Atopic dermatitis (AD) prevalence is rising worldwide. Literature data suggest the incidence of AD in developing countries is gradually getting close to that of developed ones, in which AD affects 20% of the paediatric population. Such an increment, associated with significant variations in prevalence among the various countries, underlines the importance of environmental factors in the disease onset. Among these, great importance is given to hygiene, intestinal microbiota, exposure to bacterial endotoxins, outdoor living with contact to animals, atmospheric pollution, weather, and diet. Genetic (alteration of the skin barrier function) as well as immunologic factors concur with the environmental ones. Only the systematical study of all these elements can best elucidate AD epidemiology.

The skin is the largest organ of the human body, serving as an effective mechanical barrier between the internal milieu and the external environment. The skin is widely considered the first-line defence of the body, with an essential function in rejecting pathogens and preventing mechanical, chemical, and physical damages. Keratinocytes are the predominant cells of the outer skin layer, the epidermis, which acts as a mechanical and water-permeability barrier. The epidermis is a permanently renewed tissue where undifferentiated keratinocytes located at the basal layer proliferate and migrate to the overlying layers. During this migration process, keratinocytes undertake a differentiation program known as keratinization process. Dysregulation of this differentiation process can result in a series of skin disorders. In this context, aquaporins (AQPs), a family of membrane channel proteins allowing the movement of water and small neutral solutes, are emerging as important players in skin physiology and skin diseases. Here, we review the role of AQPs in skin keratinization, hydration, keratinocytes proliferation, water retention, barrier repair, wound healing, and immune response activation. We also discuss the dysregulated involvement of AQPs in some common inflammatory dermatological diseases characterised by skin barrier disruption.

Background: Etiopathogenesis of nummular eczema is obscure; many causative factors have been proposed. Only a few studies investigated the relevance of contact allergy. Objective: This retrospective study aimed to investigate the role of contact allergy in the underlying mechanism of nummular eczema. Methods: From the 29,323 consecutive patients, we patch-tested for eczematous dermatitis of various type, 1022 (3.5%) with nummular eczema were enrolled. Data were collected for each patient, including age, sex, occupation, symptoms onset and duration, onset and spread sites, and clinical evidence or history of atopy. Histological analyses of acute phase lesions were carried out in some patients. Results: Peak incidence of age at disease onset was found in the third decade of life. Predominant sites of lesions were upper (75.8%) and lower (64.5%) limbs, followed by trunk, dorsum of the hands, and face and neck. Three hundred thirty-two (32.5%) of 1022 patients showed positive reactions to 1 or more allergens. Highest sensitization rates were found with nickel sulfate (10.2%), potassium dichromate (7.3%), and cobalt chloride (6.1%). Histopathology showed less pronounced spongiosis in atopic subjects and the elderly. Conclusions: Because this study demonstrates that contact allergy is common with nummular eczema, patch testing is strongly advisable in every patient with persistent nummular dermatitis.