Pigmentation Disorders

Vitamin D deficiency is a particular problem in individuals with skin of color, and screening of these patients should be considered given the growing list of diseases associated with the condition, said Dr. Grimes at the annual meeting of the American Academy of Dermatology.

African Americans have an increased incidence of many of the diseases also linked to vitamin D deficiency, including hypertension, diabetes, obesity, aggressive prostate and breast cancer, lupus, tuberculosis, and non-Hodgkins lymphoma, said Dr. Grimes.

Vitamin D deficiency has been shown to be associated with numerous other conditions, including neurocognitive disorders, such as Alzheimer's disease, and dermatologic disorders, such as atopic dermatitis, psoriasis, malignant melanoma, and other skin cancers.

In a recent study of 194 African American men undergoing risk assessment for prostate cancer, mean 25-hydroxyvitamin D (25[OH]D) serum concentrations were 13.7 ng/ml (BMC Public Health 2009;9:191). A concentration lower than 20 ng/ml is considered deficient; concentrations of 21-50 ng/ml are considered insufficient; and concentrations of greater than 50 ng/ml are considered sufficient.

More than 60% of the men in the study had levels less than 15 ng/ml; even 55% of the men ingesting more than 400 IU of vitamin D daily had levels less than 15 ng/ml, said Dr. Grimes, a clinical professor of dermatology at the University of California, Los Angeles. She noted the finding raises the question of whether there is a genetic, racially-induced polymorphism that predisposes African Americans to vitamin D deficiency.

Other studies from around the world have also demonstrated racial and gender differences in regard to vitamin D levels, with significantly lower levels found in African Americans and women.

In a study of 185 patients, Dr. Grimes and her colleagues found the highest vitamin D levels were seen in whites, and the lowest were in those with skin of color. Women had slightly lower levels than men. Sun exposure appeared to be a factor, with about 40% of patients using sunscreen regularly, and most only getting sun exposure on weekends.

Sun exposure is the best source of vitamin D, accounting for 80% to 90% of vitamin D levels, compared with 10% to 20% for dietary intake, said Dr. Grimes. The use of a sunscreen with an SPF of 15 can decrease vitamin D production by 99%.

The problem of vitamin D deficiency has increased over time, perhaps due in part to improved photoprotective and sun-avoidance behaviors. Data from the Centers for Disease Control's National Health and Nutrition Examination Survey (NHANES) found that 25(OH)D concentrations decreased in all ages, both genders, and all racial and ethnic groups between 1988 and 2001, she said. "In patients with [25(OH)D] less than 20 ng/ml, I invariably put them on 2,000 IU of vitamin D daily and have them come back in 3-4 months to check their levels," Dr. Grimes said.
Vitamin D3, the natural form of vitamin D when exposed to sunlight, is superior to vitamin D2, which can be found in a select group of foods, said Dr. Grimes. Doses of up to 5,000 IU are also acceptable.

Patients should be advised about the best sources of dietary vitamin D, including  fish liver, fish liver oil, fatty fish like salmon (wild is better than farm raised), egg yolks, and milk, she noted. Also, in patients with skin of color, it may be important to weigh the low risk of developing skin cancer against the risks of vitamin D deficiency.

"It is imperative that we educate patients … I think we need to have a dialogue regarding sunscreen," Dr. Grimes said. If a patient with pigmented skin is using an SPF 75 sunscreen, the wisdom of that should be questioned, as should the value of advising more outdoor activity and sun exposure.

"I don't have the answers … but as clinicians we have to think about these things as we move forward," she said.

Dr. Grimes reported she had no disclosures related to her presentation.

Vitamin D deficiency is a particular problem in individuals with skin of color, and screening of these patients should be considered given the growing list of diseases associated with the condition, said Dr. Grimes at the annual meeting of the American Academy of Dermatology.

African Americans have an increased incidence of many of the diseases also linked to vitamin D deficiency, including hypertension, diabetes, obesity, aggressive prostate and breast cancer, lupus, tuberculosis, and non-Hodgkins lymphoma, said Dr. Grimes.

Vitamin D deficiency has been shown to be associated with numerous other conditions, including neurocognitive disorders, such as Alzheimer's disease, and dermatologic disorders, such as atopic dermatitis, psoriasis, malignant melanoma, and other skin cancers.

In a recent study of 194 African American men undergoing risk assessment for prostate cancer, mean 25-hydroxyvitamin D (25[OH]D) serum concentrations were 13.7 ng/ml (BMC Public Health 2009;9:191). A concentration lower than 20 ng/ml is considered deficient; concentrations of 21-50 ng/ml are considered insufficient; and concentrations of greater than 50 ng/ml are considered sufficient.

More than 60% of the men in the study had levels less than 15 ng/ml; even 55% of the men ingesting more than 400 IU of vitamin D daily had levels less than 15 ng/ml, said Dr. Grimes, a clinical professor of dermatology at the University of California, Los Angeles. She noted the finding raises the question of whether there is a genetic, racially-induced polymorphism that predisposes African Americans to vitamin D deficiency.

Other studies from around the world have also demonstrated racial and gender differences in regard to vitamin D levels, with significantly lower levels found in African Americans and women.

In a study of 185 patients, Dr. Grimes and her colleagues found the highest vitamin D levels were seen in whites, and the lowest were in those with skin of color. Women had slightly lower levels than men. Sun exposure appeared to be a factor, with about 40% of patients using sunscreen regularly, and most only getting sun exposure on weekends.

Sun exposure is the best source of vitamin D, accounting for 80% to 90% of vitamin D levels, compared with 10% to 20% for dietary intake, said Dr. Grimes. The use of a sunscreen with an SPF of 15 can decrease vitamin D production by 99%.

The problem of vitamin D deficiency has increased over time, perhaps due in part to improved photoprotective and sun-avoidance behaviors. Data from the Centers for Disease Control's National Health and Nutrition Examination Survey (NHANES) found that 25(OH)D concentrations decreased in all ages, both genders, and all racial and ethnic groups between 1988 and 2001, she said. "In patients with [25(OH)D] less than 20 ng/ml, I invariably put them on 2,000 IU of vitamin D daily and have them come back in 3-4 months to check their levels," Dr. Grimes said.
Vitamin D3, the natural form of vitamin D when exposed to sunlight, is superior to vitamin D2, which can be found in a select group of foods, said Dr. Grimes. Doses of up to 5,000 IU are also acceptable.

Patients should be advised about the best sources of dietary vitamin D, including  fish liver, fish liver oil, fatty fish like salmon (wild is better than farm raised), egg yolks, and milk, she noted. Also, in patients with skin of color, it may be important to weigh the low risk of developing skin cancer against the risks of vitamin D deficiency.

"It is imperative that we educate patients … I think we need to have a dialogue regarding sunscreen," Dr. Grimes said. If a patient with pigmented skin is using an SPF 75 sunscreen, the wisdom of that should be questioned, as should the value of advising more outdoor activity and sun exposure.

"I don't have the answers … but as clinicians we have to think about these things as we move forward," she said.

Dr. Grimes reported she had no disclosures related to her presentation.

Vitamin D deficiency is a particular problem in individuals with skin of color, and screening of these patients should be considered given the growing list of diseases associated with the condition, said Dr. Grimes at the annual meeting of the American Academy of Dermatology.

African Americans have an increased incidence of many of the diseases also linked to vitamin D deficiency, including hypertension, diabetes, obesity, aggressive prostate and breast cancer, lupus, tuberculosis, and non-Hodgkins lymphoma, said Dr. Grimes.

Vitamin D deficiency has been shown to be associated with numerous other conditions, including neurocognitive disorders, such as Alzheimer's disease, and dermatologic disorders, such as atopic dermatitis, psoriasis, malignant melanoma, and other skin cancers.

In a recent study of 194 African American men undergoing risk assessment for prostate cancer, mean 25-hydroxyvitamin D (25[OH]D) serum concentrations were 13.7 ng/ml (BMC Public Health 2009;9:191). A concentration lower than 20 ng/ml is considered deficient; concentrations of 21-50 ng/ml are considered insufficient; and concentrations of greater than 50 ng/ml are considered sufficient.

More than 60% of the men in the study had levels less than 15 ng/ml; even 55% of the men ingesting more than 400 IU of vitamin D daily had levels less than 15 ng/ml, said Dr. Grimes, a clinical professor of dermatology at the University of California, Los Angeles. She noted the finding raises the question of whether there is a genetic, racially-induced polymorphism that predisposes African Americans to vitamin D deficiency.

Other studies from around the world have also demonstrated racial and gender differences in regard to vitamin D levels, with significantly lower levels found in African Americans and women.

In a study of 185 patients, Dr. Grimes and her colleagues found the highest vitamin D levels were seen in whites, and the lowest were in those with skin of color. Women had slightly lower levels than men. Sun exposure appeared to be a factor, with about 40% of patients using sunscreen regularly, and most only getting sun exposure on weekends.

Sun exposure is the best source of vitamin D, accounting for 80% to 90% of vitamin D levels, compared with 10% to 20% for dietary intake, said Dr. Grimes. The use of a sunscreen with an SPF of 15 can decrease vitamin D production by 99%.

The problem of vitamin D deficiency has increased over time, perhaps due in part to improved photoprotective and sun-avoidance behaviors. Data from the Centers for Disease Control's National Health and Nutrition Examination Survey (NHANES) found that 25(OH)D concentrations decreased in all ages, both genders, and all racial and ethnic groups between 1988 and 2001, she said. "In patients with [25(OH)D] less than 20 ng/ml, I invariably put them on 2,000 IU of vitamin D daily and have them come back in 3-4 months to check their levels," Dr. Grimes said.
Vitamin D3, the natural form of vitamin D when exposed to sunlight, is superior to vitamin D2, which can be found in a select group of foods, said Dr. Grimes. Doses of up to 5,000 IU are also acceptable.

Patients should be advised about the best sources of dietary vitamin D, including  fish liver, fish liver oil, fatty fish like salmon (wild is better than farm raised), egg yolks, and milk, she noted. Also, in patients with skin of color, it may be important to weigh the low risk of developing skin cancer against the risks of vitamin D deficiency.

"It is imperative that we educate patients … I think we need to have a dialogue regarding sunscreen," Dr. Grimes said. If a patient with pigmented skin is using an SPF 75 sunscreen, the wisdom of that should be questioned, as should the value of advising more outdoor activity and sun exposure.

"I don't have the answers … but as clinicians we have to think about these things as we move forward," she said.

Dr. Grimes reported she had no disclosures related to her presentation.

If you would like to learn more about issues in skin of color, and be part of an organization dedicated to promoting awareness and excellence in dermatology, please attend the Skin of Color Society's scientific symposium at the American Academy of Dermatology's annual meeting in Miami this Thursday, March 4, at 2 pm in the Loews Miami Beach Hotel (Ponciana 4 Room).

We hope to see you there!

Lily & Naissan

If you would like to learn more about issues in skin of color, and be part of an organization dedicated to promoting awareness and excellence in dermatology, please attend the Skin of Color Society's scientific symposium at the American Academy of Dermatology's annual meeting in Miami this Thursday, March 4, at 2 pm in the Loews Miami Beach Hotel (Ponciana 4 Room).

We hope to see you there!

Lily & Naissan

If you would like to learn more about issues in skin of color, and be part of an organization dedicated to promoting awareness and excellence in dermatology, please attend the Skin of Color Society's scientific symposium at the American Academy of Dermatology's annual meeting in Miami this Thursday, March 4, at 2 pm in the Loews Miami Beach Hotel (Ponciana 4 Room).

We hope to see you there!

Lily & Naissan

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.

The lifetime risk of white patients developing melanoma is currently estimated at 1 in 50, compared with 1 in 1,000 for black patients. Although darker-pigmented populations are consistently reported to have lower melanoma risk--possibly related to protection from ultraviolet radiation provided by melanin--darker skinned patients have been consistently shown to have worse outcomes than whites.

While less common in blacks, malignant melanoma is nonetheless an aggressive, deadly disease and presents at a more advanced stage at diagnosis and with a decreased chance of survival than in white patints. Underlying etiologies for the disparity in prognosis are still poorly understood.

Many of the public health interventions for melanoma prevention have focused predominantly on whites. However, recent studies in blacks and Hispanics that have elucidated advanced stage of melanoma at presentation and a higher mortality rate have led to increased efforts to characterize melanoma in ethnic minorities.

One such study found that ethnic disparities persist in the incidence of melanoma and its stage at diagnosis (Arch Dermatol. 2009;145:1369-74). Researchers analyzed information in the Florida Cancer Data System, a statewide, population-based cancer registry. They looked at three 5-year periods: 1990 to 1994, 1995 to 1999, and 2000 to 2004.

Of 41,072 cases of melanoma diagnosed from 1990 to 2004, 39,670 were in whites, 1,148 in Hispanics, and 254 in blacks. Advanced melanoma diagnosed at either regional or distant stages were seen in 26.4% of black patients, compared with 17.8% of Hispanics and 11.6% of whites. Blacks and Hispanic patients had advanced cancer odd ratios of 2.7 and 1.6, respectively, compared with whites.

The authors of the study concluded that public health efforts are one of the primary sources of ethnic disparities. However the question still remains: is race (and in essence a more aggressive tumor biology) an independent prognostic indicator? 

Multiple studies have elucidated worse prognosis in blacks even when controlling for socioeconomic status, stage, tumor thickness, ulceration, anatomic site, and histological type. This data has been refuted in other studies that show no survival advantage in whites; however, the controversy still remains.

This study is a much needed reminder that increased surveillance is needed, as well as more targeted public health efforts, prevention models, and educational programs specific to the culture and languages of ethnic groups. We also need to continue to investigate the unique genetic and biologic markers of melanoma in different ethnic populations to improve clinical detection and develop targeted therapies.

The lifetime risk of white patients developing melanoma is currently estimated at 1 in 50, compared with 1 in 1,000 for black patients. Although darker-pigmented populations are consistently reported to have lower melanoma risk--possibly related to protection from ultraviolet radiation provided by melanin--darker skinned patients have been consistently shown to have worse outcomes than whites.

While less common in blacks, malignant melanoma is nonetheless an aggressive, deadly disease and presents at a more advanced stage at diagnosis and with a decreased chance of survival than in white patints. Underlying etiologies for the disparity in prognosis are still poorly understood.

Many of the public health interventions for melanoma prevention have focused predominantly on whites. However, recent studies in blacks and Hispanics that have elucidated advanced stage of melanoma at presentation and a higher mortality rate have led to increased efforts to characterize melanoma in ethnic minorities.

One such study found that ethnic disparities persist in the incidence of melanoma and its stage at diagnosis (Arch Dermatol. 2009;145:1369-74). Researchers analyzed information in the Florida Cancer Data System, a statewide, population-based cancer registry. They looked at three 5-year periods: 1990 to 1994, 1995 to 1999, and 2000 to 2004.

Of 41,072 cases of melanoma diagnosed from 1990 to 2004, 39,670 were in whites, 1,148 in Hispanics, and 254 in blacks. Advanced melanoma diagnosed at either regional or distant stages were seen in 26.4% of black patients, compared with 17.8% of Hispanics and 11.6% of whites. Blacks and Hispanic patients had advanced cancer odd ratios of 2.7 and 1.6, respectively, compared with whites.

The authors of the study concluded that public health efforts are one of the primary sources of ethnic disparities. However the question still remains: is race (and in essence a more aggressive tumor biology) an independent prognostic indicator? 

Multiple studies have elucidated worse prognosis in blacks even when controlling for socioeconomic status, stage, tumor thickness, ulceration, anatomic site, and histological type. This data has been refuted in other studies that show no survival advantage in whites; however, the controversy still remains.

This study is a much needed reminder that increased surveillance is needed, as well as more targeted public health efforts, prevention models, and educational programs specific to the culture and languages of ethnic groups. We also need to continue to investigate the unique genetic and biologic markers of melanoma in different ethnic populations to improve clinical detection and develop targeted therapies.

The lifetime risk of white patients developing melanoma is currently estimated at 1 in 50, compared with 1 in 1,000 for black patients. Although darker-pigmented populations are consistently reported to have lower melanoma risk--possibly related to protection from ultraviolet radiation provided by melanin--darker skinned patients have been consistently shown to have worse outcomes than whites.

While less common in blacks, malignant melanoma is nonetheless an aggressive, deadly disease and presents at a more advanced stage at diagnosis and with a decreased chance of survival than in white patints. Underlying etiologies for the disparity in prognosis are still poorly understood.

Many of the public health interventions for melanoma prevention have focused predominantly on whites. However, recent studies in blacks and Hispanics that have elucidated advanced stage of melanoma at presentation and a higher mortality rate have led to increased efforts to characterize melanoma in ethnic minorities.

One such study found that ethnic disparities persist in the incidence of melanoma and its stage at diagnosis (Arch Dermatol. 2009;145:1369-74). Researchers analyzed information in the Florida Cancer Data System, a statewide, population-based cancer registry. They looked at three 5-year periods: 1990 to 1994, 1995 to 1999, and 2000 to 2004.

Of 41,072 cases of melanoma diagnosed from 1990 to 2004, 39,670 were in whites, 1,148 in Hispanics, and 254 in blacks. Advanced melanoma diagnosed at either regional or distant stages were seen in 26.4% of black patients, compared with 17.8% of Hispanics and 11.6% of whites. Blacks and Hispanic patients had advanced cancer odd ratios of 2.7 and 1.6, respectively, compared with whites.

The authors of the study concluded that public health efforts are one of the primary sources of ethnic disparities. However the question still remains: is race (and in essence a more aggressive tumor biology) an independent prognostic indicator? 

Multiple studies have elucidated worse prognosis in blacks even when controlling for socioeconomic status, stage, tumor thickness, ulceration, anatomic site, and histological type. This data has been refuted in other studies that show no survival advantage in whites; however, the controversy still remains.

This study is a much needed reminder that increased surveillance is needed, as well as more targeted public health efforts, prevention models, and educational programs specific to the culture and languages of ethnic groups. We also need to continue to investigate the unique genetic and biologic markers of melanoma in different ethnic populations to improve clinical detection and develop targeted therapies.

Dr. Cheryl Burgess of the Center for Dermatology and Dermatologic Surgery in Washington, D.C., describes typical cosmetic dermatology concerns for patients with skin of color, including Latinos, Asians, and blacks.

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Dr. Cheryl Burgess of the Center for Dermatology and Dermatologic Surgery in Washington, D.C., describes typical cosmetic dermatology concerns for patients with skin of color, including Latinos, Asians, and blacks.

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Dr. Cheryl Burgess of the Center for Dermatology and Dermatologic Surgery in Washington, D.C., describes typical cosmetic dermatology concerns for patients with skin of color, including Latinos, Asians, and blacks.

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Dr. Joanna L. Chan explains how skin grafts from a patients own body can repigment areas affected by vitiligo. This surgical option is primarily for patients who fail to respond to topical treatments or phototherapy or have more difficult-to-treat forms of the condition, such as segmental or focal vitiligo.

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Dr. Joanna L. Chan explains how skin grafts from a patients own body can repigment areas affected by vitiligo. This surgical option is primarily for patients who fail to respond to topical treatments or phototherapy or have more difficult-to-treat forms of the condition, such as segmental or focal vitiligo.

View Video Now.

Dr. Joanna L. Chan explains how skin grafts from a patients own body can repigment areas affected by vitiligo. This surgical option is primarily for patients who fail to respond to topical treatments or phototherapy or have more difficult-to-treat forms of the condition, such as segmental or focal vitiligo.

View Video Now.