Atopic dermatitis is a common chronic/chronically relapsing inflammatory skin disease, with increasing worldwide prevalence. Etiopathogenesis is complex and multifactorial, with a mix of genetic, immunological and environmental aspects. Like in other chronic inflammatory diseases, oxidative stress plays an important pathogenetic role. We reviewed in vivo research studies on humans about oxidative stress and atopic dermatitis. Although sometimes contrasting, overall, they suggest that oxidative stress may have a significant role in atopic dermatitis, but our understanding is still incomplete, at least concerning in vivo data, because of limitations of available literature. Research consists of 33 papers published in 28 years, was not always performed on large study populations, represents a limited number of countries and ethnicities—not always in proportion to their size—and is scattered over multiple papers that, in the majority of cases, cannot be pooled and/or compared because many biomarkers were studied, in different tissues and with different methods. Further, larger studies appear warranted and necessary to shed more light on this aspect of atopic dermatitis, which is important not only to improve our understanding of this disease, but also for potential clinical and therapeutic implications.

Photodynamic Therapy (PDT) is a non-invasive treatment successfully used for neoplastic, inflammatory and infectious skin diseases. One of its strengths is represented by the high safety profile, even in elderly and/or immuno-depressed subjects. PDT, however, may induce early and late onset side effects. Erythema, pain, burns, edema, itching, desquamation, and pustular formation, often in association with each other, are frequently observed in course of exposure to the light source and in the hours/days immediately after the therapy. In particular, pain is a clinically relevant short-term complication that also reduces long-term patient satisfaction. Rare complications are urticaria, contact dermatitis at the site of application of the photosensitizer, and erosive pustular dermatosis. Debated is the relationship between PDT and carcinogenesis: the eruptive appearance of squamous cell carcinoma (SCC) in previously treated areas has been correlated to a condition of local and/or systemic immunosuppression or to the selection of PDT-resistant SCC. Here we review the literature, with particular emphasis to the pathogenic hypotheses underlying these observations.

Relapsing polychondritis is an immune-mediated systemic disease characterized by recurrent episodes of inflammation of cartilaginous and proteoglycan-rich tissues, resulting in progressive anatomical deformation and functional impairment of the involved structures. Auricular and nasal chondritis and/or polyarthritis represent the most common clinical features, but potentially all types of cartilage may be involved. Because of the pleomorphic nature of the disease, with non-specific symptoms at the onset, the diagnosis of relapsing polychondritis is often delayed. In this review article we provide a comprehensive look into clinical presentation, laboratory and instrumental investigations, diagnostic criteria, and therapeutic options.

To provide an updated list of genetic and environmental causative factors of autoimmune thyroid disease, and report about the recent discoveries concerning their interaction in the pathogenesis of thyroid autoimmunity. Although significant discoveries have been made on genetic and environmental factors underlying the development of autoimmune thyroid disease, few data are available about the mechanisms by which they interact. The most interesting news in this field comes from research on molecular mimicry between microbial antigens and thyroid autoantigens. The molecular mimicry model postulates that, in predisposed subjects, a microbial antigen could trigger autoimmunity because of its structural similarity to an autoantigen of the host, and is a paradigmatic example of the multifactorial interaction of several genes and environmental factors to cause autoimmune diseases, including thyroid diseases. Recent findings help us to better understand the functional mechanisms of the immune system, which are still only partially known. Beyond the scientific interest, this knowledge has immediate repercussions on clinical practice because it can suggest possible therapeutic targets for new treatments, as well as better and more specific uses of currently available drugs and resources.