Current Issue : April-June Volume : 2026 Issue Number : 2 Articles : 5 Articles
Psoriasis is a chronic inflammatory skin disease whose pathogenesis involves not only cutaneous inflammation but also intestinal dysbiosis and oxidative stress (OxS). Monoclonal antibodies targeting interleukin (IL)-17 and IL-23 have demonstrated significant immunomodulatory effects; however, their impact on systemic parameters requires further investigation. We conducted a study on 33 patients with plaque psoriasis treated with anti-IL-17 or anti-IL-23 monoclonal antibodies. Dermatological parameters (Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index (DLQI)), biomarkers of intestinal dysbiosis (trimethylamine-N-oxide (TMAO)) and OxS (reactive oxygen metabolites (d-ROMs) and oxidized LDL (oxLDL)) were evaluated. Anthropometric, metabolic, and adipose-derived hormonal parameters (adipokines) were also monitored. After 16 weeks of therapy, significant improvements were observed in PASI and DLQI scores (p < 0.001). TMAO levels were significantly reduced (p = 0.02), as were d-ROMs and oxLDL (p < 0.001). No significant changes were found in weight, body mass index, lipid profile, or adipokine levels (visfatin, leptin and adiponectin). Our data indicate that monoclonal antibody therapy not only improves psoriasis severity but also exerts beneficial effects on systemic biomarkers of dysbiosis and OxS, independent of metabolic or hormonal changes. These findings suggest a systemic mechanism of action, supporting a multifactorial therapeutic effect with potential implications for the prevention of cardiovascular risk....
Background/Objectives: Next-generation drugs, such as JAK inhibitors and biologics, have proved to be very effective treatment choices in several autoimmune and autoinflammatory skin disorders. However, these drugs are not without risk. Due to their immunemodulating properties, these drugs may pose a risk of infection, which could vary between drug target, disorder type and pathogen. Our goal was to determine infection risk and how it may vary by drug target, pathogen and skin disorder, namely psoriasis, atopic dermatitis, alopecia areata, vitiligo and hidradenitis suppurativa. Methods: We performed a systematic search and meta-analysis where we extracted the rates of different infections from the adverse events of each trial that were found and met our inclusion criteria. Results: We found significant associations in psoriasis and atopic dermatitis where infection risk varied by drug, skin condition and pathogen type. We specifically found that there was an increased risk of viral infection for patients with atopic dermatitis with both JAK inhibitors and biologics. We also found an increased risk of fungal infections in psoriasis patients receiving targeted therapies. Lastly, we observed a decreased risk of bacterial infections in atopic dermatitis with dupilumab specifically. Additionally, there was a significantly higher incidence of herpes simplex infections in atopic dermatitis patients with target-selective JAK inhibitors, while no increased risk was observed with herpes zoster. Conclusions: There is a varied risk with these next-generation medications that needs to be considered when determining treatment regime....
Background and Objectives: Dermoscopy is a non-invasive clinical tool that allows for the in vivo visualization of pigmented and non-pigmented structures in the epidermis and the papillary dermis. The standard handheld dermoscopy offers a magnification of 10×, whereas the videodermatoscopes can obtain a magnification of up to 140×. Recently, a new method called magnified dermoscopy was introduced, in which a magnification of 400× can be achieved. Materials and Methods: This review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines. Comprehensive research was conducted using the PubMed database on 9 June 2025, using the following keywords: “high magnification” or “super high magnification” or “optical super high magnification” or “400×”, and “dermoscopy” or “dermatoscopy”. Results: Froma total of 237 records retrieved, 25 were found to be suitable for this review, and consisted of: four prospective studies, three retrospective studies, six case series, ten case reports and two image letters. Conclusions: This review summarizes the current knowledge on magnified dermoscopy, compiling existing data and exploring future perspectives for this emerging non-invasive diagnostic method....
The metabolism of hydroquinone (HQ) by tyrosinase presents significant biochemical and dermatological challenges, particularly due to its association with adverse effects such as exogenous ochronosis (EO). Despite its widespread use in skin-lightening products, the detailed mechanistic pathways of HQ metabolism by tyrosinase remain inadequately understood. This study aims to elucidate the mechanistic insights into the tyrosinasecatalyzed metabolism of HQ, leading to the production of HQ-eumelanin (HQ-EM) and HQpheomelanin (HQ-PM). We employed HPLC analysis to detect key intermediates and final metabolites. Results show that mushroom tyrosinase catalyzes the hydroxylation of HQ to 2-hydroxyhydroquinone (HHQ) via the 2-hydroxybenzoquinone (HBQ) pathway, giving rise to HQ-EM. However, in the presence of cysteine, a shift from HBQ to the benzoquinone (BQ) pathway occurs, giving rise to HQ-PM. Hydroiodic acid hydrolysis of HQ-PM and subsequent HPLC-electrochemical analysis identified 4-aminophenol (AP) as degradation product, thereby serving as a novel marker to monitor HQ oxidation in vitro. These results indicate that HQ functions both as a “pseudo” substrate for tyrosinase—undergoing redox exchange with dopaquinone to form BQ—and as a true substrate, yielding HBQ. This dual role contributes to the formation of HQ-EM and HQ-PM. It would be possible that EO is caused by a continuous oxidation of HQ mediated by tyrosinase activity in the skin....
T helper 2 (Th2)-mediated dermatoses are inflammatory skin diseases driven by CD4+ Th2 cells that produce interleukin (IL)-4, IL-5, IL-13, and IL-31, promoting immunoglobulin E (IgE) class switching, eosinophil recruitment, mast cell degranulation, and pruritus. We aimed to place these conditions in context and clarify how Th2 biology informs diagnosis and therapy. We conducted a narrative synthesis of mechanistic, translational, and clinical evidence on Th2 pathways in atopic dermatitis (AD), prurigo nodularis, bullous pemphigoid, chronic spontaneous urticaria, and selected type I/IVb hypersensitivity reactions, with focused appraisal of trials targeting IL-4Rα, IL-13, and IL-31R. Persistent Th2 activation is associated with epidermal barrier dysfunction, immune dysregulation, and pruritogenic neural signaling; AD is the archetype, showing prominent lesional IL-4/IL-13 activity correlated with severity and itch. Across disorders, pathway-directed biologics against IL-4Rα, IL-13, and IL-31R consistently reduce disease activity and pruritus in AD and prurigo nodularis, with emerging signals of benefit in bullous pemphigoid and chronic spontaneous urticaria. The Th2 axis provides a unifying pathogenic framework and actionable therapeutic target across multiple dermatoses. Integrating cytokine profiling with clinical phenotypes may refine patient stratification and optimize the deployment of existing and next-generation Th2-targeting therapies....
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