Chapter 62 Special considerations in skin of color
1. What is “skin of color”?
There are many ways to subcategorize human beings. Widely recognized racial groups include Africans, African-Americans, Asians, Middle Easterners, Northern Europeans, Native Americans, Pacific Islanders, and Hispanics, to name a few. Even within a racial group gradations exist with regard to skin pigmentation. Simply put, people with “skin of color” have darker skin tones than those of typical white skin. The term may be used also to reference other shared cutaneous characteristics, such as hair color or quality, or a common reaction pattern to skin insults, all of which may be clinically relevant. By 2050, about 54% of the United States population will be composed of people with skin of color. Accordingly, a solid understanding of the myriad differences in diagnosing and treating persons with skin of color is essential to the competent practice of dermatology.
Taylor SC, Cook-Bolden F: Defining skin of color, Cutis 69:435–437, 2002.
U.S. Census Bureau: 2008 national population projections: tables and charts. Available at: http://www.census.gov/population/www/projections/tablesandcharts.html. Accessed March 13, 2010.
2. What accounts for differences in color between ethnic and racial groups?
Although the number of melanocytes varies within anatomic regions of the body, interestingly, among different races and ethnicities, the actual number of melanocytes in the skin does not vary with skin color. Instead, among variations, it is the amount and distribution of melanin produced that changes. In mammals, two types of melanin are produced by melanocytes, eumelanin and pheomelanin. Eumelanin is a tyrosine-derived, dark brown or black pigment. Pheomelanin, derived from a biochemical shunt in the normal melanin production pathway, has a yellow to red-brown hue. Pheomelanin is the predominant pigment produced by those with freckles and red hair. It is also increased in Asian skin, and in women when compared to men. Melanin is packaged in melanosomes, which are membrane-bound vesicles containing a unique scaffolding of matrix proteins. Melanosomes within keratinocytes of white skin are distributed as membrane-bound clusters. In black skin, melanosomes tend to be larger and more diffusely located in the cell. Therefore, the quantity and composition of melanin, as well as melanosome size and distribution, vary considerably within the epidermis, both with ethnicity and with chronic sun exposure, yielding various degrees and hues of pigmentation.
3. Do any physiologic differences exist between black skin and that of other racial/ethnic groups?
Yes. In truth, the color of “black” skin ranges from light brown to very dark brown/black, and it is difficult to generalize given this tremendous variability. Nevertheless, studies have demonstrated that the stratum corneum of most black skin maintains more layers and is more compact and cohesive than white skin. This finding may explain why black skin tends to manifest a decreased susceptibility to cutaneous irritants. One study demonstrated that black skin had a spontaneous desquamation rate 2.5 times that of white skin, and this may explain why some blacks experience a particular type of xerosis commonly referred to as ashy skin. Ashy skin consists of fine white flakes yielding a dry appearance. Other differences in black skin include an increased transepidermal water loss (TEWL), lower pH, and larger mast cell granules compared with white skin. Black skin also produces less vitamin D3 in response to equivalent sunlight, and this has been postulated to possibly represent the driving evolutionary force in development of paler skin as early humans migrated away from the equator. Conflicting data exist regarding differences in resistance, capacitance, conductance, impedance, and skin microflora.
Jablonski NG, Chaplin G: The evolution of human skin coloration, J Hum Evol 39:57–106, 2000.
4. Are the brown streaks on the nails of people with skin of color always a cause for concern?
No. Pigmented streaks of the nail may be a normal variant in people with skin of color. The condition is called melanonychia striata, and it is characterized by longitudinal bands of pigmentation that may vary from light brown to dark black. Multiple bands may be seen within the same nail or, alternatively, several nails may be involved. The cause is unknown, but the rarity of bands in children may indicate that they are a sequela of accumulated trauma. Some studies have revealed that such bands are present in >75% of blacks older than 20 years. Another recent study found that simple racial variation was the most common cause of nail pigmentation in Hispanics as well, although malignancy was a cause in about 6% of cases. In general, solitary bands are of greater concern than are multiple lesions. Close examination of the nail fold may be helpful, assessing for diffusion of pigment into the surrounding skin; however, the absence of this sign does not rule out a more serious condition, such as nail unit melanoma. Other causes of nail pigmentation include drugs such as actinomycin, antimalarials, bleomycin, cyclophosphamide, doxorubicin, 5-fluorouracil, melphalan, methotrexate, minocycline, nitrogen mustard, and zidovudine, to name a few. Laugier-Hunziker syndrome, Addison’s disease, hemochromatosis, Peutz-Jegher syndrome, and vitamin B12 deficiency may also cause nail pigmentation.
Pappert AS, Scher RK, Cohen JL: Longitudinal pigmented nail bands, Dermatol Clin 9:703–716, 1991.
5. Is pigmentation of the oral mucosa in people with skin of color invariably concerning?
No. Pigmentation of the oral mucosa is often subdivided into conditions related to melanin (including racial differences in pigmentation), and non–melanin-associated conditions, such as metabolic conditions or pigmentation related to drugs. Therefore, oral pigmentation in people with skin of color is neither uncommon, nor necessarily indicative of a serious condition. Idiopathic, racially related pigmentation of the oral mucosa often involves the gingiva, hard palate, buccal mucosa, or tongue. The color may vary, but it often has a blue or gray appearance. Symmetry is frequently observed. As always, obtaining an appropriate medical history is important, particularly with respect to the length of time present and any associated symptoms.
6. Are there other areas of the body where hyperpigmentation represents a normal racial variant?
Hyperpigmented macules of the palms and soles occur in people with skin of color, particularly in those with darker skin types. Such lesions may vary in color from light tan to dark brown. The number of lesions may range from one or two lesions to dozens or more. This potential for natural racial variation must be kept in mind, particularly when one considers other diseases associated with palmoplantar lesions, such as erythema multiforme and secondary syphilis. As acral lentiginous melanoma is the most common form of melanoma occurring in blacks, Asians, and Hispanics, this potentially life-threatening diagnosis must always be considered, and excluded by biopsy where indicated. Other areas with possible increased pigmentation among persons with skin of color include the sclera, the labia and vaginal mucosa, and the glans penis.
7. What are Futcher’s lines?
Futcher’s lines, also known as Voigt’s lines or Futcher-Voigt lines or Ito’s lines, are areas of abrupt demarcation between lighter and darker pigmented skin. Common locations include the anterior arms, the sternum, and the posterior thighs and legs (Fig. 62-1). There appears to be no appreciable difference in melanin concentration between the adjacent darker and lighter areas when examined by light microscopy. The distribution and symmetry of the lines allows differentiation from other diagnoses, such as hypomelanosis of Ito, incontinentia pigmenti, linear epidermal nevus, or lichen striatus. Interestingly, drug eruptions have, on occasion, affected preferentially the skin on one side of the line, suggesting the skin in these areas has slightly different embryologic origin, at least with regard to a susceptibility to metabolic insult.
8. What causes postinflammatory hyperpigmentation?
Postinflammatory hyperpigmentation represents a residual darkening of the skin as a result of an inflammatory insult, such as lichen planus, lupus erythematosus (Fig. 62-2), or atopic dermatitis (Fig. 62-3). It is most severe in those diseases that result in significant disruption of the basal layer, which allows melanin to escape into the upper dermis where it is engulfed by macrophages. The resultant hyperpigmentation requires months to years for fading. Treatment includes bleaching creams, such as hydroquinone, tretinoin, and azelaic acid; however, if the pigmentation is significantly deep, topical management does not often augment the body’s normal, albeit slow, corrective mechanisms. Bleaching agents containing >4% hydroquinone may cause exogenous ochronosis, with a resultant blue-gray discoloration of the skin. Patients from countries in Africa and Europe may have access to harsh bleaching agents without prescription, and should be warned against such use. Disorders such as inflammatory acne, occurring in dark skin types, should be treated early and aggressively, to prevent pigmentary alterations.
Figure 62-2. Postinflammatory hyperpigmentation in a patient with lupus erythematosus.
(Courtesy of James E. Fitzpatrick, MD.)
9. What causes postinflammatory hypopigmentation?
Postinflammatory hypopigmentation, another sequela of inflammatory skin disorders in dark skin, is thought to result from impaired transfer of melanosomes from melanocytes to keratinocytes. This occurs in many diseases, such as atopic dermatitis (see Fig. 62-3) and psoriasis. The increased mitotic rate of keratinocytes, and the decreased transit time of cells within the epidermis, does not allow sufficient pigment transfer. After the inflammatory process resolves, pigment typically normalizes over weeks to months.
10. Is pityriasis alba the same thing as postinflammatory hypopigmentation?
Pityriasis alba is seen primarily in children with darker skin types, and it manifests as hypopigmented macules on the face and/or upper arms (Fig. 62-4). The lesions lack a distinct border and may have overlying fine scale. Patients often report a history of atopic dermatitis. Some studies show boys may be preferentially affected. While many consider pityriasis alba to be a mild form of postinflammatory hypopigmentation, it is often considered a separate entity. Although the condition typically resolves with time, brief treatment with low-potency topical corticosteroids and/or generous emollients may be helpful.
11. Is vitiligo more common in patients with darker skin?
Vitiligo is a common disorder, affecting 1% to 2% of the world’s population. There is no clear racial predisposition for vitiligo; however, the condition is more readily apparent in darker skin. Consequently, people with darker skin types may seek medical attention or manifest with more cosmetically debilitating disease. Also, the tendency for familial inheritance of vitiligo must be considered when conducting prevalence studies. In some societies, particularly Indian culture, there is a social stigma associated with vitiligo that pertains to a historic overlap with the appearance of cutaneous leprosy. In these cultures, patients with the condition, especially young women, may be considered “unfit for marriage,” and the sociodynamic aspects of vitiligo must always be carefully considered by the clinician.
Nordlund JJ: The epidemiology and genetics of vitiligo, Clin Dermatol 15:875–878, 1997.
12. Why does tinea versicolor cause hypopigmented spots on dark skin?
Tinea versicolor, also known as pityriasis versicolor, is a common superficial yeast infection caused by the lipophilic organism Malassezia furfur and other species in this genus. The typical presentation in darker skin types is that of multiple hypopigmented thin plaques with fine scale distributed over the densely seborrheic skin of the chest, upper back, and proximal upper extremities. The cause of the hypopigmentation is not completely understood; however, extracts from cultured organisms contain dicarboxylic acids that may competitively inhibit tyrosinase, an enzyme important in melanin production. Production of other indoles or tryptophan-based metabolites may also be involved in the resultant hypopigmentation.
13. Why is it more difficult to appreciate erythema in darker skin?
Erythema, or the amount of visible redness in the skin, is caused by increased blood flow and/or blood vessel engorgement in the dermis with the presence of oxyhemoglobin. If the epidermis is deeply pigmented, the red hues of oxyhemoglobin may be difficult to visualize. For this reason, the interpretation of patch testing for sensitivity to cutaneous allergens in black patients is challenging. This is an important point to remember, as many diseases that have erythema as a hallmark, such as seborrheic dermatitis or atopic dermatitis, may present more subtly in a black patient. Cyanosis is also difficult to perceive in a dark-skinned patient for similar reasons.
14. Can any other generalizations be made about common cutaneous reaction patterns in skin of color?
In addition to the difficulty in perceiving erythema, there exist other cutaneous reaction patterns more prevalent in darker skin. Papulosquamous diseases, such as psoriasis and nummular eczema, tend to exhibit a more violaceous color, leading to possible confusion with lichenoid conditions. Certain diseases, such as atopic dermatitis or tinea versicolor, may demonstrate a follicular accentuation (Fig. 62-5). Pityriasis rosea may present atypically, with either papular or vesiculobullous forms, in black skin. In addition, some disorders, such as lichen planus and seborrheic dermatitis, have an increased propensity toward formation of annular lesions (Fig. 62-6). The reasons for these observations remain largely unknown.
Figure 62-6. Annular lichen planus, demonstrating central postinflammatory hypopigmentation.
(Courtesy of James E. Fitzpatrick, MD.)
McLaurin CI: Unusual patterns of common dermatoses in blacks, Cutis 32:352–355, 358-360, 1983.
15. What is the significance of multiple brown papules often seen on the periorbital area, cheeks, and nose?
The condition described is dermatosis papulosa nigra, and it is commonly seen in blacks, particularly black women. They are often referred to colloquially as “flesh moles.” In truth, they are not “moles” (nevi) at all and represent a variant of seborrheic keratoses. The lesions tend to increase in number over time and do not typically resolve on their own. They have no malignant potential and are largely a cosmetic concern. Removal may be accomplished by light electrodesiccation (a personal favorite) and/or curettage. Alternatively, lesions may be treated with light application of liquid nitrogen, but care must be taken to avoid permanent hypopigmentation, a sequela of increased risk in persons with dark skin.
16. What is cutaneous sarcoidosis?
Cutaneous sarcoidosis is a granulomatous process of unknown etiology that is more prevalent among blacks, particularly among those in the southern United States, where the incidence is 3 to 4 times that of appropriately matched white patients. The cause of the disease is unknown. Cutaneous lesions may occur in association with pulmonary disease, or may be present in isolation. Diverse patterns of skin lesions occurring in black patients with sarcoidosis have been observed. Shiny, somewhat waxy papular lesions are the most frequent cutaneous manifestation of sarcoidosis in blacks. When such dermal granulomatous papules are located near the nose, the condition has been referred to as lupus pernio (Fig. 62-7), and it may be indicative of a higher association with pulmonary disease (for photos, see interactive reference). Because of its protean cutaneous manifestations, sarcoidosis should be included in the differential diagnosis of nearly all chronic dermatoses in black patients.
Figure 62-7. Multiple sarcoidal granulomas along the right eyelid, nasal margin, and lower lip in a patient with sarcoidosis.
(Courtesy of Whitney A. High, MD)
High WA: A woman with “keloids” on the nose and restrictive pulmonary disease, Medscape Dermatol Clin, September 7, 2004. Available at: http://www.medscape.com/viewarticle/488343. Accessed March 13, 2010.
17. What are keloids?
Keloids are benign dermal neoplasms composed of broad collagen bundles (Fig. 62-8). It is believed they represent an aberrant healing process. In distinction from hypertrophic scars, keloids extend beyond the bounds of the original wound. There exists a distinct tendency toward keloid formation in persons of color. Sites of predilection include the shoulders, mandible, earlobes, presternal area, and deltoid region. Any form of trauma can induce keloids, including thermal injuries, insect bites, acne scars, injection sites, or cosmetic piercings and surgical incisions. Keloids may occur spontaneously, particularly in the central chest area. It is quite possible that such a “spontaneous” keloid represents a reaction to unrecognized trauma. The causal abnormality in the normal healing process is not known with certainty. It appears, however, that genetically predisposed fibroblasts are stimulated to produce abnormally high levels of procollagen messenger RNA, leading to excessive collagen production and secretion. Treatment options have included radiation or pressure therapy, cryotherapy, intralesional corticosteroids or verapamil, interferon, fluorouracil, topical silicone dressings, and laser treatment (either pulsed dye or Nd:YAG). Surgical excision is typically followed by recurrence unless adjunct preventive therapies are employed.
Kelly AP: Update on the management of keloids, Semin Cutan Med Surg 28:71–76, 2009.
18. What are “razor bumps”?
The hair follicles of blacks and many other people of color, such as Puerto Ricans, are elliptical, leading to development of tightly curled hair. After shaving, as the hairs regrow, there is a tendency for the sharp end of the curled hair to curve back into the skin. When the hair pierces the skin, it causes an inflammatory reaction, just as one might see with a splinter. This inflammatory reaction leads to the development of pseudofolliculitis barbae. This condition is not normally seen in men who grow beards, because after attainment of a certain length, usually 3 to 6 mm, the hair does not curve back into the skin. Accordingly, the condition is most common among populations required to be clean-shaven, such as black men in the military. Acne keloidalis nuchae represents a similar condition arising on the occipital scalp and/or nuchal area of those with shaved or very tightly cropped haircuts.
Kelly AP: Pseudofolliculitis barbae and acne keloidalis nuchae, Dermatol Clin 21:645–653, 2003.
19. How is pseudofolliculitis barbae treated?
Clearly, the definitive treatment is growth of a beard; however, if this is not an option, several techniques may decrease the number of inflamed papules. The beard should be shaved in the direction of growth with a single-edged razor. The skin should not be stretched while shaving. Hairs that have clearly recurved into the skin should be released with a sterile needle, but such hairs should not be plucked. Some men with this condition may use clippers that purposefully leave short stubble. Others may obtain good results with chemical depilatories. If inflammation is severe, short-term treatment with a low-potency topical corticosteroid may be effective. Laser hair removal or topical eflornithine represent emerging treatment options for those with intractable disease and a requisite need to maintain a clean shaven appearance.
20. Are there other racial differences that may affect the treatment of hair or scalp conditions in blacks?
Blacks have elliptical follicular ostia and tightly curled hair with a small mean cross-sectional area. Asians have round ostia and straight hair with a large mean cross-sectional area. Whites have round to slightly ovoid follicles with an intermediate mean cross-sectional area. Nevertheless, these remain broad generalizations, and the entire racial and genetic makeup of the individual must be considered. The angles of curvature in the spiral structure of black hair yields multiple vulnerable points along the hair shaft, making it relatively fragile and prone to breakage. This structural arrangement also inhibits effective transmission of secreted sebum down the shaft, making the hair drier and less manageable relative to other hair types. For these reasons, the hair of blacks cannot be shampooed as often as that of other racial groups. Daily washing would lead to excessive dryness and hair breakage. A moisturizing conditioner should be used after shampooing. Such differences in hair care must be considered when prescribing treatment for scalp conditions that involve medicated shampoos. When evaluating alopecia, a thorough history of hair grooming techniques used should be obtained. Specifically, questions about the use of chemical relaxers, permanent hair dyes, curling irons, hot combs, blow dryers, braids, or weaves should be inquired of, because many of these modalities cause damage to the hair shaft or the scalp. Finally, some unusual forms of alopecia, such as lipedematous alopecia (Fig. 62-9), with associated cotton-batting textural changes of the scalp, are associated nearly exclusively with black women.
High WA, Hoang MP: Lipedematous alopecia, J Am Acad Dermatol 53:S157–S161, 2005.
McMichael AJ: Ethnic hair update: past and present, J Am Acad Dermatol 48:S127–S133, 2003.
Key Points: Skin of Color
1. Skin of color, particularly black skin, manifests minor physiologic differences, including a stratum corneum with increased layers and cohesiveness and a decreased ability to synthesize vitamin D3.
2. Erythema may be more difficult to appreciate on darkly pigmented skin, and this must be considered during clinical examination.
3. Pigmentation of the oral mucosa, benign-appearing palmoplantar macules, or multiple longitudinal pigmented streaks of the nails, may represent normal variants in persons with darker skin types.
21. Are patients with skin of color particularly susceptible to any life-threatening illnesses?
Coccidioidomycosis, also known as San Joaquin Valley fever, is a deep fungal infection caused by Coccidioides immitis. It is typically acquired via inhalation of arthrospores and demonstrates occasional hematogenous dissemination to subcutaneous tissues, bone, or skin. Endemic areas include the Sonoran life zone of southern California, Arizona, New Mexico, southwestern Texas, and northern Mexico. It has also been reported in certain areas of South America. Infection occurs equally in both sexes, and in all races and ages. For reasons that are not entirely clear, black persons are 14 times more likely to have severe disseminated disease than are caucasians (Fig. 62-10), and individuals of Filipino descent are 10 times more likely to develop coccidioidomycosis-related meninigitis than caucasians. Further investigation has revealed that certain host genetics, in particular the human leukocyte antigen (HLA) class II and ABO blood group genes, influence susceptibility to severe coccidioidomycosis. Untreated, nonmeningeal coccidioidomycosis has a 50% mortality rate; therefore, early aggressive treatment with systemic antifungal agents is essential.
Figure 62-10. Coccidioidomycosis. Disseminated coccidioidomycosis in a young black soldier.
(Courtesy of the Fitzsimons Army Medical Center teaching files.)
Pappagianis D: Epidemiology of coccidioidomycosis, Curr Top Med Mycol 2:199–238, 1988.
22. Do any special considerations exist when performing skin surgery on patients with skin of color?
Due to the increased risk of pigmentary alterations, hypertrophic scars, and keloids among black patients, any surgical undertaking should be carefully considered with respect to the risks and benefits of the procedure. Because melanocytes are more sensitive to cold injury than keratinocytes, liquid nitrogen can cause permanent loss of pigmentation, and this is generally more noticeable in darker skin types. Treatment of benign growths, such as warts or seborrheic keratoses, with cryotherapy can result, therefore, in permanent loss of pigment, and this modality must be judiciously implemented.
23. Why is skin cancer less common in skin of color?
Ultraviolet (UV) radiation-induced damage to the DNA of cells in the lower epidermis, including keratinocyte stem cells and melanocytes, is prevented to a greater degree in darker skin, suggesting that the pigmented epidermis serves as an efficient UV filter. In addition, UV radiation-induced apoptosis (programmed cell death) is significantly greater in darker skin, indicating that any damaged cells may be removed more efficiently from the epidermis in skin of color. Together, the combination of decreased DNA damage due to ultraviolet radiation and the more efficient removal of damaged cells likely play a critical role in the decreased photocarcinogenesis seen in individuals with skin of color.
24. Are there any unique presentations of skin cancer when it does occur in patients with darker skin?
Although skin cancer is decidedly less common in people with skin of color, it is often associated with greater morbidity and mortality. Squamous cell carcinoma (SCC) is the most common skin cancer in blacks and Asian Indians, and it is the second-most common cancer in Chinese and Japanese. Also, in skin of color, malignancies occur more often upon non–sun-exposed surfaces and the lower extremities. In fact, the most important risk factors for developing SCC in blacks are chronic scarring processes and areas of chronic inflammation. Acral lentiginous melanoma presents more often in persons with skin of color. Other reported risk factors for melanoma in blacks include albinism, burn scars, radiation therapy, trauma, immunosuppression, and preexisting pigmented lesions. Mycosis fungoides (MF), a type of cutaneous T-cell lymphoma (CTCL), occurs more often in persons with skin of color (see Chapter 46). Because many individuals with dark skin do not believe that they are susceptible to skin cancers, they may delay seeking care for a suspicious lesion, thereby leading to a less favorable prognosis. Public education in ethnic communities regarding the performance of self-skin examination, and the utility of regular visits to a dermatologist when skin conditions exist may lessen the associated morbidity and mortality of skin cancer in these populations.
Gloster HM, Neal K: Skin cancer in skin of color, J Am Acad Dermatol 55:741–760, 2006.
Hinds GA, Herald P: Cutaneous T-cell lymphoma in skin of color, J Am Acad Dermatol 60:359–375, 2009.
25. List skin diseases or conditions that are often considered more common in persons with skin of color.
The diseases listed in Table 62-1, while not all-inclusive, represent many skin conditions thought to be seen with higher frequency in blacks. Some diseases, particularly the tropical infections, may be more common in blacks living outside of the United States. The perception of these diseases being more common in blacks may be related purely to this geographic distribution. Furthermore, such entities may be rarely encountered within the United States but are listed here for completeness.
Table 62-1. Dermatologic Conditions More Common in Skin of Color
