Dr. Naissan Wesley

Recent studies have highlighted the rising incidence of melanoma in non-white skin. In populations with darker complexions, melanomas may appear on areas of the skin not exposed to the sun, often of the acral lentiginous type. 

The stage at diagnosis is also more advanced in non-white skin. Despite increased surveillance efforts, diagnosis of melanoma in darker skin is often difficult and delayed, which affects overall prognosis and likelihood of survival. When stratified by stage of diagnosis, melanoma in non-white skin has the same prognosis as melanoma in white skin.

Pigmented skin lesions are rarely noticed and are difficult to detect by clinical examination on dark skin because of reduced visibility of melanocytic lesions.

Using a dermatoscope to examine dark skin for melanomas could help improve the chance of correct diagnosis and earlier treatment if done properly. The use of dermoscopy is increasing in favor among dermatologists to improve diagnostic accuracy.

Few studies have reviewed the use of dermoscopy in darker skinned populations. In one study investigators evaluated the utility and efficacy of dermoscopy for pigmented lesions in black populations. The authors attempted to evaluate whether darker pigmentation influences dermatoscopic features in comparison with white populations (Brit. J. Dermatol. 2006:4;695-99).

In the study, 100 clinically doubtful or equivocal pigmented skin lesions in black patients were subjected to dermatoscopic examination. The lesions were observed using dermoscopy by two groups of dermatologists, one in Brazil (in vivo) and the other blinded evaluators in Italy (on slide images), both recording dermatoscopic features. The results showed that out of 100 cases, 79 were Clark nevi, 15 seborrheic keratoses, 4 blue nevi, 1 dermatofibroma, and 1 melanoma.

The agreement between observers was statistically evaluated and there was a high level of inter-observer agreement among dermatoscopic features. Only 3 out of the 100 suspicious lesions (Clark’s nevi) required surgical excision to confirm the diagnosis.

The melanomas presented dermatoscopic characteristics similar to the melanomas appearing in white populations with a blue-whitish veil, irregular globules and streaks at the periphery.

The increased incidence of melanoma, and decreased survival of ethnic patients due to a delay in diagnosis, is a sign of caution to dermatologists to increase surveillance of pigmented lesions in dark skin. Accurate classification of pigmented lesions is difficult; however, this study showed that dermoscopy can be a useful and even necessary tool in the identification of pigmented lesions in dark skin, as naked-eye examinations may be more difficult.

More accurate diagnoses can lead to, not only earlier treatment of clinically suspicious lesions, but also to a decrease in unnecessary biopsies in skin of color, which is more prone to hypertrophic and keloidal scarring.

Recent studies have highlighted the rising incidence of melanoma in non-white skin. In populations with darker complexions, melanomas may appear on areas of the skin not exposed to the sun, often of the acral lentiginous type. 

The stage at diagnosis is also more advanced in non-white skin. Despite increased surveillance efforts, diagnosis of melanoma in darker skin is often difficult and delayed, which affects overall prognosis and likelihood of survival. When stratified by stage of diagnosis, melanoma in non-white skin has the same prognosis as melanoma in white skin.

Pigmented skin lesions are rarely noticed and are difficult to detect by clinical examination on dark skin because of reduced visibility of melanocytic lesions.

Using a dermatoscope to examine dark skin for melanomas could help improve the chance of correct diagnosis and earlier treatment if done properly. The use of dermoscopy is increasing in favor among dermatologists to improve diagnostic accuracy.

Few studies have reviewed the use of dermoscopy in darker skinned populations. In one study investigators evaluated the utility and efficacy of dermoscopy for pigmented lesions in black populations. The authors attempted to evaluate whether darker pigmentation influences dermatoscopic features in comparison with white populations (Brit. J. Dermatol. 2006:4;695-99).

In the study, 100 clinically doubtful or equivocal pigmented skin lesions in black patients were subjected to dermatoscopic examination. The lesions were observed using dermoscopy by two groups of dermatologists, one in Brazil (in vivo) and the other blinded evaluators in Italy (on slide images), both recording dermatoscopic features. The results showed that out of 100 cases, 79 were Clark nevi, 15 seborrheic keratoses, 4 blue nevi, 1 dermatofibroma, and 1 melanoma.

The agreement between observers was statistically evaluated and there was a high level of inter-observer agreement among dermatoscopic features. Only 3 out of the 100 suspicious lesions (Clark’s nevi) required surgical excision to confirm the diagnosis.

The melanomas presented dermatoscopic characteristics similar to the melanomas appearing in white populations with a blue-whitish veil, irregular globules and streaks at the periphery.

The increased incidence of melanoma, and decreased survival of ethnic patients due to a delay in diagnosis, is a sign of caution to dermatologists to increase surveillance of pigmented lesions in dark skin. Accurate classification of pigmented lesions is difficult; however, this study showed that dermoscopy can be a useful and even necessary tool in the identification of pigmented lesions in dark skin, as naked-eye examinations may be more difficult.

More accurate diagnoses can lead to, not only earlier treatment of clinically suspicious lesions, but also to a decrease in unnecessary biopsies in skin of color, which is more prone to hypertrophic and keloidal scarring.

Recent studies have highlighted the rising incidence of melanoma in non-white skin. In populations with darker complexions, melanomas may appear on areas of the skin not exposed to the sun, often of the acral lentiginous type. 

The stage at diagnosis is also more advanced in non-white skin. Despite increased surveillance efforts, diagnosis of melanoma in darker skin is often difficult and delayed, which affects overall prognosis and likelihood of survival. When stratified by stage of diagnosis, melanoma in non-white skin has the same prognosis as melanoma in white skin.

Pigmented skin lesions are rarely noticed and are difficult to detect by clinical examination on dark skin because of reduced visibility of melanocytic lesions.

Using a dermatoscope to examine dark skin for melanomas could help improve the chance of correct diagnosis and earlier treatment if done properly. The use of dermoscopy is increasing in favor among dermatologists to improve diagnostic accuracy.

Few studies have reviewed the use of dermoscopy in darker skinned populations. In one study investigators evaluated the utility and efficacy of dermoscopy for pigmented lesions in black populations. The authors attempted to evaluate whether darker pigmentation influences dermatoscopic features in comparison with white populations (Brit. J. Dermatol. 2006:4;695-99).

In the study, 100 clinically doubtful or equivocal pigmented skin lesions in black patients were subjected to dermatoscopic examination. The lesions were observed using dermoscopy by two groups of dermatologists, one in Brazil (in vivo) and the other blinded evaluators in Italy (on slide images), both recording dermatoscopic features. The results showed that out of 100 cases, 79 were Clark nevi, 15 seborrheic keratoses, 4 blue nevi, 1 dermatofibroma, and 1 melanoma.

The agreement between observers was statistically evaluated and there was a high level of inter-observer agreement among dermatoscopic features. Only 3 out of the 100 suspicious lesions (Clark’s nevi) required surgical excision to confirm the diagnosis.

The melanomas presented dermatoscopic characteristics similar to the melanomas appearing in white populations with a blue-whitish veil, irregular globules and streaks at the periphery.

The increased incidence of melanoma, and decreased survival of ethnic patients due to a delay in diagnosis, is a sign of caution to dermatologists to increase surveillance of pigmented lesions in dark skin. Accurate classification of pigmented lesions is difficult; however, this study showed that dermoscopy can be a useful and even necessary tool in the identification of pigmented lesions in dark skin, as naked-eye examinations may be more difficult.

More accurate diagnoses can lead to, not only earlier treatment of clinically suspicious lesions, but also to a decrease in unnecessary biopsies in skin of color, which is more prone to hypertrophic and keloidal scarring.

As a follow-up to our blog about the relationship between ceramic flat iron use and trichorrhexis nodosa, we wanted to focus on the use of chemical relaxers and their association with hair damage.

Chemical relaxers have maintained their popularity over the years to make curly hair straight, especially in the African-American community. A relaxer is a chemical compound applied to curly hair to permanently break hydrogen disulfide bonds along the hair shaft to release the tight curl pattern. Typically, it is re-applied at varying intervals as new growth of unrelaxed hair occurs (Semin. Cutan. Med. Surg. 2009;28:103-8).

Relaxers have evolved from containing unusual ingredients such as lard, boiled eggs, and sodium hydroxide or lye (which is also found in many household cleaning products), to no-lye relaxers which contain guanidine hydroxide. These chemicals—whether made with or without lye—can result in hair breakage, particularly at points along the hair shaft where a new relaxer is applied to hair that has already been chemically treated.

In a recently published study, investigators performed a biochemical analysis on the hair of 30 women of African decent from Cape Town, South Africa. Of the women, 10 had natural hair (never used chemical treatments), 10 had asymptomatic relaxed hair, and 10 had symptomatic (brittle, breaking, or damaged) relaxed hair (J. Am. Acad. Dermatol. 2010; 62:402-8).

Cysteine levels were expected to be lower in chemically relaxed hair because it is estimated that 35% of cysteine changes to lanthionine during hydrolysis of the disulfide bonds (Clin. Dermatol. 1988;6:71-82).

The study found that cysteine levels were similar in proximal and distal natural hair. Levels were reduced in all relaxed hair, but were lowest in distal relaxed hair. Cysteine levels in distal and symptomatic relaxed hair were consistent with fragile, damaged hair such as that found in trichothiodystrophy.

In addition, arginine and citrulline levels were decreased, and glutamine levels were increased, in all relaxed hair when compared with natural hair. The authors noted that a decrease in arginine and citrulline has been associated with inflammation elsewhere, particularly in critically ill children, thus, relaxer use may also be associated with scalp inflammation.

However, Dr. Zoe Draelos wrote in an accompanying editorial that while cysteine levels were expected to be decreased, and this study validly confirms that, the association between decreased arginine and citrulline levels and scalp inflammation has not been as well elucidated.

Dr. Draelos, a dermatologist in High Point, N.C., also noted that prior amino acid analyses have failed to demonstrate that constituents of the body are accurately translated into the hair shaft composition in normal health. Further research is needed to elucidate whether or not relaxer use is also associated with amino acid deficiencies, which may be related to scalp inflammation, she concluded (J. Am. Acad. Dermatol. 2010;62:409-10).

As a follow-up to our blog about the relationship between ceramic flat iron use and trichorrhexis nodosa, we wanted to focus on the use of chemical relaxers and their association with hair damage.

Chemical relaxers have maintained their popularity over the years to make curly hair straight, especially in the African-American community. A relaxer is a chemical compound applied to curly hair to permanently break hydrogen disulfide bonds along the hair shaft to release the tight curl pattern. Typically, it is re-applied at varying intervals as new growth of unrelaxed hair occurs (Semin. Cutan. Med. Surg. 2009;28:103-8).

Relaxers have evolved from containing unusual ingredients such as lard, boiled eggs, and sodium hydroxide or lye (which is also found in many household cleaning products), to no-lye relaxers which contain guanidine hydroxide. These chemicals—whether made with or without lye—can result in hair breakage, particularly at points along the hair shaft where a new relaxer is applied to hair that has already been chemically treated.

In a recently published study, investigators performed a biochemical analysis on the hair of 30 women of African decent from Cape Town, South Africa. Of the women, 10 had natural hair (never used chemical treatments), 10 had asymptomatic relaxed hair, and 10 had symptomatic (brittle, breaking, or damaged) relaxed hair (J. Am. Acad. Dermatol. 2010; 62:402-8).

Cysteine levels were expected to be lower in chemically relaxed hair because it is estimated that 35% of cysteine changes to lanthionine during hydrolysis of the disulfide bonds (Clin. Dermatol. 1988;6:71-82).

The study found that cysteine levels were similar in proximal and distal natural hair. Levels were reduced in all relaxed hair, but were lowest in distal relaxed hair. Cysteine levels in distal and symptomatic relaxed hair were consistent with fragile, damaged hair such as that found in trichothiodystrophy.

In addition, arginine and citrulline levels were decreased, and glutamine levels were increased, in all relaxed hair when compared with natural hair. The authors noted that a decrease in arginine and citrulline has been associated with inflammation elsewhere, particularly in critically ill children, thus, relaxer use may also be associated with scalp inflammation.

However, Dr. Zoe Draelos wrote in an accompanying editorial that while cysteine levels were expected to be decreased, and this study validly confirms that, the association between decreased arginine and citrulline levels and scalp inflammation has not been as well elucidated.

Dr. Draelos, a dermatologist in High Point, N.C., also noted that prior amino acid analyses have failed to demonstrate that constituents of the body are accurately translated into the hair shaft composition in normal health. Further research is needed to elucidate whether or not relaxer use is also associated with amino acid deficiencies, which may be related to scalp inflammation, she concluded (J. Am. Acad. Dermatol. 2010;62:409-10).

As a follow-up to our blog about the relationship between ceramic flat iron use and trichorrhexis nodosa, we wanted to focus on the use of chemical relaxers and their association with hair damage.

Chemical relaxers have maintained their popularity over the years to make curly hair straight, especially in the African-American community. A relaxer is a chemical compound applied to curly hair to permanently break hydrogen disulfide bonds along the hair shaft to release the tight curl pattern. Typically, it is re-applied at varying intervals as new growth of unrelaxed hair occurs (Semin. Cutan. Med. Surg. 2009;28:103-8).

Relaxers have evolved from containing unusual ingredients such as lard, boiled eggs, and sodium hydroxide or lye (which is also found in many household cleaning products), to no-lye relaxers which contain guanidine hydroxide. These chemicals—whether made with or without lye—can result in hair breakage, particularly at points along the hair shaft where a new relaxer is applied to hair that has already been chemically treated.

In a recently published study, investigators performed a biochemical analysis on the hair of 30 women of African decent from Cape Town, South Africa. Of the women, 10 had natural hair (never used chemical treatments), 10 had asymptomatic relaxed hair, and 10 had symptomatic (brittle, breaking, or damaged) relaxed hair (J. Am. Acad. Dermatol. 2010; 62:402-8).

Cysteine levels were expected to be lower in chemically relaxed hair because it is estimated that 35% of cysteine changes to lanthionine during hydrolysis of the disulfide bonds (Clin. Dermatol. 1988;6:71-82).

The study found that cysteine levels were similar in proximal and distal natural hair. Levels were reduced in all relaxed hair, but were lowest in distal relaxed hair. Cysteine levels in distal and symptomatic relaxed hair were consistent with fragile, damaged hair such as that found in trichothiodystrophy.

In addition, arginine and citrulline levels were decreased, and glutamine levels were increased, in all relaxed hair when compared with natural hair. The authors noted that a decrease in arginine and citrulline has been associated with inflammation elsewhere, particularly in critically ill children, thus, relaxer use may also be associated with scalp inflammation.

However, Dr. Zoe Draelos wrote in an accompanying editorial that while cysteine levels were expected to be decreased, and this study validly confirms that, the association between decreased arginine and citrulline levels and scalp inflammation has not been as well elucidated.

Dr. Draelos, a dermatologist in High Point, N.C., also noted that prior amino acid analyses have failed to demonstrate that constituents of the body are accurately translated into the hair shaft composition in normal health. Further research is needed to elucidate whether or not relaxer use is also associated with amino acid deficiencies, which may be related to scalp inflammation, she concluded (J. Am. Acad. Dermatol. 2010;62:409-10).

A great victory for our patients suffering from cicatricial alopecia—Dr. Pratima Karnik, assistant professor of dermatology at Cleveland’s Case Western Reserve University, received a $1.77 National Institutes of Health grant to fund a 5 year study on hair follicle, stem cell specific, PPAR-gamma deficiency in scarring alopecia.

Her research, published in the Journal of Investigative Dermatology, linked a defect in lipid processing and peroxisome biogenesis to cicatricial alopecia. As a result, it paved the way for a breakthrough finding in understanding the pathophysiology of the permanent hair loss disorder (J Invest Dermatol. 2009 May;129(5):1066-70).

Dr. Karnik and her colleagues found that unprocessed lipids are responsible for developing scarring hair loss. Their research suggests that processed lipids are necessary for hair growth and unprocessed lipids are toxic to hair. The bench-side research has led to clinical findings that treating patients with drugs that enhance lipid processing may relieve the clinical symptoms of the disorder.

Central centrifugal cicatricial alopecia, a scarring hair loss prevalent in African Americans, has no well-defined cause and has been difficult to and frustrating for patients.

Dr. Karnik’s research, and the work of the Cicatricial Alopecia Research Foundation (www.carfintl.org), is helping patients and physicians understand the biology, natural history, and treatment options for patients.
 
I personally attended a session with NIH Director Dr. Francis S. Collins, on behalf of CARF, where underrepresented and underfunded organizations had a chance to voice their opinions to the NIH and gain the well deserved attention they need.

Dr. Collins suggested that a new structure of communication was being established at the NIH, noting that any organization can send a brief summary of issues it would like to bring to the attention of the NIH. The e-mail address is [email protected]. He ensured us he would look at every e-mail and respond to each one.

Often, rare diseases are difficult to study given the lack of attention and funding.  The work of Dr. Karnik and her collaborative team, and organizations like CARF, give hope to the thousands of people suffering from cicatricial alopecia.

A great victory for our patients suffering from cicatricial alopecia—Dr. Pratima Karnik, assistant professor of dermatology at Cleveland’s Case Western Reserve University, received a $1.77 National Institutes of Health grant to fund a 5 year study on hair follicle, stem cell specific, PPAR-gamma deficiency in scarring alopecia.

Her research, published in the Journal of Investigative Dermatology, linked a defect in lipid processing and peroxisome biogenesis to cicatricial alopecia. As a result, it paved the way for a breakthrough finding in understanding the pathophysiology of the permanent hair loss disorder (J Invest Dermatol. 2009 May;129(5):1066-70).

Dr. Karnik and her colleagues found that unprocessed lipids are responsible for developing scarring hair loss. Their research suggests that processed lipids are necessary for hair growth and unprocessed lipids are toxic to hair. The bench-side research has led to clinical findings that treating patients with drugs that enhance lipid processing may relieve the clinical symptoms of the disorder.

Central centrifugal cicatricial alopecia, a scarring hair loss prevalent in African Americans, has no well-defined cause and has been difficult to and frustrating for patients.

Dr. Karnik’s research, and the work of the Cicatricial Alopecia Research Foundation (www.carfintl.org), is helping patients and physicians understand the biology, natural history, and treatment options for patients.
 
I personally attended a session with NIH Director Dr. Francis S. Collins, on behalf of CARF, where underrepresented and underfunded organizations had a chance to voice their opinions to the NIH and gain the well deserved attention they need.

Dr. Collins suggested that a new structure of communication was being established at the NIH, noting that any organization can send a brief summary of issues it would like to bring to the attention of the NIH. The e-mail address is [email protected]. He ensured us he would look at every e-mail and respond to each one.

Often, rare diseases are difficult to study given the lack of attention and funding.  The work of Dr. Karnik and her collaborative team, and organizations like CARF, give hope to the thousands of people suffering from cicatricial alopecia.

A great victory for our patients suffering from cicatricial alopecia—Dr. Pratima Karnik, assistant professor of dermatology at Cleveland’s Case Western Reserve University, received a $1.77 National Institutes of Health grant to fund a 5 year study on hair follicle, stem cell specific, PPAR-gamma deficiency in scarring alopecia.

Her research, published in the Journal of Investigative Dermatology, linked a defect in lipid processing and peroxisome biogenesis to cicatricial alopecia. As a result, it paved the way for a breakthrough finding in understanding the pathophysiology of the permanent hair loss disorder (J Invest Dermatol. 2009 May;129(5):1066-70).

Dr. Karnik and her colleagues found that unprocessed lipids are responsible for developing scarring hair loss. Their research suggests that processed lipids are necessary for hair growth and unprocessed lipids are toxic to hair. The bench-side research has led to clinical findings that treating patients with drugs that enhance lipid processing may relieve the clinical symptoms of the disorder.

Central centrifugal cicatricial alopecia, a scarring hair loss prevalent in African Americans, has no well-defined cause and has been difficult to and frustrating for patients.

Dr. Karnik’s research, and the work of the Cicatricial Alopecia Research Foundation (www.carfintl.org), is helping patients and physicians understand the biology, natural history, and treatment options for patients.
 
I personally attended a session with NIH Director Dr. Francis S. Collins, on behalf of CARF, where underrepresented and underfunded organizations had a chance to voice their opinions to the NIH and gain the well deserved attention they need.

Dr. Collins suggested that a new structure of communication was being established at the NIH, noting that any organization can send a brief summary of issues it would like to bring to the attention of the NIH. The e-mail address is [email protected]. He ensured us he would look at every e-mail and respond to each one.

Often, rare diseases are difficult to study given the lack of attention and funding.  The work of Dr. Karnik and her collaborative team, and organizations like CARF, give hope to the thousands of people suffering from cicatricial alopecia.

With photographs of a much lighter-skinned Sammy Sosa in the media recently, questions about bleaching agents and their effects have been posed by our patients and by the media.

Skin-lightening agents are essential products for hyperpigmentation, particularly in persons of color, for whom the stigma of common skin disorders such as acne is magnified by the post-inflammatory hyperpigmentation these conditions leave as their mark. Although there are numerous skin-lightening agents on the market, including azelaic acid, mequinol, retinoids, glycolic acid, kojic acid, licorice, arbutin, soy, N-acetyl glucosamine, ascorbic acid, and niacinamide, hydroquinone (HQ) has been our workhorse.

In 1961, Dr. Malcolm C. Spencer evaluated the efficacy of hydroquinone 1.5% and 2% in 98 subjects with hyperpigmentation. Improvement was noted in 45% of subjects, with no reports of adverse events. Since this seminal study, HQ has been the standard for treatment of hyperpigmentation. HQ blocks the conversion of dihydroxyphenylalanine (DOPA) to melanin by inhibiting tyrosinase, a copper-containing enzyme of plant and animal tissues that catalyzes the production of melanin and other pigments. It may also inhibit RNA and DNA synthesis, degrade melanosomes, and destroy melanocytes.

Currently, HQ is commonly used in concentrations of 2% over the counter, 4% by standard prescription, or prescribed in higher concentrations or compounded with other agents (particularly retinoids or glycolic acid) to offer maximal efficacy. The Kligman formula, containing 5% HQ, 0.1% tretinoin, and 0.1% dexamethasone, and modifications of this formula, has emerged as the most popular combination. 

Side effects of HQ are both acute and chronic. Acute complications include irritant or allergic contact dermatitis and postinflammatory hyper- and hypopigmentation. Of these, irritant reactions are the most common. Review of the literature suggests that monotherapy hydroquinone agents cause irritant reactions in 0%-70% of patients. In combination therapy, the incidence rises to 10%-100%.  Reports of allergic contact sensitization to hydroquinone are infrequent.

Chronic adverse events related to exposure to hydroquinone are of greater concern. These complications include ochronosis, nail discoloration, conjunctival melanosis, and corneal degeneration. Ochronosis is the most common chronic complication related to long-term use of hydroquinone. The condition was initially described by G.H. Findlay and associates among South African Bantu women who applied high concentrations of hydroquinone (6%-8.5%) for many years (Br. J. Dermatol. 1975;93:613-22). Clinically, ochronosis is characterized by asymptomatic hyperpigmentation, erythema, papules, papulonodules, and grey-blue colloid milia on sun-exposed areas of the skin. Although ochronosis has been commonly described among women in Africa, it is uncommon in the United States despite its extensive use. There were less than 25 reported cases of hydroquinone-associated ochronosis in the United States in the past 25 years. Certainly, there may be unreported cases; however, conservative use of the data suggests that there would be one case of exogenous ochronosis for every 300-450 million units of hydroquinone sold in the United States. The majority of reported U.S. cases have occurred with 2% hydroquinone.

As Dr. Pearl Grimes stated in the Seminars of Cutaneous Medicine and Surgery: Skin of Color issue, “factors accounting for the disparity in the frequency of ochronosis in the U.S. and Africa include the routine use of sunscreens and the absence of resorcinol in formulations in the States. In addition, in contrast to Africa, there are few hydroethanolic formulations marketed in the U.S. Such formulations may permit enhanced absorption of HQ (2009;28:77-85). In addition, the Bantu women described in the original article by Findlay used higher concentrations of hydroquinone over extensive body surface areas, several times a day, for years or, in some cases, decades.

Hydroquinone has been banned in some countries, including over-the-counter dispensed formulations of 2% HQ by the European Cosmetic Product Regulation. In August 2006, the U.S. Food and Drug Administration (FDA) proposed a ban on OTC HQ and considered requiring new drug applications for 4% formulations due to concerns regarding ochronosis and possible carcinogenicity. Some animal studies have shown an increase in cancers that are species and sex specific, but there are no human studies documenting an increased incidence of skin cancer or internal malignancies in users of HQ.

Details on the FDA’s proposed ban are as follows: on Aug. 29, 2006, the FDA published a monograph in the U.S. Federal Register proposing that all hydroquinone products, which have not been approved through the new drug application process, be considered misbranded and therefore banned. This so-called “proposed rule” allowed anyone to submit comments to the FDA by a specified date (in this case Dec. 27, 2006 – later extended 30 days) before the so-called “final rule” would be published. Once the final rule is published in the Federal Register, manufacturers would have 30 days to remove noncompliant hydroquinone products from the marketplace or risk seizure, fines, and possibly imprisonment. Now, in 2010, the verdict on the proposed FDA ban is still pending.

Though controversial, hydroquinone still remains the workhorse of dermatologists for the treatment of melasma and postinflammatory hyperpigmentation. Until a safe, more widely accepted, and efficacious product is developed, we will continue the search to find the best treatment for skin of color patients.

With photographs of a much lighter-skinned Sammy Sosa in the media recently, questions about bleaching agents and their effects have been posed by our patients and by the media.

Skin-lightening agents are essential products for hyperpigmentation, particularly in persons of color, for whom the stigma of common skin disorders such as acne is magnified by the post-inflammatory hyperpigmentation these conditions leave as their mark. Although there are numerous skin-lightening agents on the market, including azelaic acid, mequinol, retinoids, glycolic acid, kojic acid, licorice, arbutin, soy, N-acetyl glucosamine, ascorbic acid, and niacinamide, hydroquinone (HQ) has been our workhorse.

In 1961, Dr. Malcolm C. Spencer evaluated the efficacy of hydroquinone 1.5% and 2% in 98 subjects with hyperpigmentation. Improvement was noted in 45% of subjects, with no reports of adverse events. Since this seminal study, HQ has been the standard for treatment of hyperpigmentation. HQ blocks the conversion of dihydroxyphenylalanine (DOPA) to melanin by inhibiting tyrosinase, a copper-containing enzyme of plant and animal tissues that catalyzes the production of melanin and other pigments. It may also inhibit RNA and DNA synthesis, degrade melanosomes, and destroy melanocytes.

Currently, HQ is commonly used in concentrations of 2% over the counter, 4% by standard prescription, or prescribed in higher concentrations or compounded with other agents (particularly retinoids or glycolic acid) to offer maximal efficacy. The Kligman formula, containing 5% HQ, 0.1% tretinoin, and 0.1% dexamethasone, and modifications of this formula, has emerged as the most popular combination. 

Side effects of HQ are both acute and chronic. Acute complications include irritant or allergic contact dermatitis and postinflammatory hyper- and hypopigmentation. Of these, irritant reactions are the most common. Review of the literature suggests that monotherapy hydroquinone agents cause irritant reactions in 0%-70% of patients. In combination therapy, the incidence rises to 10%-100%.  Reports of allergic contact sensitization to hydroquinone are infrequent.

Chronic adverse events related to exposure to hydroquinone are of greater concern. These complications include ochronosis, nail discoloration, conjunctival melanosis, and corneal degeneration. Ochronosis is the most common chronic complication related to long-term use of hydroquinone. The condition was initially described by G.H. Findlay and associates among South African Bantu women who applied high concentrations of hydroquinone (6%-8.5%) for many years (Br. J. Dermatol. 1975;93:613-22). Clinically, ochronosis is characterized by asymptomatic hyperpigmentation, erythema, papules, papulonodules, and grey-blue colloid milia on sun-exposed areas of the skin. Although ochronosis has been commonly described among women in Africa, it is uncommon in the United States despite its extensive use. There were less than 25 reported cases of hydroquinone-associated ochronosis in the United States in the past 25 years. Certainly, there may be unreported cases; however, conservative use of the data suggests that there would be one case of exogenous ochronosis for every 300-450 million units of hydroquinone sold in the United States. The majority of reported U.S. cases have occurred with 2% hydroquinone.

As Dr. Pearl Grimes stated in the Seminars of Cutaneous Medicine and Surgery: Skin of Color issue, “factors accounting for the disparity in the frequency of ochronosis in the U.S. and Africa include the routine use of sunscreens and the absence of resorcinol in formulations in the States. In addition, in contrast to Africa, there are few hydroethanolic formulations marketed in the U.S. Such formulations may permit enhanced absorption of HQ (2009;28:77-85). In addition, the Bantu women described in the original article by Findlay used higher concentrations of hydroquinone over extensive body surface areas, several times a day, for years or, in some cases, decades.

Hydroquinone has been banned in some countries, including over-the-counter dispensed formulations of 2% HQ by the European Cosmetic Product Regulation. In August 2006, the U.S. Food and Drug Administration (FDA) proposed a ban on OTC HQ and considered requiring new drug applications for 4% formulations due to concerns regarding ochronosis and possible carcinogenicity. Some animal studies have shown an increase in cancers that are species and sex specific, but there are no human studies documenting an increased incidence of skin cancer or internal malignancies in users of HQ.

Details on the FDA’s proposed ban are as follows: on Aug. 29, 2006, the FDA published a monograph in the U.S. Federal Register proposing that all hydroquinone products, which have not been approved through the new drug application process, be considered misbranded and therefore banned. This so-called “proposed rule” allowed anyone to submit comments to the FDA by a specified date (in this case Dec. 27, 2006 – later extended 30 days) before the so-called “final rule” would be published. Once the final rule is published in the Federal Register, manufacturers would have 30 days to remove noncompliant hydroquinone products from the marketplace or risk seizure, fines, and possibly imprisonment. Now, in 2010, the verdict on the proposed FDA ban is still pending.

Though controversial, hydroquinone still remains the workhorse of dermatologists for the treatment of melasma and postinflammatory hyperpigmentation. Until a safe, more widely accepted, and efficacious product is developed, we will continue the search to find the best treatment for skin of color patients.

With photographs of a much lighter-skinned Sammy Sosa in the media recently, questions about bleaching agents and their effects have been posed by our patients and by the media.

Skin-lightening agents are essential products for hyperpigmentation, particularly in persons of color, for whom the stigma of common skin disorders such as acne is magnified by the post-inflammatory hyperpigmentation these conditions leave as their mark. Although there are numerous skin-lightening agents on the market, including azelaic acid, mequinol, retinoids, glycolic acid, kojic acid, licorice, arbutin, soy, N-acetyl glucosamine, ascorbic acid, and niacinamide, hydroquinone (HQ) has been our workhorse.

In 1961, Dr. Malcolm C. Spencer evaluated the efficacy of hydroquinone 1.5% and 2% in 98 subjects with hyperpigmentation. Improvement was noted in 45% of subjects, with no reports of adverse events. Since this seminal study, HQ has been the standard for treatment of hyperpigmentation. HQ blocks the conversion of dihydroxyphenylalanine (DOPA) to melanin by inhibiting tyrosinase, a copper-containing enzyme of plant and animal tissues that catalyzes the production of melanin and other pigments. It may also inhibit RNA and DNA synthesis, degrade melanosomes, and destroy melanocytes.

Currently, HQ is commonly used in concentrations of 2% over the counter, 4% by standard prescription, or prescribed in higher concentrations or compounded with other agents (particularly retinoids or glycolic acid) to offer maximal efficacy. The Kligman formula, containing 5% HQ, 0.1% tretinoin, and 0.1% dexamethasone, and modifications of this formula, has emerged as the most popular combination. 

Side effects of HQ are both acute and chronic. Acute complications include irritant or allergic contact dermatitis and postinflammatory hyper- and hypopigmentation. Of these, irritant reactions are the most common. Review of the literature suggests that monotherapy hydroquinone agents cause irritant reactions in 0%-70% of patients. In combination therapy, the incidence rises to 10%-100%.  Reports of allergic contact sensitization to hydroquinone are infrequent.

Chronic adverse events related to exposure to hydroquinone are of greater concern. These complications include ochronosis, nail discoloration, conjunctival melanosis, and corneal degeneration. Ochronosis is the most common chronic complication related to long-term use of hydroquinone. The condition was initially described by G.H. Findlay and associates among South African Bantu women who applied high concentrations of hydroquinone (6%-8.5%) for many years (Br. J. Dermatol. 1975;93:613-22). Clinically, ochronosis is characterized by asymptomatic hyperpigmentation, erythema, papules, papulonodules, and grey-blue colloid milia on sun-exposed areas of the skin. Although ochronosis has been commonly described among women in Africa, it is uncommon in the United States despite its extensive use. There were less than 25 reported cases of hydroquinone-associated ochronosis in the United States in the past 25 years. Certainly, there may be unreported cases; however, conservative use of the data suggests that there would be one case of exogenous ochronosis for every 300-450 million units of hydroquinone sold in the United States. The majority of reported U.S. cases have occurred with 2% hydroquinone.

As Dr. Pearl Grimes stated in the Seminars of Cutaneous Medicine and Surgery: Skin of Color issue, “factors accounting for the disparity in the frequency of ochronosis in the U.S. and Africa include the routine use of sunscreens and the absence of resorcinol in formulations in the States. In addition, in contrast to Africa, there are few hydroethanolic formulations marketed in the U.S. Such formulations may permit enhanced absorption of HQ (2009;28:77-85). In addition, the Bantu women described in the original article by Findlay used higher concentrations of hydroquinone over extensive body surface areas, several times a day, for years or, in some cases, decades.

Hydroquinone has been banned in some countries, including over-the-counter dispensed formulations of 2% HQ by the European Cosmetic Product Regulation. In August 2006, the U.S. Food and Drug Administration (FDA) proposed a ban on OTC HQ and considered requiring new drug applications for 4% formulations due to concerns regarding ochronosis and possible carcinogenicity. Some animal studies have shown an increase in cancers that are species and sex specific, but there are no human studies documenting an increased incidence of skin cancer or internal malignancies in users of HQ.

Details on the FDA’s proposed ban are as follows: on Aug. 29, 2006, the FDA published a monograph in the U.S. Federal Register proposing that all hydroquinone products, which have not been approved through the new drug application process, be considered misbranded and therefore banned. This so-called “proposed rule” allowed anyone to submit comments to the FDA by a specified date (in this case Dec. 27, 2006 – later extended 30 days) before the so-called “final rule” would be published. Once the final rule is published in the Federal Register, manufacturers would have 30 days to remove noncompliant hydroquinone products from the marketplace or risk seizure, fines, and possibly imprisonment. Now, in 2010, the verdict on the proposed FDA ban is still pending.

Though controversial, hydroquinone still remains the workhorse of dermatologists for the treatment of melasma and postinflammatory hyperpigmentation. Until a safe, more widely accepted, and efficacious product is developed, we will continue the search to find the best treatment for skin of color patients.