Abstract
Atopic dermatitis (AD), a prevalent endogenous skin condition primarily diagnosed in children, involves both immunologic and compromised skin barrier components. Allergic contact dermatitis (ACD), an exogenous dermatitis, arises from allergen sensitization, triggering a type IV hypersensitivity reaction and a re-exposure leading to the dermatitis. Despite decades of exploration into the interplay between AD and ACD, a definitive conclusion has yet to come. The hypothesized relationship suggests reduced ACD in AD patients due to Th2-skewed immunology but increased ACD prevalence due to compromised skin barriers, maybe linked to filaggrin loss-of-function mutations. To complicate even further, AD treatment often involves topical products potentially containing allergens like propylene glycol (PG), a weak allergen with irritant and sensitizing properties. This prompts the central question: Does AD increase the risk of ACD towards PG? A literature review employing PubMed and the search terms atopic dermatitis or eczema; propylene glycol; topical treatment, emmolients, medication; contact dermatitis or allergy; haptens yielded 908 results, narrowing down to 18 relevant articles. Three articles explored the immunologic processes in AD-ACD interplay, 13 examined PG allergenicity, and five addressed ACD towards PG in AD patients. Current evidence fails to definitively establish whether PG heightens ACD in AD patients. Notably, strong sensitizers seem to attenuate immunologic responses in AD mice, while weak sensitizers like PG might elevate ACD prevalence in humans, especially when AD or a childhood AD history is present. The findings suggest that PG need not be strictly avoided in AD patients, but physicians should be aware of potential PG-ACD development. Tailored treatments considering this possibility are advisable. This nuanced understanding contributes to navigating the intricate relationship between AD, ACD, and topical treatments, offering insights for secure clinical decision-making.