Vitiligo is an acquired hypopigmentation of the skin due to a progressive selective loss of melanocytes; it has a prevalence of 1–2% and appears as rounded, well-demarcated white macules. The etiopathology of the disease has not been well defined, but multiple factors contribute to melanocyte loss: metabolic abnormalities, oxidative stress, inflammation, and autoimmunity. Therefore, a convergence theory was proposed that combines all existing theories into a comprehensive one in which several mechanisms contribute to the reduction of melanocyte viability. In addition, increasingly in-depth knowledge about the disease’s pathogenetic processes has enabled the development of increasingly targeted therapeutic strategies with high efficacy and fewer side effects. The aim of this paper is, by conducting a narrative review of the literature, to analyze the pathogenesis of vitiligo and the most recent treatments available for this condition.
Bullous pemphigoid is a subepidermal blistering disease associated with autoantibodies (auto-ab) to BP180 and BP230 which affects elderly patients, predominately. Although it is a rare disease, bullous pemphigoid is the most common among the autoimmune bullous skin diseases. Systemic corticosteroids and immunosuppressants represent milestones in the treatment of patients suffering from bullous pemphigoid; however, therapeutic management of patients still represents a clinical challenge, owing to the chronic nature of the disease and to potential adverse effects related to the long-term use of systemic treatments. Recent discoveries on the pathogenesis of bullous pemphigoid have allowed investigation of new target therapies against selective pro-inflammatory mediators. These therapies appear to yield satisfactory results with fewer side effects in cases of refractory disease. The review discusses current evidence on these new therapeutic targets and specific drugs under investigation.
Hidradenitis suppurativa (HS) is an immune-mediated inflammatory disorder characterized by deep-seated nodules, abscesses, sinus tracts and scars localized in the intertriginous areas. It is accompanied by pain, malodourous secretion and a dramatically decreased quality of life. Although the pathogenesis has not been entirely elucidated, the primary event is follicular hyperkeratosis of the pilosebaceous apocrine unit. Since the registration of the tumor necrosis factor-alpha inhibitor Adalimumab in 2015, several cytokines have been implicated in the pathomechanism of HS and the research of novel therapeutic targets has been intensified. We provide an update on the inflammatory cytokines with a central role in HS pathogenesis and the most promising target molecules of future HS management.
Introduction The key role of microRNAs (miRNAs) in the pathogenesis of psoriasis has been extensively discussed in the literature. Increasing evidence suggests that the analysis of miRNA levels may constitute an innovative approach for exploring the clinical efficacy of anti-inflammatory therapies in patients with psoriasis. However, so far there have been no published studies evaluating the effects of modulating circulating miRNAs and the efficacy of anti-interleukin-23 (anti-IL-23) therapy. The main objective of the present was to evaluate the diagnostic/prognostic relevance of the levels of five circulating candidate miRNAs (miR-21, miR-146a, miR-155, miR-210, miR-378) in psoriatic patients treated with the anti-IL-23 drug risankizumab. Methods A total of eight psoriatic participants were recruited consecutively from January 2021 to July 2021 at the Dermatology Clinic of Università Politecnica delle Marche (UNIVPM) "Ospedali Riuniti" of Marche. Data on anamnestic, clinical and miRNA evaluations before the initiation of risankizumab therapy and after 1 year (January 2021–July 2022) of risankizumab therapy were available for all patients. Results A significant reduction in the signs and symptoms in patients treated with risankizumab was observed after 1 year of treatment, suggesting that the drug is effective for treating psoriasis in a context of real-life clinical evaluation. Plasma levels of the two prototypical inflammamiRs, miR-146a and miR-155, were significantly reduced after 1 year of risankizumab therapy. Also, in patients before treatment, a significant positive correlation was found between circulating levels of miR-210 and miR-378 and disease severity scores. Conclusions Our results reinforce the notion that specific circulating miRNAs could have clinical relevance as diagnostic/prognostic biomarkers of psoriatic disease and suggest the potential relevance of these miRNAs as biomarkers of treatment response.
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