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.)
Figure 62-3. Postinflammatory hyperpigmentation and hypopigmentation in a child with atopic dermatitis.
(Courtesy of James E. Fitzpatrick, MD.)
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