Atopic Dermatitis in Skin of Colour: A Review

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin condition characterised by intense pruritus, eczematous lesions, and a relapsing-remitting course. While extensively studied in lighter skin types, AD in skin of colour presents unique clinical, pathophysiological, and psychosocial challenges. Patients of Asian ethnicity often display atypical morphologies, including papular or follicular lesions, and more pronounced lichenification, complicating diagnosis and management. Hyperpigmentation and post-inflammatory changes are prominent in these patients, often persisting long after active inflammation subsides, contributing to significant psychosocial distress. Cultural practices, environmental factors, and access to care further impact disease severity and outcomes. This review aims to provide a comprehensive overview of the clinical presentation, diagnostic challenges, and therapeutic approaches for AD in skin of colour, emphasising the need for culturally sensitive care and tailored interventions to improve outcomes in this underserved population. Addressing knowledge gaps through targeted research and education is crucial for advancing equitable dermatologic care.

Introduction

Atopic dermatitis (AD) is an itchy, chronic, inflammatory, relapsing, and remitting skin disorder. It has an early age of onset and poses a significant burden on healthcare resources and patients’ quality of life. It is one of the most common conditions encountered in the dermatology outpatient clinic.[1] AD is a global condition that has a rising prevalence in developing countries such as those within South-east Asia and Latin America. Recent research represents the condition as a heterogeneous disease of distinct endotypes among different ethnic groups.[2]

There remains a critical need to enhance the diagnostic acumen of dermatologists and trainees regarding AD and other dermatologic conditions in individuals with skin of colour. Variations in clinical presentation − such as the subtlety of erythema − can compromise the accuracy of existing AD assessment tools, increasing the risk of misdiagnosis and underestimation of disease severity. Although recent targeted therapies for AD have been evaluated across diverse populations, ethnicity-specific subgroup analyses are often lacking. Further studies are necessary to determine whether therapeutic outcomes or safety profiles vary across different ethnic backgrounds.[3]

Epidemiology

According to The International Study of Asthma and Allergies in Childhood (Phase 3), an increasing prevalence of AD was noted across Latin America and Southeast Asia when compared with Phase 1. This was not demonstrated in countries that originally had a high prevalence of AD, such as the UK (16.0% aged 6–7 years) and Australia (17.1% aged 6–7 years), where prevalence had plateaued.[4] Despite having overall rates of AD in geographical regions with predominance of individuals with skin of colour, most studies on AD have been conducted within Europe and the US.[5] The prevalence and incidence of AD were initially lower than what is now understood and show an increasing trend.[6] A higher prevalence, a greater severity, level of pruritus, impact of pruritus and prevalence of xerosis were noted in AD patients with darker skin as compared with those with lighter skin in studies predominantly based in the US and UK.[7] A systematic review of studies published between 2011 and 2021 reported that the prevalence of AD in paediatric populations in India ranged from 3.1% to 7.21%, while in the general population it varied between 0.98% and 9.2%. Despite these figures, a comprehensive understanding of the disease burden of AD in India − particularly in individuals with skin of colour − remains limited.[8]

Pathophysiology

Ethnic variations in skin barrier function: Ethnic variations in normal skin barrier attributes to differences between ethnicities in view of the prevalence and severity of AD, xerosis and pruritus.[9] A higher prevalence of AD and ScORing Atopic Dermatitis severity score has been reported in individuals of Black ethnicity as compared with individuals of White ethnicity.[10]

Transepidermal water loss and ceramide dysfunction: Transepidermal water loss (TEWL), a key indicator of stratum corneum barrier function since the 1960s, measures the total evaporation of water through the epidermis. Research has shown that individuals of African descent tend to exhibit higher TEWL compared to those of European ancestry, suggesting potential differences in barrier integrity across ethnicities. Ceramides, a class of sphingolipids forming the lipid matrix around corneocytes, are essential for maintaining epidermal hydration. Alterations in ceramide levels and composition − particularly a lower ceramide-to-cholesterol ratio − have been strongly implicated in the pathogenesis of AD.[11] In the Indian context, where darker skin tones are prevalent, a combination of elevated TEWL and reduced ceramide content may contribute to the high incidence of xerosis observed in patients with AD. This supports the growing use of ceramide-rich emollients as barrier-repair strategies in clinical practice across skin of colour populations. Asian skin is reportedly more ‘sensitive’.[12]

Immunological pathways across ethnicities: AD in patients of white ethnicities is typified by filaggrin dysfunction, more T helper (Th) 1 and less Th17 involvement, with less epidermal thickness compared with patients of Black or Asian ethnicities. AD in patients of Black ethnic groups is Th2/Th22-skewed, with robust IgE expression, and less Th1 and Th17 involvement than patients of Asian or White ethnicities. AD across South Asian and East Asian populations is characterised by Th17/Th22 upregulation. In skin of colour, interleukin-6 (IL-6) plays a crucial role in the inflammatory cascade of atopic dermatitis, contributing to both acute and chronic phases. IL-6 contributes to post-inflammatory hyperpigmentation (PIH) in skin of colour by stimulating melanogenesis through inflammatory mediators. In atopic dermatitis, elevated IL-6 induces cytokine-driven oxidative stress and keratinocyte-derived signals that activate melanocytes. This results in increased melanin production and uneven distribution, particularly in darker skin tones where melanocytes are more reactive. The heightened inflammatory milieu in skin of colour amplifies this pigmentary response, making PIH a common and persistent sequela of AD.[5]

Psychosocial impact on skin of colour: Differences also exist in how AD psychosocially has an impact on individuals of different ethnic groups. Individuals with skin of colour consistently report a greater impact on quality of life compared with individuals from white ethnic groups.[2]

Environmental and dietary influences in the Indian context: AD tends to be more prevalent in urban areas compared to rural settings, likely due to industrialisation, lifestyle changes, and increased exposure to environmental pollutants. Pollution is not only implicated in respiratory allergic conditions like allergic rhinitis and bronchial asthma but also plays a role in triggering or exacerbating AD. Additionally, the “hygiene hypothesis” suggests that reduced microbial exposure in early life − common in industrialised environments − may dysregulate immune development, contributing to heightened allergic responses. A comparative study showed that Indian children raised in the UK or the US had more severe AD than those raised in India, highlighting the impact of environmental factors such as climate, diet, clothing, and stress levels on disease expression.[13,14]

Role of diet in AD management: Diet also appears to play a contributory role in the pathogenesis and management of AD. An open-label pilot study conducted in India explored the impact of dietary elimination in 100 paediatric patients with AD. Over a 3-week-period, elimination of common allergens such as milk, nuts, eggs, seafood, brinjal, and soy was associated with a significant improvement in clinical severity scores. The study underscores the potential of culturally adapted dietary interventions as adjunctive management strategies for AD in Indian children.[15]

Clinical Presentation

AD is classically characterised by itchy papules, papulovesicles, erythema, excoriations, and lichenification, which occur typically in a flexural distribution. However, differences exist in the clinical presentation of AD for patients with skin of colour. AD in people with skin of colour may appear psoriasiform with clearer demarcation, lichenoid, scaly or papular, with a violaceous colour, and there is a higher prevalence of post-inflammatory dyspigmentation compared with affected individuals of White ethnicity [Figures 1 and 2].[16] More hyperkeratosis and follicular prominence can be seen. Patches in the skin of colour may appear less erythematous and more violaceous, ashen grey or a dark brown colour.[17] Pruritus remains a prominent feature in all populations with AD, but has been reported to be more severe in individuals with skin of colour.

Figure 1.

(a) A 5-year-old boy presenting with multiple, well-defined to ill-defined erythematous plaques over the face with oozing and crusting present over it. Erythema, oozing and crusting present over eyelids, suggestive of eyelid dermatitis and cheilitis. (b) A 10-year-old child presenting with thickening of palmar skin, scales, and pigmentation suggestive of chronic palmar eczema

Figure 2.

(a) An 8-year-old child presenting with follicular eczema over bilateral knees. (b) 3 well-defined erythematous plaques with oozing and crusting present over the posterior aspect of the bilateral thighs of a 2-year-old girl. Post-inflammatory pigmentation is also present, suggestive of healed dermatotic lesions

Secondary skin changes in atopic dermatitis (AD) among individuals with skin of colour often include distinctive features such as infraorbital darkening, the presence of Dennie-Morgan lines (folds beneath the lower eyelid), and palmar hyperlinearity.[18] However, infraorbital creases may occasionally be seen in children without AD as well. In Indian and other Asian populations, white dermographism − a transient pale response upon rubbing or stroking the skin − is a notable finding, and may aid clinical recognition when erythema is not apparent.[19] Erythema, a hallmark of inflammation, tends to be more difficult to discern in darker skin types, which can lead to underestimation of disease severity on visual examination.[20]

Lichenoid papules, which may mimic lichen planus, are more frequently observed in patients of Indian and African descent. Pruritus remains a consistent and distressing symptom across all ethnicities, but is often reported to be more intense in patients of African ancestry, potentially due to neuroimmune variations and chronicity of inflammation.[21]

From an Indian perspective, pityriasis alba is a commonly encountered sequela in children with AD, particularly during the post-inflammatory phase. These hypopigmented patches stand out more starkly against brown or dusky skin, contributing to significant cosmetic concern and social stigma, especially among school-aged children.[22,23] Post-inflammatory pigmentation changes − either hypo- or hyperpigmentation − are common in patients with skin of colour and can often persist longer than the active eczema itself. Such pigmentation tends to be more pronounced in chronic, relapsing cases and is often observed following scratching or inadequately treated flares.[21,24] In the Indian context, this frequently prompts the use of topical fairness products or home remedies, which may inadvertently worsen the condition.

Importantly, the development of prurigo nodularis − a chronic, intensely itchy nodular eruption − has been found to occur more commonly in individuals with darker skin tones, with studies showing a significantly higher odds ratio in Black populations. Although Indian-specific epidemiological data on prurigo in AD is limited, anecdotal experience suggests similar trends may exist, particularly in chronic and untreated cases.[6,25]

Labial melanotic macules are a distinctive cutaneous finding observed in patients with atopic dermatitis (AD) of Asian descent, including Indian populations. These appear as solitary or multiple well-demarcated, light- to dark-brown pigmented macules, most frequently located on the central upper lip. The lesions tend to occur in younger individuals, especially those with a history of chronic or recurrent cheilitis, a common feature in Indian children with AD due to frequent lip licking and climate-related dryness.[26]

These differences in clinical presentation may limit the use of AD assessment tools in people with skin of colour, leading to the potential for misdiagnosis and underestimation of severity, particularly in relation to assessment of erythema.

Differential Diagnosis of AD in Skin of Colour

Differential diagnosis of AD in individuals with skin of colour, particularly in Indian patients, requires careful clinical distinction due to overlapping features with other dermatoses. Psoriasis is an important mimic, especially in Asian skin types, as both may present with erythematous, scaly plaques. Studies from East Asia suggest a bidirectional association, possibly due to shared inflammatory pathways.

Lichen planus and lichen nitidus may also resemble AD in darker skin tones. Lichen nitidus, though less itchy, can show papular eruptions on the trunk or flexures. Careful examination of the mucosa and signs like the Koebner phenomenon help differentiate these conditions.[18]

Allergic contact dermatitis (ACD) is a frequent consideration, especially in India, where cultural practices and cosmetics often lead to sensitisation. Recalcitrant or atypical AD may benefit from patch testing.

In infants, seborrheic dermatitis is the most common differential. While both may involve the face and scalp, AD typically affects the limbs, and elevated IgE or specific food sensitivities (e.g., egg, milk) support an AD diagnosis.

Scabies, particularly in infants, can mimic AD when eczematised. Clues include intense nocturnal itching, family history, and burrows or nodules in the web spaces and axillae.

Rarely, genetic and immunodeficiency disorders (e.g., hyper-IgE syndrome) can present with eczema-like lesions and elevated IgE, especially in children with poor growth or recurrent infections.[19]

Histological findings in darker skin, including Indian patients, may show greater epidermal hyperplasia and keratinocyte proliferation, which may reflect ethnic differences in immune response and contribute to variation in clinical presentation.[27]

A range of coexisting skin conditions can worsen the severity of atopic dermatitis by triggering flare-ups or contributing to emotional stress. Recurrent infections − whether bacterial, fungal, or viral − are commonly seen and may become chronic over time. Additionally, conditions such as alopecia areata, adverse drug reactions, and pigmentary abnormalities are frequently observed in association with AD, further complicating its clinical course.[22]

Assessment of Severity

Evaluating disease severity is a key initial step in managing atopic dermatitis (AD), as it guides treatment decisions and helps track therapeutic progress. Several validated tools are available for this purpose, including the SCORAD (SCORing Atopic Dermatitis) index and the Eczema Area and Severity Index (EASI). These scales assess the extent of skin involvement and the intensity of clinical features such as lichenification and excoriation; SCORAD also incorporates patient-reported symptoms like itch and sleep disturbance.[28]

However, assessing severity in Indian patients − and broadly in those with skin of colour − can be challenging. This is primarily because erythema, a key marker in these scoring systems, is often less visible or masked in darker skin tones, potentially leading to underestimation of disease burden. To counter this limitation, some experts recommend adjusting erythema scoring upward by one level in skin of colour to better reflect true disease activity. This adaptation is particularly relevant in Indian clinical practice, where visual cues may be subtle and easily overlooked.[29]

Management

Bland topical emollients soothe, moisturise and protect the skin and are important in preventing AD flares. Moisturisers with humectant ingredients such as urea, glycerine and propylene glycol can be irritating, which may worsen the skin of patients with AD of Asian ethnicity, given the predilection of this group to have ‘sensitive skin’.[30] Moisturisers with squalene are less irritating and are preferred in populations with ‘sensitive skin. Topical corticosteroids and topical calcineurin inhibitors (e.g., pimecrolimus and tacrolimus) have proven effective and well tolerated in all skin types, although steroid-induced dyspigmentation (particularly steroid-induced hypopigmentation) more commonly affects individuals with skin of colour.[31] Traditional emollients such as natural remedies like honey and vegetable oils such as coconut oil, sunflower, olive, and safflower are commonly used by the Indian population. It is believed that an oil massage helps improve the skin barrier and increases growth.[22]

Topical therapies like corticosteroids and calcineurin inhibitors (tacrolimus, pimecrolimus) are effective across all skin types, including Indian patients. However, steroid-induced hypopigmentation is more noticeable in darker skin, making long-term use cosmetically concerning. Tacrolimus is often preferred for sensitive areas like the face. Non-steroidal agents such as crisaborole and newer PDE4 inhibitors (difamilast, roflumilast) are emerging as safe options for mild-to-moderate AD, even in children, with minimal pigmentary changes. JAK inhibitors and topical ruxolitinib are promising for moderate-to-severe disease, offering fast itch relief, though experience in Indian patients is limited.[32]

Phototherapy (NB-UVB) is an effective systemic alternative in extensive AD. Indian patients may tolerate higher doses due to increased melanin, but the risk of post-inflammatory pigmentation remains a concern. Systemic agents like cyclosporine, azathioprine, and methotrexate are used in severe cases but require monitoring for side effects and dosing adjustments based on genetic variability in metabolism.[33]

Recent targeted therapies for AD have been studied in multiple ethnic groups; however, ethnicity-based subgroup analysis is often not performed. Biologics such as dupilumab have shown good results in Indian patients, with similar efficacy and safety profiles as in Western populations. However, access and cost remain challenges in widespread use. In India, treatment choice often depends not only on disease severity but also on cosmetic outcomes, affordability, and long-term safety. Further research is required to understand whether treatment responses or safety may differ among ethnic groups.[3]

Conclusion

Atopic dermatitis presents with significant variation in clinical features, immune pathways, and tissue-level changes across different skin tones, highlighting the disease’s heterogeneity. These differences underscore the importance of including individuals with skin of colour − such as those from Indian, African, and Southeast Asian backgrounds − in clinical research. Broader representation in clinical trials is essential to understand how treatments perform across diverse populations and to identify unique safety profiles or therapeutic responses. Without this inclusivity, treatment recommendations may fall short of addressing the specific needs and challenges faced by patients with skin of colour, who often present with less visible erythema, more pigmentary changes, and different morphologic variants.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.