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Researchers shared details of a noninvasive technique that detects abnormal inflammatory cytokine profiles in the skin of asymptomatic infant patients who subsequently develop AD.
A recent study of atopic dermatitis (AD) in infant patients, published in The Journal of Allergy and Clinical Immunology, shed light on potential early predictors of AD development.1
Emollients, long considered a cornerstone in AD management, have been explored for preventive efficacy, with mixed results, according to researchers. However, recent findings hinted at the promise of early emollient initiation in high-risk infants.2
A cohort of 86 high-risk infants, enrolled in the Short-Term Topical Application for Prevention of Atopic Dermatitis (STOP AD) study, each had at least 1 parent bearing a history of allergic disease. Patients were divided into intervention (emollient use) and control groups. Skin surface samples were collected at birth and 8 weeks, with subsequent analysis focusing on biomarkers' association with AD outcomes.
Researchers found that skin biomarkers, notably S100A8/9 and IL-36γ, sampled at 2 months, emerged as potential signals of AD development, particularly in infants with wild-type filaggrin (FLGwt) genes.
Elevated levels of S100A8/9 at 8 weeks correlated significantly with AD prevalence at 6 and 12 months. FLG mutation status played a pivotal role, with FLGwt infants exhibiting distinct biomarker associations compared to FLGmut counterparts.
"Early prediction of AD development at age 8 weeks through biomarkers indicating a presymptomatic or subclinical AD phenotype may allow enrichment or stratification for early-intervention clinical trials," study authors wrote. "Furthermore, biomarkers may facilitate the identification of AD phenotypes or endotypes responsive to specific, targeted interventions in the presymptomatic stage of AD, as is possibly suggested by the different findings in the infants with FLGmut versus in the infants with FLGwt."
The study validated the predictive power of early skin biomarkers in identifying AD risk. Utilizing data from prior research, the models demonstrated robust accuracy in distinguishing active AD lesions from normal skin.
"We have shown a new, noninvasive technique that detects an abnormal inflammatory cytokine profile in the skin of asymptomatic infants who subsequently progress to development of AD. Additionally, we have shown that the presymptomatic cytokine profile of carriers of FLGmut is different from that of children with FLGwt who subsequently develop AD, illuminating the diverse molecular pathways that can lead to AD," according to Stamatas et al. "Indeed, these findings point to the existence of different paths that can lead to AD pathogenesis: one related to barrier impairment (linked to FLG genetic mutations) and another likely linked to immune-related mechanisms."
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