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Background Despite the incidence of Frontal fibrosing alopecia (FFA) has been increasing in last two decades, the pathophysiology and trigger factors of FFA have not been yet fully understood. Aims The aim of this study was to describe epidemiology, clinical and trichoscopic features and comorbidities of FFA patients, in order to improve the understanding of this disease. Patients/Methods A retrospective, observational monocentric study was conducted from 2003 to 2019. Data concerning epidemiology (age, gender, age of menopause, and age of FFA onset), comorbidities, current therapies, localization of FFA (such as frontotemporal hairline, occipital, eyebrow, eyelash, beard, sideburns, and body hair), presence of papules and sign of Lichen planus (LP) at skin, mucosae and/or nail were collected for each patient included. Results A total of 119 Caucasian, adult patients (8 men and 111 female) with FFA were enrolled in the study. Cutaneous, mucosal, or nail localization of LP were found in 16% of our subjects. Interestingly, 15 out of 119 subjects (10.61%) were affected by concomitant genital Lichen sclerosus (LS) and 5 out of these 15 patients (4.38%) presented both LS and LP in association with FFA. Conclusion Considering the high prevalence of LS in FFA patients in our case series, and the frequency of autoimmune comorbidities in both LS and FFA, it is possible to hypothesize an autoimmune process in both conditions. Further studies are needed for a better understanding of the nature of the association between LS and FFA.

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Psoriasis is a chronic immune-mediated inflammatory disease. Up to 40% of patients with psoriasis may develop psoriatic arthritis.  Currently, interleukin (IL)-17/IL-23 pathways are identified as key factors in the immunopathogenesis of both conditions. Here we describe the case of a patient who developed psoriasiform skin lesions 10 months after the initiation of anti-IL17 therapy for psoriatic arthritis. The underlying disease had responded well to the therapy, but the patient developed a striking pustular eruption at the fingers with nail involvement, onycholysis, yellow discoloration, and subungual keratosis. Clinical and histological findings were consistent with an acrodermatitis continua of Hallopeau-like eruption. Skin lesions subsided after discontinuation of the responsible anti-IL17 agent. The interpretation of this paradoxical side effect of biological therapies remains unclear but may relate to an unbalanced inflammatory cytokine response induced by the inhibition of TNF activity. It is likely that patients, who are genetically prone, may respond exaggeratedly to a cytokine imbalance. The identification of this kind of patient, in the future, could be useful in order to choose the correct therapy.

Pemphigus vulgaris is an autoimmune bullous disease that involves the skin and mucous membranes. Current therapies aim to decrease antibody production by means of the use of systemic corticosteroids, immunosuppressive agents and, recently, rituximab, an anti-CD20 monoclonal antibody. However, the chronic immune suppression could entail complications, like infections and secondary malignancies. We describe a case of a patient with pemphigus who developed a sepsis due to Citrobacter freundii infection.