Andrew F. Alexis, MD, MPH, professor of dermatology at the Icahn School of Medicine at Mount Sinai and chair of the department of dermatology at Mount Sinai St. Luke’s and Mount Sinai West in New York, NY.
Skin of color poses some unique challenges when it comes to diagnosing atopic dermatitis (AD). In an interview with The Dermatologist, Andrew F. Alexis, MD, MPH, discussed important diagnostic and treatment considerations for AD in this diverse patient population.
Dr Alexis presented on AD in this patient population at the Skin of Color Update, held from September 7 through September 8, 2019, in New York, NY.1 He is a professor of dermatology at the Icahn School of Medicine at Mount Sinai and chair of the department of dermatology at Mount Sinai St. Luke’s and Mount Sinai West in New York, NY.
At the meeting, the Journal of Drugs in Dermatology presented Dr Alexis with the Innovations in Skin of Color Dermatology Award, which recognizes individuals who fostered innovation and improvement in dermatology through increased emphasis on skin of color education and research.2
Q. What are some of the challenges for diagnosing AD in patients with skin of color?
A. One of the challenges of diagnosing AD in patients with skin of color is the ability to detect erythema, which can vary according to skin type. In the darkest skin types, redness typically seen in lighter skin types might be masked by background epidermal pigment. Erythema can present as shades of purple, red brown, gray-brown, or very dark brown instead of red.
Another diagnostic challenge is that some AD lesion morphologies are unique to patients with skin of color.3 For example, there is a tendency for eczema to present as multiple follicular papules, which can happen in the absence of other more typical signs of eczema such as scaling, lichenification, and redness. There is a greater frequency of lichenoid presentation of AD in patients of African ancestry, including African Americans and others from the African diaspora. These AD lesions tend to resemble lichen planus in terms of their violaceous hue and popular morphology, which can make it difficult to differentiate the two conditions. Patients with African ancestry also have a greater frequency of AD-associated prurigo nodularis. This might have something to do with racial ethnic variations in pruritus as some emerging work suggests that certain populations, including African Americans, may have a tendency towards more severe pruritus associated with their AD, which can lead to sequelae of longstanding pruritus and scratching, such as prurigo nodularis.3 In addition, individuals with East Asian ancestry may be more likely to present with a psoriasiform variant of AD according to recent studies.4
Q. What are your recommendations for clinically assessing AD in patients with skin of color?
A. First, clinicians have to really train the eye to assess erythema in the background of darkly pigmented skin. Again, one should think less about reds and pinks and more about violaceous, red brown, or grayish hues in areas of active lesions. Another useful approach is to identify what the patient’s normal skin, or clinically uninvolved skin, looks like compared with areas with active and symptomatic lesions, which can help assess the severity of AD.
Clinicians should also be familiar with follicular expression of AD, as a patient can present with multiple 1- to 3-mm papules in sites of predilection of eczema without other symptoms.3 Likewise, knowing the variants of AD that affect certain populations more frequently is important to make the correct diagnosis, such as psoriasiform in patients with East Asian ancestry and lichenoid in patients with African ancestry.
Differentiating AD from other conditions, such as lichen planus, can be done by examining the entire patient, looking for typical sites of predilection of AD, and assessing their personal and family history of atopy. Occasionally, there are scenarios where a biopsy might be needed to help differentiate AD from other conditions.
In addition, it is important to remember patients with skin of color can experience pigmentary alterations following the resolution of eczema, which certainly adds to the disease burden among this patient population.3
Q. What are your recommendations and treatment considerations for AD?
A. Early treatment is important for all patients but has specific implications in patients with skin of color. The earlier and more effectively we treat AD in patients with skin of color, the more likely we are to minimize the frequency, severity, and duration of these sequelae, including pigmentary sequelae and development of prurigo nodularis in severe cases. Also, it is important to treat AD as a chronic disease, because that is what it is, and to move away from episodic treatment to manage flares to more continuous treatment to manage the condition longitudinally.
We can do this more effectively than ever before with safe and efficacious noncorticosteroid medications, such as dupilumab (Dupixent), crisaborole (Eucrisa), and topical calcineurin inhibitors, among others. These noncorticosteroid options can very effectively manage the chronic disease over time.
An important treatment consideration for corticosteroid therapy is to avoid one of its well-known side effects—hypopigmentation. Due to the greater contrast between normal skin and hypopigmented skin among patients with skin of color, hypopigmentation related to corticosteroid use has a greater burden and is more disfiguring among patients with darker skin types. Therefore, it is particularly important to avoid this complication.
Strategies to mitigate the risk of hypopigmentation include limiting the duration of corticosteroids to the appropriate duration of 2 to 4 weeks, then switching patients to noncorticosteroids. For topical therapies, I typically treat patients with a corticosteroid for 2 weeks and then switch over to a topical calcineurin inhibitor or topical phosphodiesterase 4 inhibitor. For patients with moderate to severe disease who need systemic treatment, dupilumab can help limit the need for topical corticosteroids.
If patients need corticosteroids to manage flares, I prescribe them for 2-week intervals, followed by 2 weeks of a noncorticosteroid therapy. This cycle can be repeated if patients need steroids again to manage flares. In general, we have to be mindful of using corticosteroids appropriately, limit their duration, and educate patients to apply them directly to the specific lesions where the treatment is indicated and not indiscriminately to nonlesional skin.
In addition to treating the typical signs and symptoms of AD, including itching, scaling, erythema, and excoriation, clinicians will need to manage the persistent pigment alterations.
Q. Do you discuss options for a patient who wants to treat AD-associated pigmentary changes?
A. It is challenging to treat pigmentary complications because many of the agents that we use to manage hyperpigmentation also have some potential irritants. For skin that is highly reactive and sensitive to many products, we are somewhat limited on what we can use for patients with AD who have hyperpigmentation.
My approach generally consists of ensuring that the areas of hyperpigmentation are completely devoid of any active inflammation. Clinicians should make sure that eczema lesions have completely resolved and been managed with therapy in a particular area and only the hyperpigmented patches are treated with bleaching agents. I check to make sure that the barrier is visibly intact before using bleaching agents, such as hydroquinone 4%, to treat hyperpigmentation.
Q. What other key takeaways you would like to leave for our dermatologist audience?
A. There are several studies that show epidermal differences between patients with skin of color and individuals of European ancestry with lighter skin, such as differences in the lipid content in the stratum corneum, specifically ceramides.5 These studies show that the ceramide content in the stratum corneum of individuals of African ancestry is lower than in other populations studied. This might contribute to a tendency toward drier skin in black patients of African ancestry.6
With that information in mind, it is especially important to go the extra mile to use the best possible moisturizing agents and barrier repair strategies to treat AD in patients with skin of color, particularly those with African ancestry, to ensure that we are doing all we can to improve the barrier.
Patient education on which cleansers to use and effective moisturization, which is key to the long-term management of AD, is important. With respect to cleansers and moisturization, I recommend patients use moisturizing cleansers as opposed to traditional soaps, which have harsh surfactants and can dry the skin excessively. Syndet bars and moisturizing liquid cleansers with occlusives and humectants built in can minimize any drying of the skin while showering or bathing. After bathing, patients should immediately and liberally apply effective moisturizing creams, lotions, and/or barrier repair devices to maintain an intact skin barrier and avoid flares.
1. Alexis AF. Pearls for the diagnosis and treatment of atopic dermatitis & eczema in SOC patients – case-based. Presented at: Skin of Color Update; September 7-8, 2019: New York, NY.
2. Andrew F. Alexis, MD, MPH, presented Innovations Award [press release]. New York, NY: Journal of Drugs in Dermatology; September 10, 2019. https://sanovaworks.com/2019/09/10/andrew-f-alexis-md-mph-presented-with-innovations-award/.
Accessed September 18, 2019.
3. Kaufman, Bridget P, Guttman-Yassky E, Alexis AF. Atopic dermatitis in diverse racial and ethnic groups—variations in epidemiology, genetics, clinical presentation and treatment. Exp Dermatol. 2018;27(4):340–357. doi:10.1111/exd.13514
4. Noda S, Suárez-Fariñas M, Ungar B, et al. The Asian atopic dermatitis phenotype combines features of atopic dermatitis and psoriasis with increased TH17 polarization. J Allergy Clin Immunol. 2015;136(5):1254e1264. doi:10.1016/j.jaci.2015.08.015
5. Sanyal RD, Pavel AB, Glickman J, et al. Atopic dermatitis in African American patients is TH2/TH22-skewed with TH1/TH17 attenuation. Ann Allergy Asthma
Immunol. 2019;122(1):99–110.e6. doi:10.1016/j.anai.2018.08.024
6. Jungersted JM, Høgh JK, Hellgren LI, Jemec GB, Agner T. Ethnicity and stratum corneum ceramides. Br J Dermatol. 2010;163(6):1169–1173. doi:10.1111/j.1365-2133.2010.10080.x