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Atopic dermatitis (AD) is one of the most common chronic, inflammatory skin diseases encountered by dermatologists. AD is characterized by pruritus and a chronic course of exacerbations and remissions. AD is thought to involve the interplay of genetic predisposition, immune dysregulation, and environmental factors. It is also associated with other allergic conditions, including asthma.
Although AD typically presents with pruritus as the hallmark symptom in all patients, the appearance of skin lesions may vary among different skin types. In individuals with light-colored skin, AD often appears as erythematous patches and plaques. It also more commonly affects the flexor surfaces of the skin. In individuals with darker skin tones, AD may more often result in follicularly centered papules, lichenification, and pigmentary changes. Lesions may also present on extensor surfaces rather than the typical flexure surfaces. Erythema in darker skin types may appear reddish-brown, have a violaceous hue, or be an ashen gray or darker brown color rather than bright red. Because erythema is more difficult to detect in darker skin types, clinicians may mistakenly minimize the severity of AD.
Clinical severity may also differ between ethnicities. Black patients have an increased tendency toward hyperlinearity of the palms, periorbital dark circles, Dennie-Morgan lines, and diffuse xerosis. Compared with White patients, Black patients with AD are also more likely to develop prurigo nodularis and lichenification. In contrast, Asian patients with AD often experience psoriasiform features, with lesions having more well-defined borders and increased scaling and lichenification.
Beyond differences in clinical appearance, AD may appear molecularly and histologically distinct in ethnic skin. One study suggests that Black patients with AD may have decreased Th1 and Th17 but share similar upregulation of Th2 and Th22 as seen in White patients. Another study showed that Asian patients may have higher Th17 and Th22 and lower Th1/interferon compared with White patients.
Regardless of skin type, treatment goals remain the same. Treatment goals aim to repair and improve the function of the skin barrier while preventing and managing flares. Clinical studies have shown that skincare regimens incorporating ceramide-containing moisturizers may improve AD by increasing the lipid content in the skin. This may offer clinical benefit in patients with skin of color. However, some treatments often used for AD may lead to other skin issues in skin in color. For example, long-term use of topical steroids may worsen hypopigmentation in darker skin types. Management strategies should take into account the unique clinical and genetic features of AD among different patient demographic groups.
William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.
Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
Atopic dermatitis (AD) is one of the most common chronic, inflammatory skin diseases encountered by dermatologists. AD is characterized by pruritus and a chronic course of exacerbations and remissions. AD is thought to involve the interplay of genetic predisposition, immune dysregulation, and environmental factors. It is also associated with other allergic conditions, including asthma.
Although AD typically presents with pruritus as the hallmark symptom in all patients, the appearance of skin lesions may vary among different skin types. In individuals with light-colored skin, AD often appears as erythematous patches and plaques. It also more commonly affects the flexor surfaces of the skin. In individuals with darker skin tones, AD may more often result in follicularly centered papules, lichenification, and pigmentary changes. Lesions may also present on extensor surfaces rather than the typical flexure surfaces. Erythema in darker skin types may appear reddish-brown, have a violaceous hue, or be an ashen gray or darker brown color rather than bright red. Because erythema is more difficult to detect in darker skin types, clinicians may mistakenly minimize the severity of AD.
Clinical severity may also differ between ethnicities. Black patients have an increased tendency toward hyperlinearity of the palms, periorbital dark circles, Dennie-Morgan lines, and diffuse xerosis. Compared with White patients, Black patients with AD are also more likely to develop prurigo nodularis and lichenification. In contrast, Asian patients with AD often experience psoriasiform features, with lesions having more well-defined borders and increased scaling and lichenification.
Beyond differences in clinical appearance, AD may appear molecularly and histologically distinct in ethnic skin. One study suggests that Black patients with AD may have decreased Th1 and Th17 but share similar upregulation of Th2 and Th22 as seen in White patients. Another study showed that Asian patients may have higher Th17 and Th22 and lower Th1/interferon compared with White patients.
Regardless of skin type, treatment goals remain the same. Treatment goals aim to repair and improve the function of the skin barrier while preventing and managing flares. Clinical studies have shown that skincare regimens incorporating ceramide-containing moisturizers may improve AD by increasing the lipid content in the skin. This may offer clinical benefit in patients with skin of color. However, some treatments often used for AD may lead to other skin issues in skin in color. For example, long-term use of topical steroids may worsen hypopigmentation in darker skin types. Management strategies should take into account the unique clinical and genetic features of AD among different patient demographic groups.
William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.
Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
Atopic dermatitis (AD) is one of the most common chronic, inflammatory skin diseases encountered by dermatologists. AD is characterized by pruritus and a chronic course of exacerbations and remissions. AD is thought to involve the interplay of genetic predisposition, immune dysregulation, and environmental factors. It is also associated with other allergic conditions, including asthma.
Although AD typically presents with pruritus as the hallmark symptom in all patients, the appearance of skin lesions may vary among different skin types. In individuals with light-colored skin, AD often appears as erythematous patches and plaques. It also more commonly affects the flexor surfaces of the skin. In individuals with darker skin tones, AD may more often result in follicularly centered papules, lichenification, and pigmentary changes. Lesions may also present on extensor surfaces rather than the typical flexure surfaces. Erythema in darker skin types may appear reddish-brown, have a violaceous hue, or be an ashen gray or darker brown color rather than bright red. Because erythema is more difficult to detect in darker skin types, clinicians may mistakenly minimize the severity of AD.
Clinical severity may also differ between ethnicities. Black patients have an increased tendency toward hyperlinearity of the palms, periorbital dark circles, Dennie-Morgan lines, and diffuse xerosis. Compared with White patients, Black patients with AD are also more likely to develop prurigo nodularis and lichenification. In contrast, Asian patients with AD often experience psoriasiform features, with lesions having more well-defined borders and increased scaling and lichenification.
Beyond differences in clinical appearance, AD may appear molecularly and histologically distinct in ethnic skin. One study suggests that Black patients with AD may have decreased Th1 and Th17 but share similar upregulation of Th2 and Th22 as seen in White patients. Another study showed that Asian patients may have higher Th17 and Th22 and lower Th1/interferon compared with White patients.
Regardless of skin type, treatment goals remain the same. Treatment goals aim to repair and improve the function of the skin barrier while preventing and managing flares. Clinical studies have shown that skincare regimens incorporating ceramide-containing moisturizers may improve AD by increasing the lipid content in the skin. This may offer clinical benefit in patients with skin of color. However, some treatments often used for AD may lead to other skin issues in skin in color. For example, long-term use of topical steroids may worsen hypopigmentation in darker skin types. Management strategies should take into account the unique clinical and genetic features of AD among different patient demographic groups.
William D. James, MD, Professor, Department of Dermatology, University of Pennsylvania, Philadelphia.
Disclosure: William D. James, MD, has disclosed the following relevant financial relationships:
Received income in an amount equal to or greater than $250 from: Elsevier.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
A 27-year-old student presents with a pruritic rash on his hands and in the bends of his arms and legs. He recently started clinical rotations in a nursing facility and has been using hand sanitizer multiple times per day, which has exacerbated the rash on his hands, causing them to ooze and sting. He describes the rash as itchy, especially at night. At times he reports that the itching causes difficulty sleeping. In addition, his skin has little cracks that frequently bleed. He notes that he has experienced similar symptoms in the past, which resolved with moisturizers and topical cream from the drugstore. He has tried over-the-counter hydrocortisone during this episode, with minimal improvement in symptoms. He denies any change in laundry detergents or use of new household products.
Physical examination reveals large erythematous plaques on the hands and flexure surfaces of his neck, antecubital fossa, and behind the knees with scattered excoriations. Erythematous, slightly lichenified coalescing papules are noted on the proximal arms. His face is clear. General skin pigmentation is brown and free of masses and lumps.
