Comparison of Epidermal Barrier Integrity in Adults with Classic Atopic Dermatitis, Atopic Prurigo and Non-Atopic Prurigo Nodularis

Simple Summary: Atopic dermatitis, also called neurodermatitis, is one of the best-known chronic inflammatory skin diseases with eczema, strong itch and dry skin. It is based on an impaired skin barrier with changes in the fats and proteins of the horny layer, which leads to a disturbed water balance. Prurigo nodularis is a less common and intractable chronic skin disease with very itchy nodules. It can be associated with atopic dermatitis (so called atopic prurigo) or with many other diseases. The aim of this study was to compare these three skin diseases classic atopic dermatitis, atopic prurigo and non-atopic prurigo nodularis with healthy control subjects with regard to their skin barrier. In all three disease groups, we then found marked disease severity, reduced water content and increased water loss through the skin, thickening and inflammation of the skin, altered levels of certain proteins and reduced fat layers, all of which demonstrate a severe disturbance of the skin barrier. The main therapeutic consequence is that basic barrier repair, as established for patients with atopic dermatitis in the form of consistent skincare, could also be crucial for patients with non-atopic prurigo nodularis due to this verified skin barrier damage. A deficient epidermal barrier is a key feature of atopic dermatitis (AD) and comprises altered lipid and protein content and composition of the stratum corneum resulting in disturbed water balance. Clinically, eczematous lesions on dry skin and pruritus develop. Pruritic nodules occur in prurigo nodularis (PN), another chronic skin disease, which can be associated with atopy. We aimed at comparing the three clinical pictures, classic AD, atopic prurigo (AP), and non-atopic PN, to healthy controls regarding the epidermal barrier. We determined clinical parameters and performed biophysical measurements, histology/immunohistochemistry, electron microscopy, and molecular biological analysis. We found distinctively elevated clinical scores, reduced hydration and increased transepidermal water loss, epidermal hyperplasia and inflammation reduced filaggrin and increased loricrin and involucrin expression, as well as reduced intercellular lipid lamellae in all three disease groups. These findings show a severe disruption in epidermal barrier structure and function in all three disorders so that epidermal barrier impairment is now proven not only for AD but also for PN.