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.

Epidermolysis bullosa (EB) is a rare disorder characterized by inherited skin adhesion defects with abnormal disruption of the epidermal–dermal junction in response to mechanical trauma. Our aim was to investigate a set of cytokine levels in serum samples from patients suffering from epidermolysis bullosa simplex (EBS), dystrophic epidermolysis bullosa (DEB), and healthy controls (HCs), exploring their potential correlations with antiskin autoantibody titers and disease activity. Forty patients afferent to the Dermatological Ward of Bari City Hospital and 9 HCs were enrolled and subdivided according to the dystrophic (DEB) and simplex forms (EBS). We found a significant increase in interleukin (IL)-1β plasmatic levels of DEB (P = 0.0224) and EBS (P = 0.0465) patients compared to HCs; IL-6 levels were significantly higher in DEB than in EBS patients (P = 0.0004) or HCs (P = 0.0474); IL-2 levels were significantly increased in DEB compared with EBS (P = 0.0428). Plasmatic tumor necrosis factor-β and interferon-γ were higher in DEB patients than in HCs (P = 0.0448 and 0.0229). Conversely, tumor necrosis factor-α was significantly decreased in DEB (P = 0.0034). IL-5 correlated with anti-BP180 (r = −0.5018, P = 0.0338), anti-BP230 (r = −0.6097, P = 0.0122), and anticollagen VII (r = −0.5166, P = 0.0405) autoantibodies; interferon-γ correlated with anti-BP180 (r = 0.9633, P < 0.0001), anti-BP230 (r = 0.9071, P < 0.0001), and anticollagen VII (r = 0.8619, P = 0.0045) autoantibodies. Score of disease severity was significantly correlated with IL-6 (r = 0.6941, P = 0.029) and IL-12 (r = 0.5503, P = 0.0272). The present study supports that EB might be considered a systemic inflammatory disease rather than a skin-limited disorder; clinical disease activity scores could be also integrated by laboratory data such as IL-6 and IL-12 dosage; biotherapies targeting specific cytokine networks probably represent a way to go in the future.

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.

Irritant or allergic contact dermatitis usually presents as an eczematous process, clinically characterized by erythematoedematovesicous lesions with intense itching in the acute phase. Such manifestations become erythematous-scaly as the condition progresses to the subacute phase and papular-hyperkeratotic in the chronic phase. Not infrequently, however, contact dermatitis presents with noneczematous features. The reasons underlying this clinical polymorphism lie in the different noxae and contact modalities, as well as in the individual susceptibility and the various targeted cutaneous structures. The most represented forms of non-eczematous contact dermatitis include the erythema multiforme-like, the purpuric, the lichenoid, and the pigmented kinds. These clinical entities must obviously be discerned from the corresponding “pure” dermatitis, which are not associated with contact with exogenous agents.