The overlap between atopic dermatitis (AD) and allergic contact dermatitis (ACD) represents a complex clinical reality that frequently poses significant diagnostic and therapeutic challenges. The development of contact-driven aggravation within the context of AD is mediated by the interplay between skin barrier dysfunction, often linked to genetic variants of FLG, and specific immune dysregulation. Although older research hypothesized that a Th2-skewed cytokine profile might lower the risk of sensitization to certain metals, such as nickel, in atopic individuals, contemporary evidence suggests that repeated exposure to topical formulations exacerbates vulnerability to a broad range of contact allergens, including metals. Recent studies indicate a significant prevalence of contact sensitization to preservatives, most notably formaldehyde and methylisothiazolinone, as well as fragrance mixes and surfactants, such as cocamidopropyl betaine, among the AD patient population. Comorbid ACD should be particularly suspected in cases of severe AD that are refractory to conventional therapy or in cases with an atypical lesional distribution. Patch testing remains a fundamental diagnostic tool for patients with suspected AD complicated by contact sensitization; however, the interpretation of results requires heightened clinical rigor due to the increased risk of irritant reactions inherent to atopic skin. The systematic identification and avoidance of incriminated allergens can substantially improve disease control, facilitating the restoration of epidermal barrier integrity and reducing the requirement for systemic immunosuppressants. This personalized approach is essential for optimizing long-term management strategies across both pediatric and adult dermatology.
Chera et al. (2026) studied this question.