A Closer Look At Dermatologic Conditions In Skin Of Color

Author(s): 
Tracey C. Vlahovic, DPM

Given the changing population demographics in the United States, it is more important than ever to be able to recognize and treat dermatologic conditions that are more prevalent among patients with skin of color. Accordingly, this author discusses the diagnosis and treatment of skin conditions including vitiligo, melanonychia and keloids.

As a physician whose primary practice consists of patients with skin of color, I am particularly concerned with the diagnosis and management of skin conditions prevalent in this population. What does the term “skin of color” encompass? It is the accepted dermatologic term to describe our patients with all shades of pigmented skin: African-American, Hispanic, Asian (East, Southeast and South), and non-Caucasian ethnic groups such as First Nations/American Indian/Alaskan Native/Native Hawaiian.

   The United States Census has projected that half of the population will be comprised of people with skin of color by 2050.1 In most cities in the United States, 2050 has already arrived. For example, I work in Philadelphia, where people with skin of color comprise over 57 percent of the population.1 Accordingly, as the demographics of the population change, it is important that the podiatric physician is familiar with the skin conditions that are of particular concern in this group.

   First, it is important to recognize the structural and biological differences between African-American and Caucasian skin. Skin color is determined by the distribution of melanin and there is no difference in the number of melanocytes among groups. The melanocytes, which reside in the basal layer of the epidermis, contain melanosomes filled with tyrosinase that is involved in melanin synthesis. Interestingly, the amount of tyrosinase is generally equal in African-American and Caucasian skin.

   However, the distribution of melanosomes within melanocytes and keratinocytes is different between skin pigments. Besides the distribution of melanosomes contributing to skin color, tyrosinase levels are 10 times higher in African-American skin and produce 10 times more melanin than melanocytes in Caucasian skin.2 Melanocytes in those with skin of color seem to respond to injury and inflammation, which helps to explain the pigmentation changes.3

   There are other variations in the epidermis and dermis between African-American and Caucasian skin. Epidermal thickness is equivalent but there are more epidermal lipids in African-American skin.4 Transepidermal water loss is lower in African-American skin, showing statistical significance on the legs in a study by Warrier and colleagues.4 Regarding the dermis, fibroblasts are more numerous, larger and physiologically active in African-American skin, which could help to explain the prevalence of keloids and hypertrophic scars in this patient population.5

   Whether one is examining a patient with skin of color for the first time or treating a new area of pigmentation following a podiatric surgical procedure, pigmentation disorders, inflammatory conditions and abnormal scar healing are the most common issues we see as podiatric practitioners.

   When examining patients with skin of color, it is helpful to note that the angry red color in cellulitis or the erythema in psoriasis/inflammatory skin conditions may appear as a more subtle red or even have a purple hue to it. As with any patient, a thorough history and physical is warranted along with a comparison of the contralateral limb and skin on the rest of the extremity. Once a patient has recovered from an infection or an inflammatory condition, the practitioner has to be concerned with both hyper- and hypopigmentation of the affected area.

Pertinent Insights On Postinflammatory Hyperpigmentation

When exposed to an inflammation or an injury, melanocytes in individuals with darker skin seem to respond in an exaggerated manner. This marked change in pigment, or dyschromia, greatly accounts for both African-American and Hispanic patients’ need for dermatologic intervention.

   The emotional and psychological impact of the dyschromia can have a negative impact on the quality of life for the patient.3 Patients become focused on the pigmentation. Their efforts range from hiding it with clothing to the use of corrective, camouflaging makeup (Dermablend products) to negatively impacting social and work interactions.

   Dyschromia following an inflammatory condition such as acne, eczema and psoriasis is known as postinflammatory hyperpigmentation. There is either an increase in melanin production or uneven distribution of melanin following the event. This excess pigment can deposit itself in the epidermis only or in both the epidermis and dermis.3

   The exact cause of how hyperpigmentation occurs after an injury is unknown but might result as an influence of inflammatory mediators and reactive oxygen species.3 The resulting pigmentation is transient and may take months to years to resolve. Most patients seek treatment as they do not want to wait for the slow, natural progression to occur.

   If the underlying inflammatory condition is still present, it is important to treat that first. If it has resolved, topical hydroquinone 2 to 4% is the gold standard of treating postinflammatory hyperpigmentation. It is important to know that it is not a true “bleaching” agent but is rather a tyrosinase blocker, which ultimately blocks production of melanin.

   Also, when I prescribe a hydroquinone such as Aclaro PD (Innocutis) for my patient, I highly encourage the concomitant use of sunscreen (SPF 30 or higher) and will often have the patient only use it during the non-summer months to prevent further pigmentation and irritation.

   I monitor the patient who is using hydroquinone for any skin irritation to the drug and severe depigmentation. While this is less frequently seen in the U.S., a side effect of long-term hydroquinone use is exogenous ochronosis or blue-black macules and patches.

   In 2006, hydroquinone sparked some controversy after being labeled a carcinogen in rats and mice when administered orally.6 This caused the FDA to consider removing over the counter hydroquinone products from the store shelves. Currently, over the counter formulations of hydroquinone are still available while the FDA and the National Toxicology Program investigate the toxicity of the drug.

   Other topical products that one can use for treatment of postinflammatory hyperpigmentation are: topical steroids; tretinoin (Retin-A, Ortho Dermatologics); licorice extract; niacinamide (vitamin B3); and kojic acid. Cosmetic treatments such as chemical peels, microdermabrasion and lasers can help further to lighten the affected areas.

What You Should Know About Postinflammatory Hypopigmentation

Also known as excessive depigmentation of an affected area, postinflammatory hypopigmentation is as troubling to patients as hyperpigmentation. It can be a result of an inflammatory condition such as psoriasis and eczema, but it can also be a direct result of a therapeutic intervention (such as long-term topical steroid use). It represents either a localized or widespread loss of melanin in the skin.7

   I have had patients in my practice who have had both hyper- and hypopigmentation occur at the same time. This might be due to a loss of functional melanocytes in the affected area and appears clinically as depigmented macules and patches with feathered edges.7 The presence of the feathered edge assists the clinician in distinguishing it from vitiligo.

   Treatment begins with determining and treating the underlying cause. Areas that are mildly hypopigmented may resolve with time but severely depigmented areas will most likely require the application of UV phototherapy (PUVA or narrowband UVB).8

   One form of hypopigmentation that podiatric practitioners frequently see is idiopathic guttate hypomelanosis. It is the presence of small hypopigmented macules on the anterior aspect of the legs. It occurs in all ethnic groups but is especially prevalent in the darker skinned patient. It seems to be related to sun exposure but the exact cause is unknown. Avoidance of further sun damage is key in treatment but one can also use corrective cosmetics and topical tretinoin.

Essential Tips On Diagnosing And Treating Vitiligo

The incidence of vitiligo in the U.S. is about 1 percent.9 Even though the exact pathogenesis is unknown, it seems to be multifactorial as it may stem from genetic, autoimmune, viral and biochemical sources.9 More importantly, vitiligo can be devastating to a patient with skin of color since the contrast between vitiliginous skin and surrounding skin is so extreme. It can even threaten racial identity in some patients and cause patients to become ostracized in certain cultures since those uneducated about the condition think of it as contagious. It generally starts in childhood or young adulthood, and is classified as focal, segmental (unilateral) and generalized (bilateral).

   Vitiligo is generally a clinical diagnosis but laboratory screening of the thyroid and antinuclear antibody (ANA) may be useful in determining an underlying autoimmune cause. The lesions present on the feet bilaterally as well defined white macules and patches that are symmetric and enlarge evenly.9 Due to destruction of the melanocytes in this disease, these patches are devoid of melanocytes but have active T cells at the border of actively spreading areas.

   Sunscreen use is key in preventing further damage to the keratinocytes in the amelanotic patches and decreasing tanning of the non-affected skin. Corrective cosmetics can camouflage but not treat the disorder. Treatment can focus on repigmenting the amelanotic patches or causing even pigmentation in both affected and non-affected skin.

   In my experience, my first line of treatment includes topical steroids and topical immunomodulators, such as tacrolimus (Prograf, Astellas Pharma) and pimecrolimus (Elidel, Novartis) to help facilitate repigmentation.

   When I have seen repigmentation occur on the lower extremity, it seems to appear in a dot-like pattern. Physicians have used PUVA phototherapy (psoralen plus UVA light) and narrowband UVB with some success to repigment but these methods have limited success in the lower extremity. The PUVA works by restimulating the melanocytes still present in the lower portion of the hair follicle to migrate and repigment surrounding skin.9 As with PUVA and UVB therapy, researchers have noted the excimer laser as being successful for the face, but not for the hands or feet.9

   Surgical options that have been described have consisted of taking advantage of the reservoir of melanocytes in the follicles. These procedures seem to work better with unilateral, stable (non-evolving) lesions. An example of a procedure is mini-grafting, in which one takes 1.0 mm punches from the buttock and transplants the punches into the affected vitiliginous skin.9 Since transplantation depends on the density of hair follicles, sparse areas such as the toes are difficult to repigment. This would explain why feet are challenging to repigment with any type of vitiligo therapy.

   Lastly, topical monobenzone can destroy epidermal melanocytes and produce a state of widespread permanent depigmentation.10 This therapy is reserved for patients who have extensive vitiligo on the body or have recalcitrant, non-responding lesions on the hands and feet.

Keys To Managing Melanonychia

Longitudinal melanonychia describes the linear pigmented brown to black streak seen in the toenail. In the type of melanonychia in patients with skin of color, melanocytes have been activated in the nail matrix and extend to the tip of the nail plate.11 The condition may appear as a single line or encompass the entire nail plate.

   This is a common occurrence in the African-American population with 100 percent of the nails being affected by the age of 50.11 In the Japanese population, this nail pigmentation occurs in 10 to 20 percent of adults.11

   It is important to distinguish this common melanonychia that occurs in patients with skin of color from pigmentation of the nail from other causes such as melanoma, hematoma, drugs, fungus and friction from shoes. Drugs such as antiretrovirals, antimalarials, metals and psoralen (used in PUVA therapy) may cause darkening of one or more nails. Once patients discontinue use of the medication, the pigmentation may fade but this can take months to years.

   Trichophyton rubrum and many molds may generate melanin on their own to cause dark pigmentation of the nail. This would explain why some of our patients will report “nail lightening” after finishing a course of oral antifungals.

   Finally, friction from shoe gear may cause the melanocytes in the nail matrix of the fourth and fifth digits to become activated and result in “frictional,” brown-colored longitudinal melanonychia.11 Changing shoe gear may help to an extent but I am always cautious to tell patients that the nail may not return to its original color.

   When I am examining pigmented streaks on toenails, I will compare all of the toenail pigmentation to each other. I will also ask to examine the fingernails as generally all 20 nails will be involved if it is longitudinal melanonychia. If anything appears clinically suspect with this streak, I will apply the following guidelines of subungual melanoma by Levit and colleagues.12

   A is for age (with the peak occurring during the fifth to seventh decades of life with African-Americans, Asians and native Americans accounting for one third of all melanoma cases).

   B is for breadth of 3 mm or more and variegated borders at the edge of the streak.

   C is for change in the nail band or a lack of change in the nail plate even with standard of care treatments.

   D is for the digit most commonly involved. This is usually the index finger, hallux and thumb.

   E is for extension of the pigmentation into the proximal and/or lateral nail fold (known as Hutchinson’s sign).

   F is for family or personal history of melanoma.

   I use a dermatoscope and a KOH/fungal culture to assist me in my clinical diagnosis, but when I am unsure, I perform a biopsy of the nail to determine if the pigmentation is a melanoma versus nevi.

Pearls For Effective Treatment Of Keloids And Scars

Keloids, or scars that extend beyond the original area of injury or trauma, occur more often in African-American and Asian patients than Caucasian patients with a ratio range of 5:1 to 16:1 respectively.13 Interestingly, keloids do not occur in albinos.

   Keloids present a therapeutic challenge to the clinician due to their non-responsiveness to treatments. They also present a psychological challenge to the patient from a cosmetic and, at times, painful viewpoint. Hypertrophic scars, unlike keloids, stay within the boundaries of the original trauma and may regress in a few years. There is a poor understanding with both types of abnormal scar healing as to why they occur and how to prevent them. As keloids only occur in humans, there are no animal models by which to research their evolution.

   When you are consulting for surgery for patients with skin of color, you might ask if they have had their earlobes pierced. While earlobe keloids are common, it is not 100 percent predictive that the patient will form a keloid after surgery. It is also helpful to ask if there is a family history of keloid formation, any previous surgical incisions (especially any that became infected) and any chemical or thermal burns.13

   When choosing a treatment for a keloid or hypertrophic scar, both the clinician and patient must have realistic expectations. The goal is to flatten, depigment and/or soften the scar whereas a goal of having no scar visible is unrealistic.

   My first line of defense in treating both keloids and hypertrophic scars is an intralesional injection of triamcinolone 10 mg/mL both deep into the dermis and at the area of the dermo-epidermal junction. It is helpful either to block the area locally or use a topical anesthetic agent to achieve that deep injection. As I am injecting less than 1 cc (dose depending on the size and breadth of the lesion) with a 27 to 30-gauge needle, I inject the triamcinolone while withdrawing.

   I perform this once every three to four weeks. By the fourth injection, if the patient has made no progress, I will choose another modality. Researchers have reported varying success with other injectables such as bleomycin, 5-fluorouracil (Efudex, Valeant Pharmaceuticals) and interferon.13

   My other choice for treating scars is the 595 nm long-pulsed dye laser (Vbeam, Candela). Research has shown the laser, in conjunction with intralesional steroid injection, is useful in treating keloids.14 In my practice, I have found that use of the pulsed dye laser for a post-op formation of a hypertrophic or keloid scar helps to reduce the redness, thickness and hardness of the lesion. I have to especially take caution with my fluence (J/cm2) and pulse width in my patients with skin of color (Fitzpatrick skin types IV-VI) in order to avoid burning the skin or causing further pigmentation changes.

   In addition to the modalities I have described, topical treatments for keloids include: topical corticosteroids; imiquimod (Aldara, Graceway Pharmaceuticals); silicone gel sheeting (such as Kelo-cote, Advanced Bio-Technologies); and Scarguard (Scarguard Labs), a combination of silicone, cortisone and vitamin E. If the topical methods fail, surgical excision is an option but has a high recurrence rate.13

   Therefore, various adjunct therapies are recommended following excision to decrease recurrence. These modalities include intralesional injection of triamcinolone starting one week after the procedure and the application of topical imiquimod after surgery daily for eight weeks. I have had the most experience with these two modalities but of course, one can use any combination of the aforementioned topical products following surgical excision.

Final Thoughts

One should use care and exercise caution when approaching patients with skin of color in order to avoid increasing pigment in the affected areas further, making the hypopigmented area worse or creating a worse scar.

   It is my hope that after reading this article, the podiatric practitioner will gain new understanding for the fascinating dermatological conditions in patients with skin of color and recognize how much more investigation needs to be done in order to further address these concerns.

   Dr. Vlahovic is an Associate Professor at the Temple University School of Podiatric Medicine. She is a Fellow of the American Professional Wound Care Association and is board certified by the American Board of Podiatric Surgery.

   Dr. Vlahovic pens a bimonthly blog for Podiatry Today. For more info, visit http://www.podiatrytoday.com/blogs/tracey-vlahovic-dpm .

References

1. Nijhawan RI, Alexis AF. Practical approaches to medical and cosmetic dermatology in skin of color patients. Expert Reviews Dermatology April 2011, http://www.medscape.org/viewarticle/739758
2. Iozumi K, Hoganson GE, Pennella R, et al. Role of tyrosinase as the determinant of pigmentation in cultured human melanocytes. J Investigative Dermatology. 1993; 100(6):806–811.
3. Grimes PE. Management of hyperpigmentation in darker racial ethnic groups. Semin Cutan Med Surg. 2009; 28(2):77-85.
4. Warrier AG, Kligman AM, Harper RA, et al. A comparison of black and white skin using noninvasive methods. J Soc Cosmet Chem. 1996; 47: 229-240.
5. Montagna W, Carlisle K. The architecture of black and white facial skin. JAAD 1991; 24(6):929-937.
6. http://www.fda.gov/AboutFDA/CentersOffices/CDER/ucm203112.htm
7. Ruiz-Maldonado R, de la Luz Orozco-Covarrubias M. Postinflammatory hypopigmentation and hyperpigmentation. Semi Cutan Med Surg 1997; 16(1): 36-43.
8. Halder RM, Nordlund JJ. Phototherapy for pigmentary disorders. In: Nordlung JJ, Boissy RE, Hearing VL, King RA, Ortonne JP, eds. The Pigmentary System: Physiology and Pathophysiology. Oxford University Press, New York, 1998, pp. 823-977.
9. Falabella R. Treatment of localized vitiligo by autologous minigrafting. Arch Dermatol 1988; 124(11):1649-55.
10. Halder RM, Chappell JL. Vitiligo update. Semin Cutan Med Surg. 2009; 28(2):86-92.
11. Tosti A, Piraccini BM, de Farias D. Dealing with melanonychia. Semin Cutan Med Surg. 2009; 28(1):49-54 .
12. Levit EK, Kagen MH, Scher RK, et al. The ABC rule for clinical detection of subungual melanoma. JAAD; 2000; 42(2 part 1):269-74.
13. Kelly AP. Update on the management of keloids. Semin Cutan Med Surg. 2009; 28(2):71-76.
14. Connell PG, Harland CC. Treatment of keloid scars with pulsed dye laser and intralesional steroid. J Cutan Laser Ther. 2000; 2(3):147-50.

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