Skin Barrier Alteration in Atopic Eczema

Atopic Eczema (AE) is a very common chronic skin inflammatory disease characterized by flares and remission phases [1]. AE is the most common form of inflammatory skin diseases affecting up to 20% of children [2]. It is a typical disease of paediatric age with 90% of cases appearing before 5 years of age. However it could persist in adult age in 30% of affected patients [3]. Recently Margolis et al., [4] have demonstrated that AE could actually continue in up to 80% of adult subjects who have suffered AE during childhood. This shows that AE should be considered a life-long illness. Skin xerosis and itch are the hallmark of the disease pointing out that skin barrier alteration is the background condition of AE [5]. From a clinical point of view AE is characterized by erythema, oedema, skin erosion and excoriation affecting mainly face, limbs and flexural areas [6]. In chronic phases lichenification is commonly seen [7]. AE has a profound impact in quality of life especially when skin conditions negatively affect sleep [8]. Alteration in skin barrier functions and an abnormal Th2-driven immune-response are the two pathogenetic mechanisms [9]. For several years the “Inside-Outside” dilemma has characterized the debate regarding which are the culprit mechanisms involved in the starting of the disease [10]. The pivotal works of Elias [11] and Cork [12] have definitely pointed out that skin barrier alteration is the “primum movens” defect causing the development of AE.