Study: African Americans Are More Burdened by Atopic Dermatitis Severity

The patient population tends to have a more unbalanced immune profile to that of European American patients, indicating a potential for tailored treatment options to combat inflammation.

Emma Guttman-Yassky, MD, PhD

Scaly rashes, extremely dry skin, inflammation, and severe itching—the symptoms of atopic dermatitis (AD, eczema) are burdensome for its entire patient population. But a recent study indicates that African Americans (AA) may face greater prevalence and challenges in combatting the skin condition compared to European American (EA) patients.

The findings are significant for the implication of symptom severity in both populations, of which 19% and 16% are diagnosed with AD, respectively, Emma Guttman-Yassky, MD, PhD, lead study author, said.

“Our study found there are significant differences in the skin of people with AD than in those without the condition,” Guttman-Yassky said in a statement. “Furthermore, we found African Americans with AD have more inflammation than European Americans with the condition.”

The investigators conducted RNA sequencing with RT-PCR validation and immunohistochemistry studies on the lesional and non-lesional skin of the respective populations of AD patients, versus healthy controls. They observed a greater infiltration of dendritic cells/(DCs) marked by the high-affinity IgE receptor/(FcεR1+) in AA AD lesions compared with EA AD (P < .05).

Strong upregulation of Th2-related (CCL17/18/26) and Th22-related markers (IL- 22, S100A8/9/12) were also observed in both AD cohorts. However, decreased expression of innate immune (TNF, IL-1β), Th1-related (IFN-γ, MX1, IL-12RB1) and Th17-related markers (IL-23p19, IL-36G, CXCL1) versus EA AD (P < .05).

In African American patients, clinical severity (SCORAD) also correlated with Th2 (IL-13) and Th22-related products (IL-22, S100A8/9/12) and serum IgE.

Additionally, in EA AD patients exclusively, fillagrin (FLG) was downregulated. On the converse, in both AD cohorts, loricrin (LOR) was downregulated and negatively correlated with SCORAD in AA.

From their findings, the team concluded that reduced Th1 and Th17 characterizes the molecular phenotype of AA AD, but the disease also shares Th2/Th22-skewing attributes to EA AD.

“This study looked for differences in the molecular profile of the skin of African Americans with AD compared to the skin of European Americans with AD to determine if there are differences that might improve treatment options for African Americans,” Guttman-Yassky added. “The results indicated that the immune profile was more unbalanced in African Americans with AD compared to European Americans.”

While more effective treatment for AD are being developed by molecular profiling of skin, the profiling technique has only included EA AD patients to date. However, with this first molecular study of the skin of AA AD patients that assesses responses to similar treatments and differences that could explain variances, better treatments may come into development.

“This may prove to be a valuable enhancement for treatment options for African Americans with AD,” Donald Leung, MD, PhD, allergist, executive editor of Annals of Allergy, Asthma and Immunology, shared. “It will also reinforce the importance of racial diversity in clinical research studies for effective treatment for AD.”

The study authors echoed Leung’s takeaway, writing that their data promotes a personalized medicine approach that includes phenotypespecific characteristics in future development of targeted therapeutics and clinical trial designs for patients with AD.

The study, “Atopic dermatitis in African American patients is TH2/TH22-skewed with TH1/TH17 attenuation,” was published online in the Annals of American College of Allergy, Asthma and Immunology.