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Psoriasis is a chronic, immune-mediated inflammatory skin disorder characterized by keratinocyte hyperproliferation, dysregulated immune signaling and systemic comorbidities, affecting nearly 2-3% of the global population. Although conventional therapies have improved disease management, they remain limited by poor drug penetration, systemic toxicity, adverse effects, high costs and relapse after discontinuation. The distinctive pathophysiology of psoriatic skin, with its thickened stratum corneum and aberrant immune microenvironment, poses persistent challenges to achieving targeted, sustained drug delivery. To address these limitations, emerging drug delivery systems and devices are being engineered to optimize therapeutic outcomes. Nanocarrier-based platforms are enabling enhanced drug localization, improved bioavailability and modulation of key inflammatory pathways. In parallel, microneedle-assisted delivery, hydrogel scaffolds and nanofiber matrices are establishing themselves as versatile technologies for localized, sustained and patient-friendly administration. Furthermore, stimuli-responsive and bio-inspired systems, incorporating plant-derived bioactives or extracellular vesicles, are advancing the paradigm of personalized and precision medicine in dermatology. This review critically evaluates recent progress in advanced therapeutics, nanotechnology-driven platforms and bioengineered systems for psoriasis therapy, with emphasis on their mechanisms, drug targeting, translational potential and future integration into clinical practice. Additionally, this review provides insight into how advanced delivery systems may redefine the future landscape of psoriasis management.Weiterlesen

BackgroundPsoriasis is a chronic, inflammatory and systemic skin disease. Currently, none of the treatment can effectively prevent the recurrent of psoriasis. α-Hederin is the main active ingredient of the traditional Chineses medicine Ivy, which has been proven to have anti-inflammatory effects. However, its effects on psoriasis and mechanisms of action remain unclear.ObjectiveThis study aimed to investigate the effects of α-Hederin on murine psoriasis and its underlying mechanisms.MethodsThis study firstly evaluated the therapeutic effects of α-Hederin on psoriasis using imiquimod-induced psoriatic mice. H&E and Ki67 immunohistochemical stainings were used to observe the pathological changes and proliferation of the skin lesions. The expression of inflammatory cytokines in skin lesions was analyzed by ELISA. Subsequently, the network pharmacology was employed to predict the molecular targets of α-Hederin in psoriasis. CXCL2 expression and neutrophil infiltration in skin lesions were evaluated via immunohistochemical staining, immunofluorescent staining and flow cytometry. Finally, the effects of α-Hederin on NF-κB p65 pathway were evaluated. The binding of α-Hederin to NF-κB p65 protein was verified through molecular docking, molecular dynamics simulation, CETSA and DARTS.Resultsα-Hederin significantly improved IMQ-induced psoriasiform skin lesions and inflammation in mice. It also reduced the expression of CXCL2 and infiltration of CD11b+Ly6G+ neutrophils in the skin of psoriatic mice. Importantly, administration of recombinant CXCL2 protein aggravated the skin lesions and increased CD11b+Ly6G+ neutrophil infiltration in psoriatic mice previously treated with α-Hederin. Furthermore, α-Hederin inhibited the production of CXCL2 in HaCaT cells and migration of neutrophils to HaCaT cells. But these effects were completely reversed by the CU-T12-9, an NF-κB p65 agonist. Similarly, α-Hederin failed to further alleviate psoriasiform skin lesions and inflammation in mice treated with SC75741 (NF-κB p65 inhibitor). Finally, based on molecular docking, molecular dynamics simulation, CETSA and DARTS, NF-κB p65 was revealed as the direct target of α-Hederin in treating psoriasis.ConclusionThis study has provided the first evidence that α-Hederin may be a promising anti-psoriatic drug by inhibiting NF-κB p65/CXCL2 axis.Weiterlesen

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The human gut microbiota is involved in immune regulation, metabolism, and skin homeostasis. In recent years, gut microbiota alterations have been linked with several inflammatory skin disorders, such as atopic dermatitis (AD), psoriasis, and hidradenitis suppurativa (HS). This systematic review synthesises current evidence on gut microbiota composition and functional alterations in these dermatoses. A comprehensive literature search was conducted in the PubMed database, identifying studies from inception to January 2025. Eligible studies included human observational, interventional, and genetic studies investigating gut microbiota alterations in AD, psoriasis, or HS, using microbiome profiling or genetic causal-inference approaches. Studies lacking control groups or relying on culture-based techniques were excluded. Sixty-two studies were included: 38 on AD, 22 on psoriasis and 5 on HS, with three addressing more than one disease. In AD, most studies focused on paediatric populations, leaving a knowledge gap regarding adult-specific data. Reduced alpha-diversity and decreased abundance of Faecalibacterium prausnitzii, Bifidobacterium spp., and Akkermansia muciniphila were recurrent findings. In psoriasis, in addition to dysbiosis, microbial metabolic pathways were also found to be altered. In HS, data remain limited, but increased Ruminococcus gnavus and reduced alpha-diversity have been reported, mirroring findings in inflammatory bowel diseases. Gut microbiota has been increasingly implicated in skin inflammation. Despite advances in microbiota analysis, significant gaps remain-especially in adult AD and HS. Future research should prioritize standardised methodologies, larger and more diverse cohorts, and leverage emerging tools such as Mendelian randomization and AI-based models to develop precision medicine interventions.Weiterlesen

BackgroundDurability of response to IL-17A blockade (secukinumab) varies, representing a major clinical challenge. Psoriasis is inherently linked to immunometabolic dysfunction. We hypothesized that simple, routine metabolic indices could predict long-term treatment stability, offering crucial pre-treatment stratification tools.MethodsThis was a 52-week prospective, single-center cohort study of 118 patients with moderate-to-severe plaque psoriasis initiating secukinumab. We defined Durable Response (DR) as PASI90 at Week 12 maintained as absolute PASI ≤ 2 until Week 52. Multivariable logistic regression and Cox models were used to identify independent predictors of DR and drug survival.ResultsIndependent predictors of durable response were biologic-naïve status (adjusted OR = 3.52, 95% CI: 1.58-7.85) and a lower baseline TG/HDL-C ratio (adjusted OR = 0.61, 95% CI: 0.47-0.79). Conversely, obesity (BMI≥30) (OR = 0.42) and higher baseline PASI (OR = 0.91) were associated with reduced odds of DR. Conventional systemic inflammatory markers (CRP, NLR) showed no significant difference. Drug survival was significantly higher in DRs (92.6% vs 78.3% at Week 52) and was independently reduced by psoriatic arthritis.ConclusionThe routine baseline TG/HDL-C ratio is a strong, independent predictor of sustained secukinumab efficacy. These easily accessible clinical and metabolic features capture the immunometabolic milieu influencing IL-17A inhibition durability. Integrating the TG/HDL-C ratio into pre-treatment assessment can support patient stratification and optimize long-term management strategies for plaque psoriasis.Weiterlesen

Ethnopharmacological relevanceThe traditional Chinese herbal medicine called Xiao-bi decoction (XBD) has been used for decades to treat psoriasis, but its mechanism of action is poorly understood.Aim of the studyTo investigate the underlying mechanism of XBD against psoriasis using systematic pharmacological techniques.Materials and methodsA psoriasis model was established in mice using imiquimod (IMQ). The efficacy of XBD was evaluated based on psoriasis severity scores and immune cell infiltration. Core components and targets were screened using UPLC-QE-MS/MS and network pharmacology. The mechanism was further explored via transcriptome sequencing, ELISA, western blotting, immunolocalization, and molecular docking.ResultsXBD treatment significantly alleviated IMQ-induced psoriatic symptoms like erythema, scaling, and thickening. It reduced CD4+ T cell infiltration in skin and decreased serum levels of IL-17, IL-1β, IL-23, and IL-36. XBD specifically decreased CD4+-IL-17+ cells while increasing CD4+-FoxP3+ cells in both blood and skin. A total of 1223 chemical components were identified in XBD, including 78 blood-entering components. Network pharmacology and transcriptome analysis collectively demonstrate that XBD inhibits the activation of the JAK2/STAT3 signaling pathway, indicating its potential role in modulating this pathway. Our results also showed that XBD modulated Th17/Treg balance in serum and ameliorating skin inflammation in IMQ-induced psoriatic model.ConclusionThe herbal medicine Xiao-bi decoction may regulate the JAK2/STAT3 pathway, thereby influencing the Th17 response and Treg differentiation, and thereby alleviating the skin inflammation of psoriasis.Weiterlesen

Psoriasis affecting special anatomical sites (scalp, face, intertriginous areas, and genitals) poses unique treatment challenges and often shows inadequate responses. This study evaluates the real-world efficacy and safety of IL-17 inhibitors in treating psoriasis affecting special sites, and identifies clinical determinants for achieving PASI75 and PASI90 responses.A retrospective cohort of 1,469 patients receiving IL-17 therapy was analyzed.Generalized linear models, univariate and multivariate logistic regression analyses were used to identify clinical factors influencing the PASI75 and PASI90 response.At week 12, significant improvements were observed in various measures of disease severity and quality of life (BSA, IGA, PASI, DLQI), with all comparisons yielding P < 0.0001. Treatment response rates were 74.0% for PASI50, 58.6% for PASI75, and 41.5% for PASI90, while adverse events were rare (0.75%). Prediction models for PASI75 and PASI90 responses exhibited moderate discriminative ability. Independent predictors for both PASI75 and PASI90 included clinical BMI, DLQI, BSA, and IGA (all P < 0.05), while job status was an independent predictor for PASI90 only (P < 0.05).Overall, IL-17 inhibitors show substantial efficacy and a favorable safety profile for psoriasis in special sites, with treatment response variability influenced primarily by baseline clinical characteristics such as BMI and disease severity indices.Weiterlesen

ObjectiveIndividuals with psoriasis (PsO) or psoriatic arthritis (PsA) have an elevated risk of major adverse cardiac events (MACE), which include congestive heart failure (CHF), myocardial infarction (MI), and cerebrovascular accident (CVA). Biologic disease-modifying antirheumatic drugs (bDMARDs) may reduce cardiovascular risk; however, whether MACE risk differs by bDMARD class for this population is unknown.MethodsUsing data from TriNetX database, we identified patients with PsO/PsA who were new bDMARD users, including tumor necrosis factor inhibitors (TNFi), interleukin (IL)-17A inhibitors (-i), IL-23i, or IL-12/23i. Time-dependent risk for MACE was calculated using weighted multinomial Cox proportional hazards regression with TNFi exposure as the referent. Additional analyses evaluated components of the primary outcome and baseline cardiovascular disease. A negative control outcome was used to assess bias.ResultsWe identified 32,758 patients with PsO/PsA who were new bDMARD users. Patients had PsO/PsA for a mean of 3.5 (SD 4.5) years prior to starting a biologic, the most common being TNFi (62.9%), followed by IL-17i (15.4%), IL-23i (11%), and IL-12/23i (10.7%). In weighted multinomial Cox proportional hazards regression, the adjusted risk of MACE was similar for IL-17Ai (adjusted hazard ratio [aHR] 0.98, 95% CI 0.73-1.32), IL-23i (aHR 0.84, 95% CI 0.54-1.31), and IL-12/23i (aHR 1.08, 95% CI 0.80-1.47) as compared to TNFi. Subset analyses supported the primary analysis. Negative control outcomes suggested adequate control of bias confounding.ConclusionMACE risk does not significantly differ across bDMARD classes in patients with PsO/PsA. Therefore, cardiovascular risk should not guide biologic selection in this population.Weiterlesen

BackgroundGeneral Practitioners (GPs) act as primary gatekeepers for patients with psoriasis and their screening practice for cardiovascular disease (CVD) and psoriastic arhtiris (PsA) y. This study aimed to assess the awareness and screening routines of Danish GPs regarding CVD and PsA in patients with psoriasis.MethodsA nationwide cross-sectional survey on screening practice was conducted involving 490 randomly selected Danish GPs. Data were analyzed descriptively based on 101 responses (21% response rate).ResultsThe survey revealed a high level of awareness regarding CVD risk (84%), with 60% of GPs reporting routine screening for cardiovascular issues. Commonly assessed parameters included blood pressure (93%) and cholesterol (67%). Conversely, screening for PsA was notably less frequent, with only 32% of GPs actively screening for PsA.ConclusionWhile screening and awareness of CVD risk among primary care professionals, PsA screening remains suboptimal. The findings suggest an urgent need for updated guidelines endorsing simple, validated PsA screening tools and targeted education to prevent missed opportunities for early diagnosis.Weiterlesen

Originaltitel: Bimekizumab longer-term safety profile in adult patients with axial spondyloarthritis or psoriatic arthritis: an updated analysis of six phase IIb/III clinical studies. Link zur Quelle

Originaltitel: Macronutrient intakes and associations with psoriasis severity: a cross-sectional analysis of the asking people with psoriasis about lifestyle and eating (APPLE) study - European Journal of Nutrition Link zur Quelle

# Psoriasis erhöht das Risiko für Lungenkrankheiten Eine aktuelle Studie zeigt, dass Menschen mit Psoriasis deutlich häufiger an Asthma oder COPD erkranken als andere.[1] Das Risiko für COPD ist 2,6-fach erhöht. Bei Asthma liegt das Risiko immerhin noch 1,7-fach höher. Der Grund liegt in der Entzündung, die Psoriasis verursacht. Diese Entzündung passiert nicht nur in der Haut. Pro-Entzündungsstoffe gelangen durch den Blutkreislauf in die Lunge und verstärken dort Atemwegsprobleme.[1] Allerdings gibt es auch gute Nachrichten. Das erhöhte Risiko hängt stark mit bekannten Risikofaktoren zusammen. Rauchen, Übergewicht und fehlende Bewegung spielen eine wichtige Rolle.[2] Deshalb ist die beste Vorbeugung überraschend einfach: mit dem Rauchen aufhören, ein gesundes Gewicht halten und regelmäßig Sport treiben.[2] Die gute Nachricht für Betroffene: Echte Lungenkrankheiten sind bei Menschen mit Psoriasis trotzdem selten. Wenn die Luft knapp wird, liegt es meist an den bekannten Risikofaktoren und nicht an komplizierter Lungenschädigung. Originaltitel: Exploring the risk association between psoriasis and chronic obstructive pulmonary disease, and asthma using the NHIS database Link zur Quelle

# Neue Hoffnung bei Pusteln an Händen und Füßen Palmoplantare Pustulosis und palmoplantare Psoriasis sind zwei unterschiedliche Erkrankungen, die lange Zeit verwechselt wurden[1]. Sie zeigen sich durch Pusteln an Handflächen und Fußsohlen und lassen sich oft schwer behandeln[1][3]. Die gute Nachricht: Es gibt mittlerweile mehr Möglichkeiten als früher. Ärzte beginnen meistens mit Kortisoncremes, die man unter Plastikfolie aufträgt[1][3]. Das hilft vielen Patienten schon weiter. Wenn das nicht reicht, probiert man Lichttherapie mit speziellen Lampen aus. Die Excimer-Laser-Therapie funktioniert besonders gut und hilft etwa 95 Prozent der Patienten[2]. Auch innerlich wirksame Medikamente bringen Erfolg. Das Medikament Apremilast half etwa 78 Prozent der Patienten[2]. Neuere Biologika wie Guselkumab oder Secukinumab zeigen ebenfalls positive Ergebnisse, auch wenn die Forschung noch nicht vollständig abgeschlossen ist[2][3]. Experten raten dazu, die Behandlung an den Krankheitsverlauf anzupassen[3]. Was dem einen hilft, funktioniert bei einem anderen vielleicht nicht. Deshalb ist es wichtig, mit dem Arzt über die richtige Strategie zu sprechen. Originaltitel: The Relative Efficacy of Monotherapies for Palmoplantar Pustulosis and Palmoplantar Psoriasis: A Network Meta-Analysis Study of the Palmoplantar Spectrum | MDPI Link zur Quelle

Die Suchergbnisse enthalten leider nicht die spezifische Studie über Leitungswasser-UVA, Salzwasser-UVA und klassisches Bad-PUVA für Palmoplantar-Pustulosis (PPP), die Sie zusammengefasst haben möchten. Die verfügbaren Suchergebnisse behandeln allerdings andere wirksame Phototherapie-Optionen für PPP, die ich gerne zusammenfassen kann: **PUVA-Therapien zeigen gute Ergebnisse** Die Kombination von PUVA mit Vitamin-A-Derivaten (re-PUVA) oder Fumarsäure-Estern (FAE-PUVA) wirkt bei PPP besonders gut.[1] Re-PUVA führt zu schnellerer Besserung. FAE-PUVA hält die Verbesserung aber länger an.[1] Bei schweren Fällen hilft auch Excimer-Laser-Therapie mit hohen Dosen.[1] **Stufenweiser Behandlungsplan** Ärzte beginnen mit Salben, dann Tabletten, dann Phototherapie wie PUVA.[1] Wenn das nicht reicht, kommen neuere Medikamente wie Antikörper-Therapien in Frage.[3] Um die genaue Studie zu Leitungswasser und Salzwasser bei UVA-Therapie zu finden, brauchen Sie möglicherweise eine direkte Suche nach dieser Publikation. Originaltitel: A Randomized Clinical Trial: The Comparative Therapeutic Efficacy of Tap Water‐UVA, Saltwater‐UVA, and Conventional Bath PUVA in Palmoplantar Pustulosis Link zur Quelle

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Psoriasis is a chronic inflammatory skin disease affecting millions of people worldwide. Although growing evidence links chronic inflammation with increased cancer risk, the association between psoriasis and cutaneous squamous cell carcinoma (cSCC) is still elusive. Using cell transplantation and chemical-induced models of cSCC combined with inducible genetically engineered mouse models of psoriasis, we investigated how chronic skin and systemic inflammation affects squamous skin tumor initiation and progression. Here we show that in the context of severe psoriasis-like disease, neutrophil-dependent inflammation prevents squamous skin tumor development. Cellular and molecular analyses of psoriasis-like skin at the tumor initiation stage revealed a marked infiltration of CD54-expressing neutrophils, associated with the release of cytotoxic granules and neutrophil extracellular traps (NETs), as well as enhanced senescence and the expression of senescence-associated secretory phenotype in keratinocytes. Furthermore, single-cell RNA sequencing demonstrated that inflammatory N1-like neutrophils mediate reprogramming of the cell-cell communication networks, while keratinocytes displayed diminished responsiveness to mitogenic signals, including epidermal growth factor and Wnt/β-catenin. Importantly, neutrophil depletion ameliorated psoriasis-like inflammation, abolished the senescence-like phenotype in keratinocytes and restored tumor growth. We propose that the release of neutrophil granules and NETs in psoriasis-like skin eliminate tumor cells and/or mediate oxidative and inflammatory stress-induced senescence in keratinocytes, thereby preventing tumor growth. Taken together, we have defined an innate control of skin tumorigenesis in psoriasis-like disease, which will be relevant for developing cancer prevention strategies.Weiterlesen

To investigate bimekizumab efficacy in scalp, nail and palmoplantar psoriasis.In this analysis, data are included from the BE SURE, BE VIVID, BE READY, and BE RADIANT phase 3/3b trials (48-56 weeks) and BE BRIGHT open-label extension (144 weeks). Adults with moderate to severe plaque psoriasis and scalp/palmoplantar Investigator's Global Assessment (IGA) score ≥3 or modified Nail Psoriasis Severity Index (mNAPSI) >10 at baseline were randomized to bimekizumab or comparators (adalimumab, ustekinumab, secukinumab, placebo). Higher rates of complete clearance of scalp and palmoplantar psoriasis were generally observed at Week 4 with bimekizumab than comparators.At Week 24, rates of complete resolution of scalp/nail/palmoplantar psoriasis were 77.7%/39.8%/78.7% with bimekizumab and 58.1%/24.5%/73.3% with adalimumab; at Week 52, 71.9%/54.0%/85.2% with bimekizumab and 51.8%/30.6%/75.0% with ustekinumab; and at Week 48, 80.6%/69.5%/82.4% with bimekizumab and 71.6%/52.5%/76.8% with secukinumab. Complete scalp/nail/palmoplantar clearance rates were sustained through 4 years' bimekizumab treatment (79.5%/61.6%/88.7%). Bimekizumab consistently showed higher rates of complete clearance of psoriasis in high-impact areas along with greater patient-reported health-related quality of life benefits than comparators. Responses were sustained over 4 years, which may lead to improvements in patients' quality of life.Trial registrationBE SURE (NCT03412747), BE VIVID (NCT03370133), BE RADIANT (NCT03536884), BE READY (NCT03410992), BE BRIGHT (NCT03598790).Weiterlesen

ObjectivePsoriasis is a chronic inflammatory autoimmune disease that affects physical and mental health. Mental stress has been shown to exacerbate human psoriasis by unknown mechanism.MethodsPeripheral blood mononuclear cells (PBMCs) were collected from patients with psoriasis and mental stress-treated psoriatic mice. The expression levels of TLR9/MyD88/NF-κB pathway-related molecules were analyzed by qRT-PCR and western blotting. Histological examination of skin lesions was examined using hematoxylin-eosin staining. The ratios of Treg/CD4+T cells and Th17/Treg cells were determined by flow cytometry. The associations among mental stress, the TLR9/MyD88/NF-κB pathway, and psoriasis were explored using pharmacological inhibitors and lentiviral transfection.ResultsOur findings demonstrated a significant upregulation of TLR9/MyD88/NF-κB pathway-associated molecules in the PBMCs of psoriasis patients, accompanied by elevated expression of inflammatory factors. These observations were validated using a mouse model of psoriasis. Notably, mental stress was shown to activate the TLR9/MyD88/NF-κB pathway and enhance inflammatory factor production, while simultaneously increasing the Th17/Treg ratio and decreasing the Treg/CD4+T ratio. Therapeutic interventions including antipsychotic sertraline, pathway-specific inhibitors, and lentiviral transfection significantly ameliorated inflammatory markers and improved psoriasis severity grading.ConclusionThe results of this study demonstrates that mental stress induces inflammation and immune dysregulation, exacerbating psoriasis progression. These findings provide valuable insights into the pathophysiological mechanisms underlying psoriasis progression, particularly the mental stress-mediated immunoregulatory axis.Weiterlesen

IntroductionGeneralized pustular psoriasis (GPP) is rare, chronic, and associated with life-threatening complications. We investigated the burden of GPP in France.MethodsUsing data from 2010 to 2021 in the Système National des Données de Santé database, healthcare resource utilization (HCRU), costs, comorbidities, mortality, and treatments were compared among GPP (N = 4351), plaque psoriasis (N = 12,945), and general population (N = 12,981) cohorts, matched for sex, age, Charlson Comorbidity Index (CCI) score, and region. GPP prevalence and incidence were also investigated.ResultsAnnually, there were 0.5-0.8 new GPP cases per 100,000 people. Across the cohorts, 54.5-54.7% of people were male, with mean age 58.7-59.5 years and mean CCI score 1.98-2.06. The GPP cohort incurred significantly greater HCRU and costs versus the plaque psoriasis and general population cohorts, including greater proportions of patients receiving emergency care (78% vs 63% and 55%) and intensive care (28% vs 17% and 14%), longer hospitalizations (mean 38.5 vs 26.2 and 22.4 days per patient), and higher medication costs (€4360 vs €1991 and €1543 per patient-year), respectively. Despite similar CCI scores, GPP was associated with more cardiometabolic and psychological comorbidities versus the plaque psoriasis and general population cohorts, e.g., hypertension (37% vs 21% and 20%), obesity (21% vs 9% and 6%), depression (13% vs 4% and 4%), alcohol abuse (16% vs 3% and 3%), and sleep disorders (8% vs 4% and 3%), respectively. Treatments in the GPP cohort were those used for plaque psoriasis, including topical steroids (77%), systemic steroids (50%), and biologics (23%). Twelve-month survival was 86.9% (GPP), 97.5% (plaque psoriasis), and 90.0% (the general population).ConclusionHCRU, costs, and comorbidities with GPP were often double those for comparator cohorts, and mortality was higher. These findings highlight the need to use GPP-targeted treatments that improve patient outcomes and may reduce the burden on healthcare systems.Weiterlesen