medication.19 Also, there have been no clinically significant drug interactions noted between finasteride and other medications.20 The cost of this drug averages between $30 and $60 per month.8

Multiple randomized double-blind clinical trials of finasteride versus placebo in men aged 18 to 41 years with both vertex and frontal hair thinning showed that patients who took finasteride 1 mg/d for one year had significantly increased scalp coverage and hair counts than patients taking placebo.19,21,22 With continuous treatment of finasteride daily for 2 years, approximately two thirds of men have improved hair regrowth, one third of men see no change, and approximately 1% of men actually have less hair than at baseline.3 This product has shown more efficacy in younger men than it has in men older than 60 years, most likely because of decreased scalp type-2 5α-reductase activity in older men.3

Finasteride also has been tested for efficacy in women with AGA. A randomized double-blind study of 137 postmenopausal women with AGA who took finasteride 1 mg/d or placebo for one year showed no significant difference in hair count between the 2 groups. In fact, both groups of patients actually showed significant loss of hair during the study period.23 Another randomized open-label study tested finasteride 5 mg/d versus no treatment in premenopausal women with hyperandrogenic alopecia and elevated serum androgens (levels >2 SD above the mean in ovulatory control patients). This study found that the women using finasteride at this elevated dose did not see any significant improvement as opposed to the women receiving no treatment.24 Some clinicians have had more success with the use of finasteride in their female patients with AGA. In a letter published in the British Journal of Dermatology, 2 physicians describe successful treatment of AGA in a postmenopausal woman who was given finasteride 5 mg/wk. Success was measured via patient report of improved hair density and review of stereotactic photographs of the scalp.25 Despite this anecdotal evidence of success, the larger body of evidence weighs against the use of finasteride in postmenopausal women with AGA.

Because there are only 2 FDA-approved treatments for AGA, patients may wonder which is more effective. In a recent letter published in the Archives of Dermatology, finasteride 1 mg/d was compared with topical minoxidil 2% in 99 men aged 18 to 45 years with mid frontal and/or vertex hair thinning.26 The researchers found that both treatments worked equally well in stopping the progression of hair loss in patients; however, patients given minoxidil had quicker initial improvement whereby patients given finasteride had slightly better results as treatment progressed.26 Choice of treatment therefore may be more a factor of side-effect profile, expense, and preferred form of medication (oral vs topical).

Some patients may ask about combining finasteride with minoxidil. One case study described the improvement of one man's alopecia from Hamilton-Norwood class V to class III after using a combination therapy of finasteride 5 mg/d plus a topical solution of minoxidil 3% and tretinoin 0.01%.27 The combined use of finasteride and minoxidil topical solution has been studied in the animal model of AGA; in stumptail macaques, the combined use of finasteride with minoxidil had greater effects on hair loss than either treatment alone.28 Because both treatments have different modes of action, it is plausible that combining them may yield better results.

Off-Label Uses for FDA-Approved Medications Spironolactone—This medication is often prescribed for the treatment of hypertension because of its action as an aldosterone antagonist, but it also is able to inhibit the biosynthesis of androgens and to competitively inhibit androgen receptor protein binding.29 The main side effects of this medication are menstrual irregularities, hyperkalemia, gynecomastia in men, and gastrointestinal distress.29 Women using this medication must be warned about the potential for feminization of male fetuses if pregnancy occurs during the course of treatment.30 The cost of this medication at a dose of 200 mg/d is approximately $60 per month, though it typically is covered by insurance policies.8

Spironolactone has shown efficacy in treating women with hirsutism,31 and it also may have mild efficacy in treating AGA at a dose of 200 mg/d.32 One study examining the efficacy of spironolactone in women with AGA showed that the women taking the medication had less hair loss than control patients after one year, but the women taking spironolactone still did not have more hair after treatment than at the start of the study.33 Another study that examined the use of spironolactone 200 mg/d in 2 men and 2 women with AGA showed that the patients had an increase in the number of hairs in anagen phase from 22% at baseline to 84.5% at the end of 6 months of treatment.34 Because this medication only has weak evidence for its use as a treatment for hair loss, clinicians should consider this medication only in addition to other, more proven, means of therapy.

Yasmin®—This is an oral contraceptive pill composed of ethinyl estradiol and drospirenone, an analogue of spironolactone. Each pill contains drospirenone 3 mg, which is equivalent to spironolactone 25 mg.35 According to the manufacturer of Yasmin, this oral contraceptive antagonizes androgen receptors without affecting sex-hormone–binding globulin synthesis or affecting the binding of testosterone to sex-hormone–binding globulin. The manufacturer also claims that the drug inhibits ovarian androgen production.36 The most common side effects are similar to side effects of other oral contraceptives and include breast tenderness, nausea, headache, emotional lability, dysmenorrhea, intermenstrual bleeding, and depression.35 Some insurance plans will cover the cost of oral contraceptives, but for patients paying out of pocket, Yasmin costs approximately $30 per month.8

Because spironolactone is sometimes prescribed for AGA, some clinicians recommend Yasmin to patients with alopecia who also are looking for effective contraceptive methods. However, to our knowledge, there are no known published studies showing that Yasmin prevents hair loss or promotes hair regrowth. Because spironolactone has shown only slight efficacy in treatment of women with AGA,3 it is unclear what the effect of Yasmin may be on hair loss. However, this may be a reasonable choice of contraceptive in a woman with AGA.

Dutasteride—This new 5α-reductase inhibitor blocks both type-1 and type-2 isoenzymes.37 By inhibiting both types of 5α-reductase, dutasteride is able to achieve a greater than 90% suppression of DHT.37 This medication was developed for the treatment of benign prostatic hyperplasia, with side effects similar to those of finasteride.38 As with finasteride, women are advised not to take this product because of the potential risk of birth defects in male fetuses.37 In November 2002, dutasteride was approved by the FDA for use in patients with benign prostatic hyperplasia.39 This medication costs approximately $75 for a 1-month supply.8

Although dutasteride is not yet FDA approved for alopecia, the manufacturers have completed phase 2 clinical trials of the medication for the treatment of hair loss and are hopeful it will be approved by the FDA in 2006.40 There are no studies published regarding this medication's effect on AGA, but preliminary results from the manufacturer showed that dutasteride reduced scalp DHT in men to a greater extent than finasteride.41 

Herbal/Dietary Remedies Saw Palmetto—Saw palmetto, or Serenoa repens, is an herbal remedy that is processed from fruit of the American dwarf pine tree.42 It often is used to treat benign prostatic hypertrophy because of its ability to inhibit 5α-reductase levels by 32% without affecting testosterone levels in men.43 Extracts of saw palmetto also have been shown to have a partial antagonistic affect on testosterone receptors.44 It is most likely that these 2 actions led to saw palmetto being used as a hair loss remedy. Saw palmetto is believed to be a safe herbal supplement, with a primary side effect of mild gastrointestinal distress.42 Also, clinical trials conducted in human patients showed that consumption of saw palmetto supplements did not result in any clinically significant alterations in laboratory parameters.45 Saw palmetto has no known drug interactions.42 The cost of this supplement varies by manufacturer, but consumers should be able to find saw palmetto supplements for as little as $3 for a month's supply.8

One double-blind placebo-controlled study examined saw palmetto's effect on AGA.46 In this study, researchers studied the efficacy of a softgel containing β-sitosterol 50 mg and saw palmetto 200 mg extract (components of the HairGenesis™ Softgels discussed later) versus placebo in treating AGA. They found that 60% of patients taking the active softgel rated their hair growth as improved from baseline as opposed to only 10% of the patients taking placebo. However, this study had a limited patient population and also concurrently tested β-sitosterol, so any improvement cannot be attributed to saw palmetto alone.

Biotin—This is a water-soluble B complex vitamin that is used in the body as a cofactor for biochemical carboxylations. Patients that are deficient in this vitamin often have alopecia, brittle nails, and a scaly erythematous dermatitis.47,48 Biotin is water-soluble, and there are no known side effects of supplementation and no documented cases of biotin overdose.49 As with other supplements, cost of treatment will depend on the manufacturer, but consumers should be able to find biotin for as little as $2 for a month's supply.8

Dietary supplementation with biotin has been shown to improve the clinical condition of brittle nails,48 but no studies have been conducted looking at biotin's effect on AGA. Although it is true that biotin deficiency can lead to alopecia, such a deficiency has not been demonstrated in healthy humans eating a mixed diet.47 The only 2 situations in which human biotin deficiency has been demonstrated are in patients with extended consumption of raw egg whites50-52 and in patients with malabsorption syndromes receiving parenteral nutrition without biotin supplementation.50,53 Supplementing the diet with biotin is unlikely to harm a patient, but there is no data to suggest any improvement in hair regrowth.

Other Hair Regrowth Products Avacor™—Sold through the Internet and directly from the manufacturer, Avacor is a hair regrowth product marketed toward both sexes for treatment of AGA.54 The product line consists of a scalp detoxifying shampoo, an herbal supplement, and a topical solution. The purpose of the shampoo as stated by the manufacturer is to deep clean the scalp to improve the absorbency of the topical treatment. The herbal supplements are to be taken twice daily to "maintain a healthy hair follicle" and consist of bilberry, ginkgo biloba, saw palmetto, and horsetail. The topical solution, which is marketed to men only, claims to dilate blood vessels in the scalp, allowing increased nutrient and oxygen delivery to the scalp. The Web site claims that these products must be used together and that they have no known side effects.54 The cost of this product is $239.95 for a 3-month supply.55

The official Avacor Web site has a summary of a clinical study performed by The New York Hair Clinic and the Hair and Skin Treatment Center in which 200 men aged 18 to 65 years used the 3-part system for 24 weeks.55 The Web site claims that 91% of the men had a decrease in hair loss and an increase in strength and thickness of preexisting hair within 3 months.55 However, this study does not appear to be published in any journal and consumers can only receive a copy of the study if they purchase the product.

A Wellness Letter highlighting dietary supplements, published by the University of California at Berkeley, showed that Avacor contains minoxidil in its topical solution despite its claims to be made from only natural ingredients.56 In April 2003, the FDA sent the makers of Avacor a letter informing them that their products are considered drugs under section 201(g) of the Federal Food, Drug, and Cosmetic Act and should have had an approved New Drug Application prior to being marketed in the United States. The FDA also points out that the 3 individual components are mislabeled because the active ingredients are not listed on their labels.57

Given the lack of peer-reviewed evidence of hair growth and with all of the controversy surrounding this product, it would not be wise for clinicians to recommend this therapy to any patient.

HairGenesis™—This product line consists of 4 items: Revitalizing Oral Softgel™ supplements (β-sitosterol 50 mg and saw palmetto 200 mg extract) that claim to strengthen and protect hair; Topical Activator Serum that consists of various 5α-reductase inhibitors; Hair Revitalizing Formulation, a shampoo that has similar components to the Topical Activator Serum; and Hair and Scalp Conditioner that also is meant to strengthen and protect hair. Although the company states that the products may be used individually, it recommends using them all synergistically, at a cost of $200 for a 3-month supply.58 The efficacy of the oral softgel containing saw palmetto is discussed above; there are no known research studies published about the other 3 components of the HairGenesis system.

Nioxin®—This product line is sold only through hair salons and does not aim to regrow hair; rather, it claims to "create an optimum scalp environment" for regrowth and maintenance of the current hair count. The manufacturer claims to accomplish this by clearing the scalp of excess sebum that may contain high levels of DHT. Ingredients include various vitamin-B coenzymes, biotin, saw palmetto, aloe, ginseng, and amino acids. The manufacturer claims that the Nioxin system has no known side effects.59 As this product is sold only in salons, the cost for a month's supply will vary depending on the place of purchase. One salon that we contacted offered a one-month starter kit for $30. The manufacturer does not disclose its clinical studies but claims that its studies are conducted by "world-renowned" researchers who are experts in hair thinning.59 However, there is no known published scientific evidence that any of the ingredients in Nioxin are effective in treating hair loss or maintaining hair count, or that excess sebum leads to hair thinning.

Laser Light Therapy—Low-intensity laser light therapy has been shown to be effective in promoting wound healing60 and in improving circulation.61,62 For these reasons, some hair loss treatment centers are offering the use of lasers for treating alopecia in both men and women. To date, there are no known studies looking at the efficacy of these lasers for treating hair loss. The use of low-intensity laser light for treating alopecia is FDA approved for safety only, not for efficacy.29 This therapy is expensive, costing as much as $3500 for the recommended 6 months of treatment.63

Although various Web sites claim efficacy based on double-blind placebo-controlled studies of laser light treatment versus placebo laser treatment,64,65 such studies are not available for viewing anywhere on the Web sites. To the best of our knowledge, there are no peer-reviewed articles supporting efficacy of this type of treatment for AGA. Until reliable evidence of the effectiveness of laser light therapy for alopecia is published, this treatment remains experimental, at best.

Conclusion

Any consumer looking on the Internet for a treatment for hair loss is exposed to a multitude of remedies. However, only the FDA-approved treatments for AGA, finasteride and minoxidil, have any well-studied factual evidence of efficacy. Smaller studies have shown possible benefit of combining topical tretinoin with minoxidil, as well as combining finasteride and minoxidil. Spironolactone in high doses (100–200 mg), dutasteride, and saw palmetto, also may provide benefit; however, larger studies are needed to consider these agents as first-line treatments for AGA. In addition to efficacy, clinicians need to consider patient preferences, safety profile, and cost when counseling patients about treatment options for AGA.

Androgenetic alopecia (AGA) is a common patient complaint, affecting approximately half of all men and women by the age of 50 years.1 Hair loss often can have significant negative effects on self-esteem and body image.2 Clinicians may be bombarded by questions from patients who have information about hair loss remedies from the Internet or testimonials from friends. However, it may be difficult or time-consuming for doctors to learn about the dozens of products claiming to promote hair growth and to then appropriately counsel their patients. In this article, we have interposed information obtained from the Internet with that obtained from peer-reviewed journals, when available, to support or refute claims made by the manufacturers or marketers of various products. We intend for this information to serve as a "consumer report" for healthcare providers and patients and help to separate some of the valid claims for hair regrowth from those that are purely fiction.

FDA-Approved Hair Loss Remedies Minoxidil—In 1988, the US Food and Drug Administration (FDA) approved minoxidil 2% topical solution for use in treating AGA in men. A 2% solution marketed toward women became available in 1991, and a 5% solution for use in men became available over-the-counter in 1997.3 Since that time, generic formulations of minoxidil topical solution also have become available. Minoxidil is a vasodilator and a potassium channel opener,3 but its mechanism of action in promoting hair regrowth is unknown and appears to be independent of its vasodilatation properties.3-7 The most common adverse side effects of minoxidil topical solution include scalp irritation, which occurs in about 7% of patients using the 2% solution, and hypertrichosis, which is noted in women.3 Because there are both generic and brand-name formulations of minoxidil topical solution, the cost of this therapy varies depending on which solution patients choose. However, most consumers pay between $10 and $20 for a 1-month supply.8

Minoxidil 2% topical solution has been proven to be effective both in stimulating new hair growth and in helping to prevent continued hair loss in both sexes.3 A recent study comparing minoxidil 2% and 5% topical solution in men showed that the men using the extra-strength formulation had 45% more hair regrowth after 48 weeks and an earlier response to the drug.9 A study published in 1992 showed that a year's treatment with minoxidil 5% was effective in improving hair density in 9 women,10 though the company has not yet obtained FDA approval for the use of this concentration in women. Minoxidil topical solution has even been found to be effective and safe in adolescents, which is an important finding because AGA can occur in older children or teenagers and can cause significant psychological distress.11

Some Web sites are claiming that products used in combination with minoxidil can increase the drug's efficacy. For example, the Hair Loss Control Clinic Web site claims that sebum on the hair follicle at the level of the scalp prevents minoxidil's penetration into the hair follicle, causing it to be absorbed ineffectively.12 The site also claims that the high alcohol content of over-the-counter minoxidil can cause hair damage. The clinic is promoting a product called HLCC Scalp Therapy Dexpanthenol 12% to be used prior to shampooing to dissolve sebum, theoretically allowing the minoxidil solution to better penetrate the hair follicle.12 Another product advertised on this site is Carrier Enhancement Agent, which supposedly neutralizes the alcohol in minoxidil to prevent scalp irritation.12 There are no peer-reviewed studies supporting these claims. Because it is unclear how minoxidil topical solution works, it also is unclear why such additives would increase its effectiveness.

Patients also may see Web sites promoting the use of retinoids with minoxidil to enhance minoxidil's effectiveness. To date, one nonblinded study tested tretinoin 0.025% combined with minoxidil 0.5% topical solution in 36 patients and showed that the tretinoin increased the percutaneous absorption of the minoxidil. The combination of the 2 drugs led to visible hair growth in 66% of the patients tested.13 Therefore, the application of both topical minoxidil solution and tretinoin may give some patients better results than application of topical minoxidil alone. Patients may want to try minoxidil by itself at first and then add the tretinoin only if they are not satisfied with their initial results.

Finasteride—In 1997, finasteride was approved by the FDA for treatment of male AGA at a dose of 1 mg/d.3 This medication is a competitive inhibitor of type-2 5α-reductase, which inhibits testosterone's conversion to dihydrotestosterone (DHT).14-17 Finasteride is able to decrease serum DHT by about 70%.18 Due to the potential for teratogenic effects in male fetuses, finasteride is not FDA approved for use in women.3 The main side effects of finasteride therapy are sexual side effects such as decreased libido and erectile/ejaculatory dysfunction, which occurred in fewer than 2% of men in one trial. In one study, these negative side effects were reversed with cessation of the medication.19 Also, there have been no clinically significant drug interactions noted between finasteride and other medications.20 The cost of this drug averages between $30 and $60 per month.8

Multiple randomized double-blind clinical trials of finasteride versus placebo in men aged 18 to 41 years with both vertex and frontal hair thinning showed that patients who took finasteride 1 mg/d for one year had significantly increased scalp coverage and hair counts than patients taking placebo.19,21,22 With continuous treatment of finasteride daily for 2 years, approximately two thirds of men have improved hair regrowth, one third of men see no change, and approximately 1% of men actually have less hair than at baseline.3 This product has shown more efficacy in younger men than it has in men older than 60 years, most likely because of decreased scalp type-2 5α-reductase activity in older men.3

Finasteride also has been tested for efficacy in women with AGA. A randomized double-blind study of 137 postmenopausal women with AGA who took finasteride 1 mg/d or placebo for one year showed no significant difference in hair count between the 2 groups. In fact, both groups of patients actually showed significant loss of hair during the study period.23 Another randomized open-label study tested finasteride 5 mg/d versus no treatment in premenopausal women with hyperandrogenic alopecia and elevated serum androgens (levels >2 SD above the mean in ovulatory control patients). This study found that the women using finasteride at this elevated dose did not see any significant improvement as opposed to the women receiving no treatment.24 Some clinicians have had more success with the use of finasteride in their female patients with AGA. In a letter published in the British Journal of Dermatology, 2 physicians describe successful treatment of AGA in a postmenopausal woman who was given finasteride 5 mg/wk. Success was measured via patient report of improved hair density and review of stereotactic photographs of the scalp.25 Despite this anecdotal evidence of success, the larger body of evidence weighs against the use of finasteride in postmenopausal women with AGA.

Because there are only 2 FDA-approved treatments for AGA, patients may wonder which is more effective. In a recent letter published in the Archives of Dermatology, finasteride 1 mg/d was compared with topical minoxidil 2% in 99 men aged 18 to 45 years with mid frontal and/or vertex hair thinning.26 The researchers found that both treatments worked equally well in stopping the progression of hair loss in patients; however, patients given minoxidil had quicker initial improvement whereby patients given finasteride had slightly better results as treatment progressed.26 Choice of treatment therefore may be more a factor of side-effect profile, expense, and preferred form of medication (oral vs topical).

Some patients may ask about combining finasteride with minoxidil. One case study described the improvement of one man's alopecia from Hamilton-Norwood class V to class III after using a combination therapy of finasteride 5 mg/d plus a topical solution of minoxidil 3% and tretinoin 0.01%.27 The combined use of finasteride and minoxidil topical solution has been studied in the animal model of AGA; in stumptail macaques, the combined use of finasteride with minoxidil had greater effects on hair loss than either treatment alone.28 Because both treatments have different modes of action, it is plausible that combining them may yield better results.

Off-Label Uses for FDA-Approved Medications Spironolactone—This medication is often prescribed for the treatment of hypertension because of its action as an aldosterone antagonist, but it also is able to inhibit the biosynthesis of androgens and to competitively inhibit androgen receptor protein binding.29 The main side effects of this medication are menstrual irregularities, hyperkalemia, gynecomastia in men, and gastrointestinal distress.29 Women using this medication must be warned about the potential for feminization of male fetuses if pregnancy occurs during the course of treatment.30 The cost of this medication at a dose of 200 mg/d is approximately $60 per month, though it typically is covered by insurance policies.8

Spironolactone has shown efficacy in treating women with hirsutism,31 and it also may have mild efficacy in treating AGA at a dose of 200 mg/d.32 One study examining the efficacy of spironolactone in women with AGA showed that the women taking the medication had less hair loss than control patients after one year, but the women taking spironolactone still did not have more hair after treatment than at the start of the study.33 Another study that examined the use of spironolactone 200 mg/d in 2 men and 2 women with AGA showed that the patients had an increase in the number of hairs in anagen phase from 22% at baseline to 84.5% at the end of 6 months of treatment.34 Because this medication only has weak evidence for its use as a treatment for hair loss, clinicians should consider this medication only in addition to other, more proven, means of therapy.

Yasmin®—This is an oral contraceptive pill composed of ethinyl estradiol and drospirenone, an analogue of spironolactone. Each pill contains drospirenone 3 mg, which is equivalent to spironolactone 25 mg.35 According to the manufacturer of Yasmin, this oral contraceptive antagonizes androgen receptors without affecting sex-hormone–binding globulin synthesis or affecting the binding of testosterone to sex-hormone–binding globulin. The manufacturer also claims that the drug inhibits ovarian androgen production.36 The most common side effects are similar to side effects of other oral contraceptives and include breast tenderness, nausea, headache, emotional lability, dysmenorrhea, intermenstrual bleeding, and depression.35 Some insurance plans will cover the cost of oral contraceptives, but for patients paying out of pocket, Yasmin costs approximately $30 per month.8

Because spironolactone is sometimes prescribed for AGA, some clinicians recommend Yasmin to patients with alopecia who also are looking for effective contraceptive methods. However, to our knowledge, there are no known published studies showing that Yasmin prevents hair loss or promotes hair regrowth. Because spironolactone has shown only slight efficacy in treatment of women with AGA,3 it is unclear what the effect of Yasmin may be on hair loss. However, this may be a reasonable choice of contraceptive in a woman with AGA.

Dutasteride—This new 5α-reductase inhibitor blocks both type-1 and type-2 isoenzymes.37 By inhibiting both types of 5α-reductase, dutasteride is able to achieve a greater than 90% suppression of DHT.37 This medication was developed for the treatment of benign prostatic hyperplasia, with side effects similar to those of finasteride.38 As with finasteride, women are advised not to take this product because of the potential risk of birth defects in male fetuses.37 In November 2002, dutasteride was approved by the FDA for use in patients with benign prostatic hyperplasia.39 This medication costs approximately $75 for a 1-month supply.8

Although dutasteride is not yet FDA approved for alopecia, the manufacturers have completed phase 2 clinical trials of the medication for the treatment of hair loss and are hopeful it will be approved by the FDA in 2006.40 There are no studies published regarding this medication's effect on AGA, but preliminary results from the manufacturer showed that dutasteride reduced scalp DHT in men to a greater extent than finasteride.41 

Herbal/Dietary Remedies Saw Palmetto—Saw palmetto, or Serenoa repens, is an herbal remedy that is processed from fruit of the American dwarf pine tree.42 It often is used to treat benign prostatic hypertrophy because of its ability to inhibit 5α-reductase levels by 32% without affecting testosterone levels in men.43 Extracts of saw palmetto also have been shown to have a partial antagonistic affect on testosterone receptors.44 It is most likely that these 2 actions led to saw palmetto being used as a hair loss remedy. Saw palmetto is believed to be a safe herbal supplement, with a primary side effect of mild gastrointestinal distress.42 Also, clinical trials conducted in human patients showed that consumption of saw palmetto supplements did not result in any clinically significant alterations in laboratory parameters.45 Saw palmetto has no known drug interactions.42 The cost of this supplement varies by manufacturer, but consumers should be able to find saw palmetto supplements for as little as $3 for a month's supply.8

One double-blind placebo-controlled study examined saw palmetto's effect on AGA.46 In this study, researchers studied the efficacy of a softgel containing β-sitosterol 50 mg and saw palmetto 200 mg extract (components of the HairGenesis™ Softgels discussed later) versus placebo in treating AGA. They found that 60% of patients taking the active softgel rated their hair growth as improved from baseline as opposed to only 10% of the patients taking placebo. However, this study had a limited patient population and also concurrently tested β-sitosterol, so any improvement cannot be attributed to saw palmetto alone.

Biotin—This is a water-soluble B complex vitamin that is used in the body as a cofactor for biochemical carboxylations. Patients that are deficient in this vitamin often have alopecia, brittle nails, and a scaly erythematous dermatitis.47,48 Biotin is water-soluble, and there are no known side effects of supplementation and no documented cases of biotin overdose.49 As with other supplements, cost of treatment will depend on the manufacturer, but consumers should be able to find biotin for as little as $2 for a month's supply.8

Dietary supplementation with biotin has been shown to improve the clinical condition of brittle nails,48 but no studies have been conducted looking at biotin's effect on AGA. Although it is true that biotin deficiency can lead to alopecia, such a deficiency has not been demonstrated in healthy humans eating a mixed diet.47 The only 2 situations in which human biotin deficiency has been demonstrated are in patients with extended consumption of raw egg whites50-52 and in patients with malabsorption syndromes receiving parenteral nutrition without biotin supplementation.50,53 Supplementing the diet with biotin is unlikely to harm a patient, but there is no data to suggest any improvement in hair regrowth.

Other Hair Regrowth Products Avacor™—Sold through the Internet and directly from the manufacturer, Avacor is a hair regrowth product marketed toward both sexes for treatment of AGA.54 The product line consists of a scalp detoxifying shampoo, an herbal supplement, and a topical solution. The purpose of the shampoo as stated by the manufacturer is to deep clean the scalp to improve the absorbency of the topical treatment. The herbal supplements are to be taken twice daily to "maintain a healthy hair follicle" and consist of bilberry, ginkgo biloba, saw palmetto, and horsetail. The topical solution, which is marketed to men only, claims to dilate blood vessels in the scalp, allowing increased nutrient and oxygen delivery to the scalp. The Web site claims that these products must be used together and that they have no known side effects.54 The cost of this product is $239.95 for a 3-month supply.55

The official Avacor Web site has a summary of a clinical study performed by The New York Hair Clinic and the Hair and Skin Treatment Center in which 200 men aged 18 to 65 years used the 3-part system for 24 weeks.55 The Web site claims that 91% of the men had a decrease in hair loss and an increase in strength and thickness of preexisting hair within 3 months.55 However, this study does not appear to be published in any journal and consumers can only receive a copy of the study if they purchase the product.

A Wellness Letter highlighting dietary supplements, published by the University of California at Berkeley, showed that Avacor contains minoxidil in its topical solution despite its claims to be made from only natural ingredients.56 In April 2003, the FDA sent the makers of Avacor a letter informing them that their products are considered drugs under section 201(g) of the Federal Food, Drug, and Cosmetic Act and should have had an approved New Drug Application prior to being marketed in the United States. The FDA also points out that the 3 individual components are mislabeled because the active ingredients are not listed on their labels.57

Given the lack of peer-reviewed evidence of hair growth and with all of the controversy surrounding this product, it would not be wise for clinicians to recommend this therapy to any patient.

HairGenesis™—This product line consists of 4 items: Revitalizing Oral Softgel™ supplements (β-sitosterol 50 mg and saw palmetto 200 mg extract) that claim to strengthen and protect hair; Topical Activator Serum that consists of various 5α-reductase inhibitors; Hair Revitalizing Formulation, a shampoo that has similar components to the Topical Activator Serum; and Hair and Scalp Conditioner that also is meant to strengthen and protect hair. Although the company states that the products may be used individually, it recommends using them all synergistically, at a cost of $200 for a 3-month supply.58 The efficacy of the oral softgel containing saw palmetto is discussed above; there are no known research studies published about the other 3 components of the HairGenesis system.

Nioxin®—This product line is sold only through hair salons and does not aim to regrow hair; rather, it claims to "create an optimum scalp environment" for regrowth and maintenance of the current hair count. The manufacturer claims to accomplish this by clearing the scalp of excess sebum that may contain high levels of DHT. Ingredients include various vitamin-B coenzymes, biotin, saw palmetto, aloe, ginseng, and amino acids. The manufacturer claims that the Nioxin system has no known side effects.59 As this product is sold only in salons, the cost for a month's supply will vary depending on the place of purchase. One salon that we contacted offered a one-month starter kit for $30. The manufacturer does not disclose its clinical studies but claims that its studies are conducted by "world-renowned" researchers who are experts in hair thinning.59 However, there is no known published scientific evidence that any of the ingredients in Nioxin are effective in treating hair loss or maintaining hair count, or that excess sebum leads to hair thinning.

Laser Light Therapy—Low-intensity laser light therapy has been shown to be effective in promoting wound healing60 and in improving circulation.61,62 For these reasons, some hair loss treatment centers are offering the use of lasers for treating alopecia in both men and women. To date, there are no known studies looking at the efficacy of these lasers for treating hair loss. The use of low-intensity laser light for treating alopecia is FDA approved for safety only, not for efficacy.29 This therapy is expensive, costing as much as $3500 for the recommended 6 months of treatment.63

Although various Web sites claim efficacy based on double-blind placebo-controlled studies of laser light treatment versus placebo laser treatment,64,65 such studies are not available for viewing anywhere on the Web sites. To the best of our knowledge, there are no peer-reviewed articles supporting efficacy of this type of treatment for AGA. Until reliable evidence of the effectiveness of laser light therapy for alopecia is published, this treatment remains experimental, at best.

Conclusion

Any consumer looking on the Internet for a treatment for hair loss is exposed to a multitude of remedies. However, only the FDA-approved treatments for AGA, finasteride and minoxidil, have any well-studied factual evidence of efficacy. Smaller studies have shown possible benefit of combining topical tretinoin with minoxidil, as well as combining finasteride and minoxidil. Spironolactone in high doses (100–200 mg), dutasteride, and saw palmetto, also may provide benefit; however, larger studies are needed to consider these agents as first-line treatments for AGA. In addition to efficacy, clinicians need to consider patient preferences, safety profile, and cost when counseling patients about treatment options for AGA.

Androgenetic alopecia (AGA) is a common patient complaint, affecting approximately half of all men and women by the age of 50 years.1 Hair loss often can have significant negative effects on self-esteem and body image.2 Clinicians may be bombarded by questions from patients who have information about hair loss remedies from the Internet or testimonials from friends. However, it may be difficult or time-consuming for doctors to learn about the dozens of products claiming to promote hair growth and to then appropriately counsel their patients. In this article, we have interposed information obtained from the Internet with that obtained from peer-reviewed journals, when available, to support or refute claims made by the manufacturers or marketers of various products. We intend for this information to serve as a "consumer report" for healthcare providers and patients and help to separate some of the valid claims for hair regrowth from those that are purely fiction.

FDA-Approved Hair Loss Remedies Minoxidil—In 1988, the US Food and Drug Administration (FDA) approved minoxidil 2% topical solution for use in treating AGA in men. A 2% solution marketed toward women became available in 1991, and a 5% solution for use in men became available over-the-counter in 1997.3 Since that time, generic formulations of minoxidil topical solution also have become available. Minoxidil is a vasodilator and a potassium channel opener,3 but its mechanism of action in promoting hair regrowth is unknown and appears to be independent of its vasodilatation properties.3-7 The most common adverse side effects of minoxidil topical solution include scalp irritation, which occurs in about 7% of patients using the 2% solution, and hypertrichosis, which is noted in women.3 Because there are both generic and brand-name formulations of minoxidil topical solution, the cost of this therapy varies depending on which solution patients choose. However, most consumers pay between $10 and $20 for a 1-month supply.8

Minoxidil 2% topical solution has been proven to be effective both in stimulating new hair growth and in helping to prevent continued hair loss in both sexes.3 A recent study comparing minoxidil 2% and 5% topical solution in men showed that the men using the extra-strength formulation had 45% more hair regrowth after 48 weeks and an earlier response to the drug.9 A study published in 1992 showed that a year's treatment with minoxidil 5% was effective in improving hair density in 9 women,10 though the company has not yet obtained FDA approval for the use of this concentration in women. Minoxidil topical solution has even been found to be effective and safe in adolescents, which is an important finding because AGA can occur in older children or teenagers and can cause significant psychological distress.11

Some Web sites are claiming that products used in combination with minoxidil can increase the drug's efficacy. For example, the Hair Loss Control Clinic Web site claims that sebum on the hair follicle at the level of the scalp prevents minoxidil's penetration into the hair follicle, causing it to be absorbed ineffectively.12 The site also claims that the high alcohol content of over-the-counter minoxidil can cause hair damage. The clinic is promoting a product called HLCC Scalp Therapy Dexpanthenol 12% to be used prior to shampooing to dissolve sebum, theoretically allowing the minoxidil solution to better penetrate the hair follicle.12 Another product advertised on this site is Carrier Enhancement Agent, which supposedly neutralizes the alcohol in minoxidil to prevent scalp irritation.12 There are no peer-reviewed studies supporting these claims. Because it is unclear how minoxidil topical solution works, it also is unclear why such additives would increase its effectiveness.

Patients also may see Web sites promoting the use of retinoids with minoxidil to enhance minoxidil's effectiveness. To date, one nonblinded study tested tretinoin 0.025% combined with minoxidil 0.5% topical solution in 36 patients and showed that the tretinoin increased the percutaneous absorption of the minoxidil. The combination of the 2 drugs led to visible hair growth in 66% of the patients tested.13 Therefore, the application of both topical minoxidil solution and tretinoin may give some patients better results than application of topical minoxidil alone. Patients may want to try minoxidil by itself at first and then add the tretinoin only if they are not satisfied with their initial results.

Finasteride—In 1997, finasteride was approved by the FDA for treatment of male AGA at a dose of 1 mg/d.3 This medication is a competitive inhibitor of type-2 5α-reductase, which inhibits testosterone's conversion to dihydrotestosterone (DHT).14-17 Finasteride is able to decrease serum DHT by about 70%.18 Due to the potential for teratogenic effects in male fetuses, finasteride is not FDA approved for use in women.3 The main side effects of finasteride therapy are sexual side effects such as decreased libido and erectile/ejaculatory dysfunction, which occurred in fewer than 2% of men in one trial. In one study, these negative side effects were reversed with cessation of the medication.19 Also, there have been no clinically significant drug interactions noted between finasteride and other medications.20 The cost of this drug averages between $30 and $60 per month.8

Multiple randomized double-blind clinical trials of finasteride versus placebo in men aged 18 to 41 years with both vertex and frontal hair thinning showed that patients who took finasteride 1 mg/d for one year had significantly increased scalp coverage and hair counts than patients taking placebo.19,21,22 With continuous treatment of finasteride daily for 2 years, approximately two thirds of men have improved hair regrowth, one third of men see no change, and approximately 1% of men actually have less hair than at baseline.3 This product has shown more efficacy in younger men than it has in men older than 60 years, most likely because of decreased scalp type-2 5α-reductase activity in older men.3

Finasteride also has been tested for efficacy in women with AGA. A randomized double-blind study of 137 postmenopausal women with AGA who took finasteride 1 mg/d or placebo for one year showed no significant difference in hair count between the 2 groups. In fact, both groups of patients actually showed significant loss of hair during the study period.23 Another randomized open-label study tested finasteride 5 mg/d versus no treatment in premenopausal women with hyperandrogenic alopecia and elevated serum androgens (levels >2 SD above the mean in ovulatory control patients). This study found that the women using finasteride at this elevated dose did not see any significant improvement as opposed to the women receiving no treatment.24 Some clinicians have had more success with the use of finasteride in their female patients with AGA. In a letter published in the British Journal of Dermatology, 2 physicians describe successful treatment of AGA in a postmenopausal woman who was given finasteride 5 mg/wk. Success was measured via patient report of improved hair density and review of stereotactic photographs of the scalp.25 Despite this anecdotal evidence of success, the larger body of evidence weighs against the use of finasteride in postmenopausal women with AGA.

Because there are only 2 FDA-approved treatments for AGA, patients may wonder which is more effective. In a recent letter published in the Archives of Dermatology, finasteride 1 mg/d was compared with topical minoxidil 2% in 99 men aged 18 to 45 years with mid frontal and/or vertex hair thinning.26 The researchers found that both treatments worked equally well in stopping the progression of hair loss in patients; however, patients given minoxidil had quicker initial improvement whereby patients given finasteride had slightly better results as treatment progressed.26 Choice of treatment therefore may be more a factor of side-effect profile, expense, and preferred form of medication (oral vs topical).

Some patients may ask about combining finasteride with minoxidil. One case study described the improvement of one man's alopecia from Hamilton-Norwood class V to class III after using a combination therapy of finasteride 5 mg/d plus a topical solution of minoxidil 3% and tretinoin 0.01%.27 The combined use of finasteride and minoxidil topical solution has been studied in the animal model of AGA; in stumptail macaques, the combined use of finasteride with minoxidil had greater effects on hair loss than either treatment alone.28 Because both treatments have different modes of action, it is plausible that combining them may yield better results.

Off-Label Uses for FDA-Approved Medications Spironolactone—This medication is often prescribed for the treatment of hypertension because of its action as an aldosterone antagonist, but it also is able to inhibit the biosynthesis of androgens and to competitively inhibit androgen receptor protein binding.29 The main side effects of this medication are menstrual irregularities, hyperkalemia, gynecomastia in men, and gastrointestinal distress.29 Women using this medication must be warned about the potential for feminization of male fetuses if pregnancy occurs during the course of treatment.30 The cost of this medication at a dose of 200 mg/d is approximately $60 per month, though it typically is covered by insurance policies.8

Spironolactone has shown efficacy in treating women with hirsutism,31 and it also may have mild efficacy in treating AGA at a dose of 200 mg/d.32 One study examining the efficacy of spironolactone in women with AGA showed that the women taking the medication had less hair loss than control patients after one year, but the women taking spironolactone still did not have more hair after treatment than at the start of the study.33 Another study that examined the use of spironolactone 200 mg/d in 2 men and 2 women with AGA showed that the patients had an increase in the number of hairs in anagen phase from 22% at baseline to 84.5% at the end of 6 months of treatment.34 Because this medication only has weak evidence for its use as a treatment for hair loss, clinicians should consider this medication only in addition to other, more proven, means of therapy.

Yasmin®—This is an oral contraceptive pill composed of ethinyl estradiol and drospirenone, an analogue of spironolactone. Each pill contains drospirenone 3 mg, which is equivalent to spironolactone 25 mg.35 According to the manufacturer of Yasmin, this oral contraceptive antagonizes androgen receptors without affecting sex-hormone–binding globulin synthesis or affecting the binding of testosterone to sex-hormone–binding globulin. The manufacturer also claims that the drug inhibits ovarian androgen production.36 The most common side effects are similar to side effects of other oral contraceptives and include breast tenderness, nausea, headache, emotional lability, dysmenorrhea, intermenstrual bleeding, and depression.35 Some insurance plans will cover the cost of oral contraceptives, but for patients paying out of pocket, Yasmin costs approximately $30 per month.8

Because spironolactone is sometimes prescribed for AGA, some clinicians recommend Yasmin to patients with alopecia who also are looking for effective contraceptive methods. However, to our knowledge, there are no known published studies showing that Yasmin prevents hair loss or promotes hair regrowth. Because spironolactone has shown only slight efficacy in treatment of women with AGA,3 it is unclear what the effect of Yasmin may be on hair loss. However, this may be a reasonable choice of contraceptive in a woman with AGA.

Dutasteride—This new 5α-reductase inhibitor blocks both type-1 and type-2 isoenzymes.37 By inhibiting both types of 5α-reductase, dutasteride is able to achieve a greater than 90% suppression of DHT.37 This medication was developed for the treatment of benign prostatic hyperplasia, with side effects similar to those of finasteride.38 As with finasteride, women are advised not to take this product because of the potential risk of birth defects in male fetuses.37 In November 2002, dutasteride was approved by the FDA for use in patients with benign prostatic hyperplasia.39 This medication costs approximately $75 for a 1-month supply.8

Although dutasteride is not yet FDA approved for alopecia, the manufacturers have completed phase 2 clinical trials of the medication for the treatment of hair loss and are hopeful it will be approved by the FDA in 2006.40 There are no studies published regarding this medication's effect on AGA, but preliminary results from the manufacturer showed that dutasteride reduced scalp DHT in men to a greater extent than finasteride.41 

Herbal/Dietary Remedies Saw Palmetto—Saw palmetto, or Serenoa repens, is an herbal remedy that is processed from fruit of the American dwarf pine tree.42 It often is used to treat benign prostatic hypertrophy because of its ability to inhibit 5α-reductase levels by 32% without affecting testosterone levels in men.43 Extracts of saw palmetto also have been shown to have a partial antagonistic affect on testosterone receptors.44 It is most likely that these 2 actions led to saw palmetto being used as a hair loss remedy. Saw palmetto is believed to be a safe herbal supplement, with a primary side effect of mild gastrointestinal distress.42 Also, clinical trials conducted in human patients showed that consumption of saw palmetto supplements did not result in any clinically significant alterations in laboratory parameters.45 Saw palmetto has no known drug interactions.42 The cost of this supplement varies by manufacturer, but consumers should be able to find saw palmetto supplements for as little as $3 for a month's supply.8

One double-blind placebo-controlled study examined saw palmetto's effect on AGA.46 In this study, researchers studied the efficacy of a softgel containing β-sitosterol 50 mg and saw palmetto 200 mg extract (components of the HairGenesis™ Softgels discussed later) versus placebo in treating AGA. They found that 60% of patients taking the active softgel rated their hair growth as improved from baseline as opposed to only 10% of the patients taking placebo. However, this study had a limited patient population and also concurrently tested β-sitosterol, so any improvement cannot be attributed to saw palmetto alone.

Biotin—This is a water-soluble B complex vitamin that is used in the body as a cofactor for biochemical carboxylations. Patients that are deficient in this vitamin often have alopecia, brittle nails, and a scaly erythematous dermatitis.47,48 Biotin is water-soluble, and there are no known side effects of supplementation and no documented cases of biotin overdose.49 As with other supplements, cost of treatment will depend on the manufacturer, but consumers should be able to find biotin for as little as $2 for a month's supply.8

Dietary supplementation with biotin has been shown to improve the clinical condition of brittle nails,48 but no studies have been conducted looking at biotin's effect on AGA. Although it is true that biotin deficiency can lead to alopecia, such a deficiency has not been demonstrated in healthy humans eating a mixed diet.47 The only 2 situations in which human biotin deficiency has been demonstrated are in patients with extended consumption of raw egg whites50-52 and in patients with malabsorption syndromes receiving parenteral nutrition without biotin supplementation.50,53 Supplementing the diet with biotin is unlikely to harm a patient, but there is no data to suggest any improvement in hair regrowth.

Other Hair Regrowth Products Avacor™—Sold through the Internet and directly from the manufacturer, Avacor is a hair regrowth product marketed toward both sexes for treatment of AGA.54 The product line consists of a scalp detoxifying shampoo, an herbal supplement, and a topical solution. The purpose of the shampoo as stated by the manufacturer is to deep clean the scalp to improve the absorbency of the topical treatment. The herbal supplements are to be taken twice daily to "maintain a healthy hair follicle" and consist of bilberry, ginkgo biloba, saw palmetto, and horsetail. The topical solution, which is marketed to men only, claims to dilate blood vessels in the scalp, allowing increased nutrient and oxygen delivery to the scalp. The Web site claims that these products must be used together and that they have no known side effects.54 The cost of this product is $239.95 for a 3-month supply.55

The official Avacor Web site has a summary of a clinical study performed by The New York Hair Clinic and the Hair and Skin Treatment Center in which 200 men aged 18 to 65 years used the 3-part system for 24 weeks.55 The Web site claims that 91% of the men had a decrease in hair loss and an increase in strength and thickness of preexisting hair within 3 months.55 However, this study does not appear to be published in any journal and consumers can only receive a copy of the study if they purchase the product.

A Wellness Letter highlighting dietary supplements, published by the University of California at Berkeley, showed that Avacor contains minoxidil in its topical solution despite its claims to be made from only natural ingredients.56 In April 2003, the FDA sent the makers of Avacor a letter informing them that their products are considered drugs under section 201(g) of the Federal Food, Drug, and Cosmetic Act and should have had an approved New Drug Application prior to being marketed in the United States. The FDA also points out that the 3 individual components are mislabeled because the active ingredients are not listed on their labels.57

Given the lack of peer-reviewed evidence of hair growth and with all of the controversy surrounding this product, it would not be wise for clinicians to recommend this therapy to any patient.

HairGenesis™—This product line consists of 4 items: Revitalizing Oral Softgel™ supplements (β-sitosterol 50 mg and saw palmetto 200 mg extract) that claim to strengthen and protect hair; Topical Activator Serum that consists of various 5α-reductase inhibitors; Hair Revitalizing Formulation, a shampoo that has similar components to the Topical Activator Serum; and Hair and Scalp Conditioner that also is meant to strengthen and protect hair. Although the company states that the products may be used individually, it recommends using them all synergistically, at a cost of $200 for a 3-month supply.58 The efficacy of the oral softgel containing saw palmetto is discussed above; there are no known research studies published about the other 3 components of the HairGenesis system.

Nioxin®—This product line is sold only through hair salons and does not aim to regrow hair; rather, it claims to "create an optimum scalp environment" for regrowth and maintenance of the current hair count. The manufacturer claims to accomplish this by clearing the scalp of excess sebum that may contain high levels of DHT. Ingredients include various vitamin-B coenzymes, biotin, saw palmetto, aloe, ginseng, and amino acids. The manufacturer claims that the Nioxin system has no known side effects.59 As this product is sold only in salons, the cost for a month's supply will vary depending on the place of purchase. One salon that we contacted offered a one-month starter kit for $30. The manufacturer does not disclose its clinical studies but claims that its studies are conducted by "world-renowned" researchers who are experts in hair thinning.59 However, there is no known published scientific evidence that any of the ingredients in Nioxin are effective in treating hair loss or maintaining hair count, or that excess sebum leads to hair thinning.

Laser Light Therapy—Low-intensity laser light therapy has been shown to be effective in promoting wound healing60 and in improving circulation.61,62 For these reasons, some hair loss treatment centers are offering the use of lasers for treating alopecia in both men and women. To date, there are no known studies looking at the efficacy of these lasers for treating hair loss. The use of low-intensity laser light for treating alopecia is FDA approved for safety only, not for efficacy.29 This therapy is expensive, costing as much as $3500 for the recommended 6 months of treatment.63

Although various Web sites claim efficacy based on double-blind placebo-controlled studies of laser light treatment versus placebo laser treatment,64,65 such studies are not available for viewing anywhere on the Web sites. To the best of our knowledge, there are no peer-reviewed articles supporting efficacy of this type of treatment for AGA. Until reliable evidence of the effectiveness of laser light therapy for alopecia is published, this treatment remains experimental, at best.

Conclusion

Any consumer looking on the Internet for a treatment for hair loss is exposed to a multitude of remedies. However, only the FDA-approved treatments for AGA, finasteride and minoxidil, have any well-studied factual evidence of efficacy. Smaller studies have shown possible benefit of combining topical tretinoin with minoxidil, as well as combining finasteride and minoxidil. Spironolactone in high doses (100–200 mg), dutasteride, and saw palmetto, also may provide benefit; however, larger studies are needed to consider these agents as first-line treatments for AGA. In addition to efficacy, clinicians need to consider patient preferences, safety profile, and cost when counseling patients about treatment options for AGA.