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Tinea capitis is a dermatophyte scalp infection with a marked prevalence among the pediatric population. However, in the last few years, its epidemiology has changed due to increasing population migration worldwide. Host-specific and environmental factors contribute to the pathogenesis of tinea capitis. Clinically, tinea capitis may present as a subtle hair loss accompanied by scalp scaling, alopecia with scaly patches, or alopecia with black dots. A more severe form of tinea capitis is represented by kerion celsi, which clinically presents as a tender plaque covered by pustules and crusts. If left untreated, this dermatophytic infection may resolve with permanent scarring and alopecia. The pathological changes found in tinea capitis are reflected by a spectrum of clinical changes. Zoophilic infections typically prompt an extensive inflammatory reaction, while anthropophilic dermatophytoses often lack inflammation and result in more persistent lesions. Tinea capitis typically requires systemic antifungal therapy. Griseofulvin, terbinafine, itraconazole, and fluconazole are the main antifungal agents used. Currently, the duration of antifungal therapy varies based on the clinical presentation and type of dermatophyte involved. Through the reported cases and literature review, we aim to emphasize the importance of the early recognition of atypical variants of tinea capitis in immunocompetent children for the prompt initiation of systemic antifungal therapy, minimizing the need for prolonged treatment. Additionally, we emphasize the importance of regular laboratory testing during systemic antifungal therapy, particularly liver enzyme tests, to prevent adverse events, especially in cases requiring long-term treatment. [ABSTRACT FROM AUTHOR]

Psoriasis is a chronic, inflammatory, multisystemic disease whose onset is triggered by genetic and environmental factors. Psoriasis has been associated with a wide range of comorbid conditions, namely metabolic syndrome, psoriatic arthritis, cardiovascular disease, psychiatric disorders, malignancy, as well as inflammatory bowel disease. Nowadays, patients affected by chronic plaque psoriasis may benefit from safe and efficient novel therapeutic options. Nevertheless, for patients affected by both psoriasis and inflammatory bowel disease, there is a strong recommendation to avoid biologic therapy with interleukin 17 inhibitors since they may trigger an exacerbation of the gastrointestinal symptoms. Moreover, inflammatory bowel disease in psoriasis patients under biologic therapy with interleukin 17 inhibitors has been reported. In this paper we present the case of a 33-year-old Male patient with a long-standing history of chronic plaque psoriasis under interleukin 17 inhibitors, previously treated with metho-trexate. Throughout the period under immunosuppressive therapy with methotrexate, the patient mentioned mild gastrointestinal symptoms, who persisted after switching to biologic therapy. The patient correlated these symptoms with poor dietary habits. Nevertheless, the patient was referred to the Gastroenterology Department for further investigations. The correlation between the levels of the fecal calprotectin, the endoscopic and histopathologic examination of the biopsies from the terminal ileum led to the diagnosis of Crohn's-like ileitis possibly in the context of biologic therapy with an interleukin 17 inhibitor. The therapeutic approach consisted in cessation of biologic therapy with secukinumab and corticosteroid therapy, with proper control of the inflammatory bowel disease. The management of chronic plaque psoriasis consisted in initiating the patient on risankizumab, an interleukin 23 inhibitor. [ABSTRACT FROM AUTHOR]

Pemphigus refers to a group of rare and severe autoimmune blistering diseases. Autoantibodies are directed against the cell surface of keratinocytes, resulting in a process called acantholysis. Considering that pemphigus has a molecular mechanism and that there is an immune response alteration during the disease, several possible triggers have been discussed, including pregnancy. However, pemphigus is a disease that rarely occurs during pregnancy. In response to the COVID-19 pandemic, various anti-COVID-19 vaccines have been developed. In the literature, there are extremely rare cases of flares or de novo development of autoimmune diseases, such as pemphigus vulgaris and bullous pemphigoid, within 2 weeks after COVID-19 vaccination. We are presenting the case of a 34-year-old patient, from an urban area, who is admitted to the hospital for a well demarcated eruption consisting of crusted erosions placed on an erythematous base, with a seborrheic distribution, including the scalp, face and trunk, with no mucous membrane involvement. The lesions appeared two months ago, in the third trimester of pregnancy, 5 days after the second-dose of COVID-19 vaccine. The onset of the disease was subtle with a transient small flaccid blister located on her left breast, followed by the scalp and trunk involvement. In order to confirm the clinical diagnosis, a skin lesion biopsy was performed that certified the diagnosis of foliaceus pemphigus. Given the patient's postpartum status at the time of hospitalisation and the clinical appearance of the disease, it was decided to initiate systemic therapy with methylprednisolone, approximately 1 mg/kg/day that was slowly tapered. Considering the relatively recent onset after vaccination and the low incidenceof pemphigus in pregnancy, we can hypothesise that the vaccine might actually be the trigger. [ABSTRACT FROM AUTHOR]