ABSTRACT
Atopic dermatitis (AD) is a frequent inflammatory condition that usually begins during early childhood, but it increasingly starts to debut, even in the elderly. Based on immunoglobulin E (IgE) levels and clinical features, two subsets of this disease have been recognized: intrinsic and extrinsic. When speaking about AD, most specialists think about filaggrin (FLG) mutations resulting in epidermal barrier defects, which is the case in most atopic patients, but some have a normal barrier, as seen by imaging, and still have specific clinical lesions along with metal allergies. Specific molecules (IL-10, IFN-γ, and HBD-3) have been shown to greatly impact the interactions between internal and external factors in this peculiar form of AD. A less-known protein, suprabasin, has been highlighted as a promising explanation for nickel anomalies in intrinsic AD.
