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BackgroundPsoriasis represents a prevalent long-term inflammatory skin condition marked by the dysregulation of immune responses. T cells are integral to the pathogenesis of psoriasis. This study conducted a comprehensive analysis to recognize biomarkers associated with T cell infiltration in psoriasis and to elucidate their underlying molecular mechanisms.ResultsThree biomarkers (AKR1B10, C10orf99, and CKS2) demonstrated high sensitivity and specificity in receiver operating characteristic (ROC) curve, and the reliability of the developed nomogram diagnostic model was observed. In addition, gene set enrichment analysis (GSEA) revealed notable enrichment of the biomarkers in the NOD-like receptor signaling pathway and focal adhesion. Immune infiltration analysis indicated elevated levels of activated B cells and CD8 T cells in psoriasis samples, with the biomarkers showing meaningful correlations with the majority of immune cell infiltration statuses. Importantly, preliminary reverse transcription quantitative PCR (RT-qPCR) validation showed increased expression of AKR1B10, C10orf99, and CKS2 in psoriasis tissues, confirmed higher expression of AKR1B10, C10orf99, and CKS2 in psoriasis patients.ConclusionAKR1B10, C10orf99, and CKS2 may serve as candidate molecules for future mechanistic studies and provide potential diagnostic biomarkers for further investigation of psoriasis-related immune regulation.Weiterlesen

Eine große Studie zeigt, dass sich Psoriasis Arthritis und axiale Spondyloarthritis im Immunsystem deutlich unterscheiden. Die Forschenden haben Blut von fast 180 Betroffenen geprüft und es mit gesunden Menschen verglichen. Bei axialer SpA fanden sie mehr Zellen der angeborenen Abwehr und viele stark aktivierte Abwehrzellen. Bei Psoriasis Arthritis sahen sie eher Zellen, die zur Gedächtnisabwehr gehören. Beide Krankheiten haben ähnliche T Helferzellen, doch bei axialer SpA gibt es mehr stark entzündliche Varianten. Durch solche Muster stellen Ärztinnen und Ärzte in Zukunft die Diagnose genauer und wählen die Therapie gezielter. Vielleicht entstehen daraus später Bluttests die die Wahl eines passenden Medikaments erleichtern. Originaltitel: Deep Immunophenotyping Reveals Distinct Immune Signatures in Axial Spondyloarthritis and Psoriatic Arthritis. Link zur Quelle

Die Studie zeigt: Seit Beginn der Corona‑Pandemie werden manche entzündliche Gelenkerkrankungen seltener erkannt als vorher[1][4]. Das betrifft auch Psoriasis‑Arthritis und rheumatoide Arthritis[1][4]. Fünf Jahre nach Pandemiebeginn liegen die Diagnosen für Psoriasis‑Arthritis etwa ein Viertel niedriger als erwartet, für rheumatoide Arthritis etwa ein Zehntel[1][4]. Gleichzeitig nehmen Diagnosen der axialen Spondyloarthritis zu, besonders bei Frauen[1][4]. ## Was bedeutet das für Euch? Die Ergebnisse sprechen dafür, dass weiterhin Menschen mit Gelenkbeschwerden ohne klare Diagnose leben[1][4]. Wenn Ihr anhaltende Gelenk‑ oder Rückenschmerzen oder Morgensteifigkeit oder Schwellungen bemerkt, sucht früh ärztlichen Rat beim Rheumatologen[1]. Notiert Symptome und macht Fotos von Hautveränderungen, das kann die Diagnose erleichtern[1]. Die Forschenden schlagen vor, Gesundheitsdaten besser zu nutzen und so Lücken zu erkennen und Angebote zu verbessern[1][4]. Das kann helfen, dass Psoriasis und mögliche Gelenkbeteiligung künftig schneller erkannt und behandelt werden. Originaltitel: Trends in autoimmune rheumatic disease diagnoses before and after the COVID-19 pandemic in England: a population-based cohort study using OpenSAFELY Link zur Quelle

Icotrokinra ist eine neue Tablette gegen mittelschwere bis schwere Schuppenflechte. In zwei großen Studien nahmen über 1500 Erwachsene einmal täglich 200 mg Icotrokinra oder Vergleichsmedikamente. Nach einem Jahr hatten rund 70 bis 75 Prozent fast klare Haut und etwa die Hälfte komplett klare Haut. Wer nach 16 Wochen gut ansprach, blieb meist stabil bis Woche 52. Auch Juckreiz und Lebensqualität besserten sich deutlich. Nebenwirkungen waren ähnlich wie unter Placebo und geringer als bei Deucravacitinib, schwerwiegende Probleme traten nicht auf. Die Daten sprechen dafür dass Icotrokinra die Schuppenflechte langfristig gut in Schach hält. Die Ergebnisse klingen vielversprechend. Originaltitel: Durability of Response to Icotrokinra in Adults With Moderate-to-Severe Plaque Psoriasis: One-Year Results From the Phase 3, Placebo- and Active Comparator-Controlled ICONIC-ADVANCE 1 & ICONIC-ADVANCE 2 Trials. Link zur Quelle

IntroductionTopical therapy plays an essential role in psoriasis management. However, lack of rapid improvement may negatively impact adherence. The calcipotriol and betamethasone dipropionate (CAL/BDP) cream based on polyaphron dispersion (PAD) technology has demonstrated high efficacy, favorable safety, and convenience compared with CAL/BDP gel in phase III trials. This post-hoc analysis aims to assess early treatment response to CAL/BDP PAD-cream at Week (W) 4.MethodsThis was a post-hoc pooled analysis of adults with mild-to-moderate psoriasis from two multicenter, investigator-blind, phase III trials (MC2-01-C2 and MC2-01-C7). Patients were randomized 3:1:3 to CAL/BDP PAD-cream (N = 551), PAD-cream vehicle (N = 178), or CAL/BDP gel (N = 542) once daily for 8 weeks. Physician's Global Assessment (PGA) and Subject's Global Assessment (SGA) were assessed at W1 and W4. At W4, early responders were defined as patients achieving PGA controlled disease (i.e., any improvement from baseline to a PGA score of 0-1), while PGA success was defined as a PGA score of 0-1 combined with a minimum 2-point improvement from baseline. SGA controlled disease and SGA success were also assessed. Comparisons between groups were performed by logistic regression models using multiple imputation. Rates of PGA/SGA concordance were assessed by simple percent agreement.ResultsAt W4, CAL/BDP PAD-cream was associated with a significantly higher proportion of patients achieving early response compared with CAL/BDP gel (32.1% vs 21.4%, P < 0.0001). Differences were already significant at W1 (7.8% vs 4.8%, P = 0.0410). PGA success at W4 was also higher with CAL/BDP PAD-cream than with CAL/BDP gel (23.6% vs 14.8%, P < 0.0001). Rates of SGA controlled disease and success were also statistically significantly higher for CAL/BDP PAD-cream at W4. Concordance between PGA/SGA assessments at W4 was observed in 65.5% (controlled disease) and 69.5% (success) of patients treated with CAL/BDP PAD-cream.ConclusionCAL/BDP PAD-cream was associated with significantly higher early response rates at W4 than CAL/BDP gel, suggesting earlier clinical improvements.Weiterlesen

IntroductionPsoriasis imposes a substantial clinical and quality-of-life burden across the Asia-Pacific (APAC) region. Despite advances in systemic therapies, variability in disease severity classification, assessment tools, and treatment escalation criteria continues to contribute to undertreatment and delayed access to effective care.MethodsA modified Delphi panel was conducted to develop APAC-contextualised consensus recommendations for psoriasis management. Statements were generated from a literature review and refined through Steering Committee interviews and review. The steering committee (n = 6) and Delphi panellists (n = 12) was comprised of dermatology experts from six APAC markets (Australia, China, Japan, South Korea, Malaysia, Taiwan). Consensus was generated through two structured online voting rounds involving all panellists, followed by a moderated consensus meeting, involving only the steering committee, to deliberate on any remaining non-consensus items. Consensus was defined a priori as ≥ 75% agreement among panellists.ResultsIn rounds 1 and 2, 92/130 (71%) and 17/24 (71%) statements achieved consensus, respectively. Eight statements were discussed during the steering committee meeting, during which consensus was reached on all eight. In total, 121 statements achieved formal consensus, which includes an additional 4 non-consensus statements from round 1 that were retained in the final recommendations based on steering committee determination of clinical relevance. Recommendations focused on severity classification and assessment thresholds, treatment goals and response criteria, and systemic therapy eligibility and escalation.ConclusionThese Delphi-derived recommendations provide a practical, patient-centred framework to standardise psoriasis assessment and guide timely treatment escalation in APAC. Adoption may reduce variability in care, support equitable access to appropriate systemic therapies, and improve outcomes across diverse APAC health systems.Weiterlesen

Psoriasis is a chronic autoinflammatory skin disease lacking curative options. Ronomilast is a novel PDE4i inhibitor with potent anti-inflammatory properties. To evaluate the therapeutic efficacy of topical ronomilast, alone and combined with clobetasol, in an imiquimod (IMQ)-induced psoriasis mouse model. Fifty BALB/c male albino mice were randomly assigned to five groups (n = 10): healthy control, imiquimod-induced, clobetasol-treated (0.05%), ronomilast-treated (0.3%), and combination-treated (ronomilast 0.15% + clobetasol 0.025%). Psoriasis-like lesions were induced by daily topical application of 5% imiquimod for five consecutive days. Treatments were applied topically 3 h after imiquimod. Skin samples were analyzed for IL-17A and IL-23 levels via ELISA, TNF-α expression via immunohistochemistry, and histopathological changes. In silico molecular docking with PDE4B and PDE4D targets was also conducted. Ronomilast significantly reduced IL-17A and IL-23 levels compared to the induction group. The combination therapy produced the greatest reduction in IL-17A and IL-23. TNF-α expression scores were also significantly decreased by ronomilast and the combination relative to the induction group, consistent with histopathological improvements. Molecular docking demonstrated that ronomilast has higher binding affinity than roflumilast for PDE4B and comparable affinity for PDE4D. Topical ronomilast alone or combined with clobetasol, substantially ameliorates psoriasiform dermatitis by inhibiting key inflammatory cytokines. These results strengthen its prospects as an antipsoriatic candidate; nonetheless, more clinical investigations are necessary to validate its effectiveness and safety in humans.Weiterlesen

Abstract Psoriasis is a chronic immune-mediated disease driven by interacting pro-inflammatory, angiogenic, and regulatory cytokine pathways. While individual cytokines of the IL-23/Th17 and Th1 axes have been widely studied, less is known about how multiple mediators behave collectively in relation to clinical severity. This study evaluated the integrated serum profile of IL-17A, IL-22, TNF-α, VEGF-A, IL-12(p40), and IL-10 in 34 patients with chronic plaque psoriasis and 19 matched healthy controls, and examined their associations with the Psoriasis Area and Severity Index (PASI). Psoriasis patients showed significantly elevated IL-17A, IL-22, TNF-α, VEGF-A, and IL-12(p40), whereas IL-10 displayed inverse pattern. Hierarchical clustering revealed a tightly interconnected pro-inflammatory cytokine network in untreated patients, with IL-17A, IL-22, and TNF-α forming a core synergistic cluster strongly associated with PASI. Systemic therapy reduced PASI and significantly decreased IL-17A, IL-22, IL-12(p40), and VEGF-A, accompanied by partial normalization of cytokine correlations. ROC analysis identified IL-22 and IL-12(p40) as potential biomarkers of treatment response. These findings demonstrate that psoriasis severity reflects coordinated activity across multiple immune pathways. Integrated cytokine profiling offers a more comprehensive understanding of disease biology and may support development of multi-marker tools for monitoring disease activity and guiding personalized therapy. Weiterlesen

Assessing disease activity in psoriatic arthritis (PsA) remains challenging, and additional biomarkers that can complement conventional inflammatory markers are still needed. The CRP-albumin-lymphocyte (CALLY) index integrates inflammatory, immune, and nutritional components into a single measure. This study examined the relationship between the CALLY index and disease activity in patients with PsA. This retrospective longitudinal cohort study included 150 patients with PsA and 50 age- and sex-matched healthy controls. Blood-derived inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), pan-immune inflammation value (PIV), and the CALLY index, were calculated using routine laboratory data. Disease activity was evaluated with the clinical Disease Activity Index for Psoriatic Arthritis (cDAPSA). Correlation analyses, receiver operating characteristic (ROC) analyses, subgroup analyses, and multivariable logistic regression models were performed. Patients with moderate-to-high disease activity had markedly lower CALLY index values than those with remission or low disease activity. The CALLY index showed a moderate inverse correlation with cDAPSA scores (r = - 0.529, p < 0.001). During follow-up, CALLY values increased significantly in both csDMARD-treated and biologic-treated patients (both p < 0.001), whereas no significant differences were observed between treatment groups. In multivariable analysis, lower log-transformed CALLY index values remained independently associated with moderate-to-high disease activity (OR 0.39, 95% CI 0.23-0.66). The discriminative performance of the CALLY index was similar to that of CRP (AUC 0.724 vs. 0.738; p = 0.42). Lower CALLY index values were linked to greater disease activity in PsA and improved alongside reductions in inflammatory burden during follow-up. Although its performance was comparable to CRP rather than superior, the CALLY index may represent a useful complementary biomarker for disease activity assessment in PsA. Prospective studies are needed to further clarify its clinical utility.Weiterlesen

BackgroundPsoriasis is a chronic immune-mediated skin disorder characterized by excessive keratinocyte proliferation and abnormal T-cell activation. Cluster of Differentiation 28 (CD28), a costimulatory protein, plays a crucial role in psoriasis pathophysiology by enhancing T-cell activation and promoting cytokine release.MethodsA case-control study was involving 168 newly diagnosed psoriasis patients and 159 healthy control individuals (HC), Genotyping of rs1879877 in promoter of CD28 gene was performed using the tetra-primer amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR), and serum levels of soluble CD28 (sCD28) and selected cytokines (Interleukin (IL), IL-38, IL-39 and Granulocyte Macrophage Colony Stimulating Factor (GM-CSF)) were measured using sandwich enzyme-linked immunosorbent assay (ELISA).ResultsThe heterozygous GT genotype was predominant among psoriasis patients and was significantly associated with elevated serum sCD28 levels compared to controls, who predominantly carried the wild type GG genotype. Elevated sCD28 levels were linked to increased T-cell activation, contributing to immune dysregulation and disease severity. This was evidenced by increased production of pro-inflammatory cytokines, including IL-39 and GM-CSF, with a concurrent decrease in the anti-inflammatory cytokine IL-38.ConclusionSerum sCD28 levels were significantly elevated in psoriasis patients. The CD28 gene variant rs1879877 (-1198 G/T) appears to be associated with psoriasis pathogenesis, potentially due to increased transcriptional activity that elevates sCD28 expression, thereby influencing T-cell activation and immune modulation.Weiterlesen

Pediatric psoriasis accounts for approximately 2% of dermatological conditions in children under 16 years of age. The objective of this study is to describe the clinical characteristics, treatment regimens, and observed efficacy and safety profiles in a real-world cohort. This retrospective study analyzed 15 pediatric patients treated with biologics in Argentina between 2010 and 2024. The median age at treatment initiation was 8 years, with a predominance of female patients. The biologics used were primarily adalimumab, followed by secukinumab, etanercept, and ixekizumab. Five patients experienced treatment failure secondary to adalimumab. The therapy was well tolerated, with no adverse events reported.The data suggest that early intervention can alter the course of the disease and prevent long-term complications.Weiterlesen

BackgroundGeneralized pustular psoriasis (GPP) is a rare and severe inflammatory disease characterized by widespread pustular eruptions and systemic inflammation.ObjectiveTo evaluate the clinical characteristics and disease burden of patients with GPP in Taiwan using a national claims database.MethodsPatients with GPP and no prior diagnosis of psoriasis vulgaris (PV) who experienced an incident flare between January 1, 2017, and September 30, 2020, were identified from Taiwan's National Health Insurance Database. Clinical characteristics, comorbidities, and treatment patterns were described. Recurrent flare frequency, healthcare resource utilization (HCRU) and costs were compared with those of a propensity score-matched PV cohort at a ratio of up to 1:4. Outpatient-managed flares were classified as moderate, whereas hospitalized flares were classified as severe.ResultsA total of 245 patients with GPP were included (mean age 51.3 years; 49.8% male). During follow-up, 1,156 moderate-to-severe flares were identified. Compared with matched patients with PV, patients with GPP had a higher recurrent flare rate (rate ratio 1.14; 95% CI 1.06-1.23). Patients with GPP also had greater HCRU, including more outpatient visits (incidence rate ratio [IRR] 1.03 [95% CI 1.01-1.05]), emergency room visits (IRR 1.33, 95% CI 1.19-1.49), and hospital admissions (IRR 1.69 [1.50-1.91]). Median monthly healthcare costs were approximately twice as high among patients with GPP as among matched patients with PV.ConclusionPatients with GPP experienced recurrent flares, greater healthcare utilization, and higher healthcare costs than matched patients with PV, underscoring the substantial real-world clinical and economic burden of GPP.Weiterlesen

There are no real-world studies on the long-term effectiveness of anti-interleukin-23 antibody tildrakizumab in Japanese patients with psoriasis stratified by pretreatment status. To evaluate the 52-week real-world effectiveness of tildrakizumab for psoriasis patients, stratified by prior systemic therapy, prior biologic therapy, or prior deucravacitinib treatment, and to assess the maintenance of week 16 responses and achievement of delayed responses in patients without week 16 responses. This study included 57 patients with psoriasis treated with tildrakizumab. Psoriasis area and severity index (PASI) and static physician's global assessment (sPGA) were analyzed through week 52 in subgroups stratified by the presence or absence of prior systemic therapy, prior biologic therapy, or prior deucravacitinib treatment. Patients who achieved PASI 75, PASI 90, PASI 100, absolute PASI ≤ 3, absolute PASI ≤ 2, or sPGA 0/1 at week 16 were assessed for the maintenance of respective responses, and patients without week 16 responses were assessed for the achievement of delayed responses through week 52. Analyses were descriptive and used an as-observed approach. Tildrakizumab reduced PASI throughout 52 weeks regardless of the presence or absence of prior systemic therapy, prior biologic therapy, or prior deucravacitinib treatment. Responses achieved at week 16 were mostly maintained through week 52. Some patients without week 16 responses achieved delayed responses by week 52. Tildrakizumab reduced PASI throughout 52 weeks in patients with psoriasis regardless of prior systemic therapy, prior biologic therapy, or prior deucravacitinib treatment. Responses achieved at week 16 were mostly sustained through week 52. Some patients without week 16 responses could achieve delayed responses by week 52.Weiterlesen

Psoriasis is a chronic inflammatory disease characterized by thickened erythematous skin lesions covered with white and silvery scales and accompanied by macrophage infiltration into the dermis. Although 2-3% of the world's population suffers from psoriasis, there is still a requirement for novel, safe, and effective treatment options. Previously, our group demonstrated the theranostic effects of two-dimensional germanium telluride nanosheets (GeTe-NSs) in the treatment of inflammatory bowel disease. However, the precise mechanisms underlying their therapeutic action remained unclear. In this study, the specific anti-inflammatory mechanisms of GeTe-NSs in lipopolysaccharide-stimulated RAW 264.7 macrophages were evaluated, along with their therapeutic potential for psoriasis treatment in an imiquimod (IMQ)-induced murine model. GeTe-NS treatment significantly decreased cell proliferation and reduced the production of reactive nitrogen and oxygen species in activated RAW 264.7 macrophages. The GeTe-NSs lowered the mRNA levels of key pro-inflammatory mediators (Nos2, Tnf, Ccl2, and Cxcl15), while enhancing the mRNA levels of an anti-inflammatory factor (Arg1) and an antioxidant enzyme (Nqo1). Flow cytometric analysis revealed that the GeTe-NSs promoted a shift from the M1 (pro-inflammatory) macrophage phenotype toward the M2 (anti-inflammatory) phenotype. Western blot analysis demonstrated that anti-inflammatory effects were achieved by inhibiting the activation of the TLR4/CD14 and ERK/NF-kB/STAT1/STAT3 pathways. In vivo, the oral administration of GeTe-NSs in an IMQ-induced psoriasis mouse model resulted in significant improvements in clinical scores, epidermal thickening, and the proportions of M1/M2 macrophages in spleen and skin lesions. Taken together, these findings suggest that GeTe-NSs could be a promising nanomaterial for treating inflammatory diseases, including psoriasis.Weiterlesen

Trial number: 2023-507039-39-00 Overall trial status: Authorised, recruiting Trial title: A Phase 3 Multicenter, Randomized, Double-blind, Placebo-controlled and Deucravacitinib Active Comparator-controlled Study to Evaluate the Efficacy and Safety of JNJ-77242113 for the Treatment of Participants With Moderate to Severe Plaque Psoriasis Medical conditions: Moderate to Severe Plaque Psoriasis Status in each country: Italy:Not authorised, Germany:Ongoing, recruitment ended, Romania:Ongoing, recruitment ended, Spain:Ongoing, recruitment ended, Poland:Ongoing, recruitment ended, Hungary:Ongoing, recruitment ended Trial phase: Therapeutic confirmatory (Phase III) Therapeutic Areas: Diseases [C] - Immune System Diseases [C20] Primary end point: IGA score of 0 or 1 and a ≥2-grade improvement from baseline at Week 16., PASI 90 at Week 16. Secondary end point: N/A Age of participants: 65+ years, 18-64 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 342 Sponsor: Janssen - Cilag International Sponsor type: Pharmaceutical company Trial product: JNJ-77242113, DEUCRAVACITINIB, Film-Coated Tablet without Deucravacitinib, Film-Coated Tablet without JNJ-77242113 Results posted: No Overall decision date: 19/03/2024 Countries decision date: IT: 21/03/2024, RO: 21/03/2024, HU: 04/04/2024, DE: 20/03/2024, PL: 25/03/2024, ES: 21/03/2024 Last updated date: 02/07/2026Den kompletten Artikel zeigen

Normalerweise raten Ärztinnen und Ärzte zu einem klaren Plan für Impfungen unter Guselkumab[4][5]. Lebendimpfstoffe wie die **Masern Mumps Röteln Impfung** gelten dabei als Tabu[4][5]. Ein aktueller Bericht beschreibt nun eine Person mit Psoriasis, die trotz laufender Guselkumab Therapie eine MMR Impfung bekam. Sie bildete schützende Antikörper und hatte keine schweren Nebenwirkungen. Das klingt beruhigend, ist aber nur ein einzelner Fall. Für dich heißt das, du solltest Impfungen immer früh mit deiner Ärztin planen[5][6]. Oft ist ein Abstand von mindestens zwölf Wochen zur letzten Guselkumab Spritze sinnvoll[5][8]. Originaltitel: Safe seroconversion after receiving measles, mumps, and rubella live vaccine during guselkumab treatment for psoriasis. Link zur Quelle

Orales CBD-Öl hat die Schwere der Psoriasis in dieser Studie nicht deutlich verringert.[1] Es zeigte nur vorübergehend etwas weniger Juckreiz und schnelleres Einschlafen.[1] ## Was bedeutet das für Euch? Die Teilnehmenden bekamen täglich 60 mg CBD-Öl oder ein Scheinpräparat.[1] Die Plaques wurden dadurch im Durchschnitt nicht besser, die PASI-Werte blieben ähnlich.[1] Kurzzeitig nahm der Juckreiz ab und einige schliefen schneller ein, dieser Effekt hielt aber nicht an.[1] Nebenwirkungen waren meist mild und traten in beiden Gruppen ähnlich oft auf.[1] Für Eure Hoffnung heißt das: CBD-Öl in dieser Dosis ist derzeit keine eigenständige Behandlung, die Psoriasis klar abschwächt.[1] Es könnte als Ergänzung einmal Juckreiz oder Einschlafprobleme etwas lindern, ersetzt aber keine bewährten Therapien.[1] Für den Alltag: Setzt Eure verordnete Behandlung und Hautpflege weiter konsequent fort. Wenn Ihr CBD ausprobieren möchtet, besprecht das vorher mit Eurem Hautarzt, besonders wegen möglicher Wechselwirkungen mit anderen Medikamenten.[3][5] Weitere Studien mit höheren Dosen und längerer Einnahme sind geplant, bis dahin ist ein vorsichtiger, gut begleiteter Einsatz sinnvoll.[1][5] Originaltitel: Efficacy and safety of cannabidiol oil in psoriasis: a randomized, double-blind, placebo-controlled trial - PubMed Link zur Quelle

Wer cremt, will schnell etwas sehen. Genau das zeigt eine neue Studie zu einer Kombi Creme mit Calcipotriol und Betamethason. Die PAD Creme wirkt bei leichter und mittlerer Plaque Psoriasis oft schneller als das bekannte Gel. Nach vier Wochen hatten etwa ein Drittel der Menschen mit PAD Creme fast klare Haut, mit Gel war es nur gut ein Fünftel. Erste Effekte gab es schon nach einer Woche. Auch die Patienten selbst fanden Haut und Befinden eher besser. Für den Alltag heißt das, dranbleiben lohnt sich. Mit dieser Creme sieht man oft früh einen Unterschied. Originaltitel: Early Response to Calcipotriol and Betamethasone Dipropionate PAD-Cream at Week 4 in Patients with Mild-to-Moderate Plaque Psoriasis: A Post-Hoc Pooled Analysis of Two Phase III Trials. Link zur Quelle

Psoriasis Arthritis greift oft erst wenige Gelenke an, später können mehr Gelenke dazukommen. Die Studie FOREMOST schaute auf Menschen mit früher PsA, sie hatten höchstens vier betroffene Gelenke. Nach 16 Wochen hatte etwa ein Viertel mehr als vier entzündete Gelenke. Wer Apremilast nahm, hatte deutlich seltener neue Gelenkprobleme. Frauen und Menschen ohne früh eingesetzte Basismittel sowie mit Wurstfingern hatten ein höheres Risiko. Wer bis zu 48 Wochen Apremilast nahm, berichtete weniger Schmerzen und blieb meist stabil. Das spricht dafür Originaltitel: Progression from oligoarticular to polyarticular psoriatic arthritis and apremilast as a disease modifier: novel insights from FOREMOST. Link zur Quelle

Eine große Studie hat Menschen mit axialer Spondyloarthritis und Psoriasis Arthritis drei Jahre lang begleitet. Sie bekamen alle vier Wochen Bimekizumab, ein modernes Entzündungsmedikament. Die meisten fühlten sich deutlich besser und konnten im Alltag mehr schaffen. Auch bei der Arbeit ließen sie sich weniger bremsen und waren mit ihrer Situation eher zufrieden. Viele fühlten sich fast so gut wie Menschen ohne diese Krankheiten. Firmen sparten dadurch viel Geld, weil Beschäftigte seltener bei der Arbeit ausfielen. Für Betroffene zeigt die Studie, dass Bimekizumab nicht nur Schmerzen und Steifigkeit senken kann sondern auch Job und Sozialleben stärken. Originaltitel: Bimekizumab Improves Health Status and Work Productivity, With Reduced Productivity Costs, to 3 Years in Axial Spondyloarthritis and Psoriatic Arthritis. Link zur Quelle

Chronische Entzündungen wie bei Psoriasis hören oft nicht von selbst auf. Ein Forscherteam schlägt dafür das CURE Modell vor. CURE heißt CONTROL UNLOAD and RESET EQUILIBRATE und läuft in drei Phasen. In CONTROL bremst eine starke Therapie zuerst die Entzündung deutlich. In UNLOAD and RESET fährt man die Medikamente Schritt für Schritt runter und stärkt die eigene Abwehr. In EQUILIBRATE folgt eine leichte Dauertherapie die das Gleichgewicht hält und Rückfälle vermeiden soll. Ziel ist nicht Heilung sondern ein stabiles Leben mit möglichst wenig Beschwerden. Originaltitel: CURE: a phase-based therapeutic framework for chronic inflammation. Link zur Quelle

Trial number: 2025-522567-15-00 Overall trial status: Ongoing, recruiting Trial title: A Phase 3, Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial to Evaluate the Efficacy, Safety, Tolerability, and Pharmacokinetics of Zasocitinib in Pediatric Participants Aged 4 to Less Than 18 Years With Moderate-to-Severe Plaque Psoriasis Medical conditions: Plaque Psoriasis Status in each country: Spain:Authorised, recruiting, Poland:Ongoing, recruiting, Germany:Ongoing, recruiting, Italy:Authorised, recruitment pending Trial phase: Therapeutic confirmatory (Phase III) Therapeutic Areas: Diseases [C] - Skin and Connective Tissue Diseases [C17] Primary end point: Part A: Coprimary Endpoints (vs Placebo) at Week 16 • sPGA 0/1 response: Proportion of participants achieving an sPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline. • PASI-75 response: Proportion of participants achieving ≥75% improvement from baseline in PASI score. Part A Cohort 1: Includes adolescent participants aged 12 to <18 years. Part A Cohort 2: Includes children participants aged 4 to <12 years., Part B: PK Primary Endpoints • PK parameters (that is Cmax, Tmax, AUC0-Last) of zasocitinib on Day 7. Part B: Includes only children participants aged 4 to <12 years. Part B participants will be separate from Part A Cohort 2 participants. Secondary end point: Part A: Key Secondary Efficacy Endpoints (vs Placebo) at Week 16 • PASI-90 response: Proportion of participants achieving PASI-90. • Enhanced sPGA response: Proportion of participants achieving an sPGA of clear (0). • PASI-100 response: Proportion of participants achieving PASI-100., Part A: Additional Secondary Efficacy Endpoints (vs Placebo) at Week 16 • ssPGA response: Proportion of participants achieving an ssPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline for participants with a baseline ssPGA ≥3. • Change and percent change from baseline in BSA affected by psoriasis., • DLQI response: Proportion of participants with a DLQI score of 0/1 (for participants with a baseline DLQI score ≥2). • CDLQI response: Proportion of participants with a CDLQI score of 0/1 (for participants with a baseline CDLQI score ≥2). • Change from baseline in DLQI. • Change from baseline in CDLQI., Part A (Cohort 1 only): Additional Secondary Efficacy Endpoints (vs Placebo) at Week 16 • Itch NRS response: Proportions of participants achieving a ≥4-point improvement in Itch NRS for participants in Cohort 1 who had an itch NRS ≥4 at baseline. • Change and percent change from baseline in Itch NRS for participants in Cohort 1., Parts A and B: Additional Secondary Efficacy Endpoints at Each Scheduled Visit Over the Duration of the Open-Label Period • PASI-75 response: Proportion of participants achieving PASI-75. • PASI-90 response: Proportion of participants achieving PASI-90. • PASI-100 response: Proportion of participants achieving PASI-100., • sPGA 0/1 response: Proportion of participants achieving an sPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline. • Enhanced sPGA response: Proportion of participants achieving an sPGA of clear (0)., • ssPGA response: Proportion of participants achieving an ssPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline for participants with a baseline ssPGA ≥3. • Change and percent change from baseline in BSA affected by psoriasis., • DLQI response: Proportion of participants with a DLQI score of 0/1 (for participants with a baseline DLQI score ≥2). • CDLQI response: Proportion of participants with a CDLQI score of 0/1 (for participants with a baseline CDLQI score ≥2)., • Change from baseline in DLQI. • Change from baseline in CDLQI., Part A (Cohort 1 only): Additional Secondary Efficacy Endpoints at Each Scheduled Visit Over the Duration of the Open- Label Period • Itch NRS responses: Proportions of participants achieving a ≥4-point improvement in Itch NRS for participants in Cohort 1 who had an itch NRS ≥4 at baseline. • Change and percent change from baseline in Itch NRS for participants in Cohort 1., Part A: Additional Secondary PK Endpoint • Plasma concentrations of zasocitinib in participants receiving active treatment., Part B: Additional Secondary Endpoint • Acceptability/palatability assessment scores. Age of participants: 0-17 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 54 Sponsor: Takeda Development Center Americas Inc. Sponsor type: Pharmaceutical company Trial product: ZASOCITINIB, Matching Placebo for TAK-279 Results posted: No Overall decision date: 01/04/2026 Countries decision date: DE: 07/04/2026, IT: 01/04/2026, ES: 06/04/2026, PL: 03/04/2026 Last updated date: 22/06/2026View the full article

Trial number: 2025-522567-15-00 Overall trial status: Ongoing, recruiting Trial title: A Phase 3, Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial to Evaluate the Efficacy, Safety, Tolerability, and Pharmacokinetics of Zasocitinib in Pediatric Participants Aged 4 to Less Than 18 Years With Moderate-to-Severe Plaque Psoriasis Medical conditions: Plaque Psoriasis Status in each country: Spain:Authorised, recruiting, Poland:Ongoing, recruiting, Germany:Ongoing, recruiting, Italy:Authorised, recruitment pending Trial phase: Therapeutic confirmatory (Phase III) Therapeutic Areas: Diseases [C] - Skin and Connective Tissue Diseases [C17] Primary end point: Part A: Coprimary Endpoints (vs Placebo) at Week 16 • sPGA 0/1 response: Proportion of participants achieving an sPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline. • PASI-75 response: Proportion of participants achieving ≥75% improvement from baseline in PASI score. Part A Cohort 1: Includes adolescent participants aged 12 to <18 years. Part A Cohort 2: Includes children participants aged 4 to <12 years., Part B: PK Primary Endpoints • PK parameters (that is Cmax, Tmax, AUC0-Last) of zasocitinib on Day 7. Part B: Includes only children participants aged 4 to <12 years. Part B participants will be separate from Part A Cohort 2 participants. Secondary end point: Part A: Key Secondary Efficacy Endpoints (vs Placebo) at Week 16 • PASI-90 response: Proportion of participants achieving PASI-90. • Enhanced sPGA response: Proportion of participants achieving an sPGA of clear (0). • PASI-100 response: Proportion of participants achieving PASI-100., Part A: Additional Secondary Efficacy Endpoints (vs Placebo) at Week 16 • ssPGA response: Proportion of participants achieving an ssPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline for participants with a baseline ssPGA ≥3. • Change and percent change from baseline in BSA affected by psoriasis., • DLQI response: Proportion of participants with a DLQI score of 0/1 (for participants with a baseline DLQI score ≥2). • CDLQI response: Proportion of participants with a CDLQI score of 0/1 (for participants with a baseline CDLQI score ≥2). • Change from baseline in DLQI. • Change from baseline in CDLQI., Part A (Cohort 1 only): Additional Secondary Efficacy Endpoints (vs Placebo) at Week 16 • Itch NRS response: Proportions of participants achieving a ≥4-point improvement in Itch NRS for participants in Cohort 1 who had an itch NRS ≥4 at baseline. • Change and percent change from baseline in Itch NRS for participants in Cohort 1., Parts A and B: Additional Secondary Efficacy Endpoints at Each Scheduled Visit Over the Duration of the Open-Label Period • PASI-75 response: Proportion of participants achieving PASI-75. • PASI-90 response: Proportion of participants achieving PASI-90. • PASI-100 response: Proportion of participants achieving PASI-100., • sPGA 0/1 response: Proportion of participants achieving an sPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline. • Enhanced sPGA response: Proportion of participants achieving an sPGA of clear (0)., • ssPGA response: Proportion of participants achieving an ssPGA of clear (0) or almost clear (1) with a ≥2-point decrease from baseline for participants with a baseline ssPGA ≥3. • Change and percent change from baseline in BSA affected by psoriasis., • DLQI response: Proportion of participants with a DLQI score of 0/1 (for participants with a baseline DLQI score ≥2). • CDLQI response: Proportion of participants with a CDLQI score of 0/1 (for participants with a baseline CDLQI score ≥2)., • Change from baseline in DLQI. • Change from baseline in CDLQI., Part A (Cohort 1 only): Additional Secondary Efficacy Endpoints at Each Scheduled Visit Over the Duration of the Open- Label Period • Itch NRS responses: Proportions of participants achieving a ≥4-point improvement in Itch NRS for participants in Cohort 1 who had an itch NRS ≥4 at baseline. • Change and percent change from baseline in Itch NRS for participants in Cohort 1., Part A: Additional Secondary PK Endpoint • Plasma concentrations of zasocitinib in participants receiving active treatment., Part B: Additional Secondary Endpoint • Acceptability/palatability assessment scores. Age of participants: 0-17 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 54 Sponsor: Takeda Development Center Americas Inc. Sponsor type: Pharmaceutical company Trial product: ZASOCITINIB, Matching Placebo for TAK-279 Results posted: No Overall decision date: 01/04/2026 Countries decision date: DE: 07/04/2026, IT: 01/04/2026, ES: 06/04/2026, PL: 03/04/2026 Last updated date: 22/06/2026Den kompletten Artikel zeigen

### Suchtverhalten bei chronischen Hauterkrankungen Die Übersicht zeigt: Suchtverhalten kommt bei Menschen mit chronisch‑entzündlichen Hauterkrankungen wie Psoriasis häufiger vor als in der Allgemeinbevölkerung.[1][4][7] Dazu gehören Rauchen, Alkohol, Medikamente und Essverhalten, aber auch Internet und Glücksspiel.[1][7] Diese Suchtformen können Schwere der Hauterkrankung, Therapieerfolg und Lebensqualität deutlich beeinflussen.[1][4] Die Autorinnen empfehlen, Sucht systematisch in der Hautarztpraxis zu erfassen, auch nach Alter und Geschlecht differenziert.[1] Das bedeutet für Euch: Die Haut soll nicht mehr getrennt von Psyche und Sucht betrachtet werden. Ihr dürft erwarten, dass Ärztinnen aktiv nach Belastungen fragen und bei Bedarf an Psychotherapie oder Suchtberatung vermitteln.[1][4] Für den Alltag heißt das: Achtet gut auf Euer Rauchen, Euren Alkoholkonsum, Essen, Medikamente oder Gaming. Wenn Ihr das Gefühl habt, die Kontrolle zu verlieren, sprecht es in der Sprechstunde offen an. Früh Hilfe zu holen kann Eure Haut und Euren Alltag entlasten.[4][6] Originaltitel: Addiction in chronic inflammatory skin diseases: A systematic review of prevalence, impact and screening practices - PubMed Link zur Quelle

Die Übersichtsarbeit zeigt: Bei chronisch entzündlichen Hauterkrankungen wie Psoriasis treten **Nikotin**‑ und **Alkoholkonsum** sowie andere **Suchtformen** häufiger auf als in der Allgemeinbevölkerung.[2][3] ### Was heißt das für euch? Rauchen und viel Alkohol können Entzündungen verstärken und Therapien schwächen.[2] Das kann Plaques und Schmerzen verschlimmern.[8] Die Forschenden betonen: Haut und Psyche hängen eng zusammen.[1] Belastung durch Juckreiz und Aussehen und soziale Probleme kann dazu führen dass ihr zu Alkohol, Nikotin oder anderen Gewohnheiten greift.[1][5] Wichtig ist dass ihr mit euren Ärztinnen und Ärzten offen über euren Konsum sprecht.[2][3] So können sie euch passende Hilfe anbieten, zum Beispiel Psychotherapie oder Suchtberatung.[3][7] Im Alltag helfen kleine Schritte: Stress senken und Entspannung üben und Unterstützung annehmen.[1][6] Ihr müsst das nicht allein schaffen. Originaltitel: emJournal of the European Academy of Dermatology and Venereology/em | Wiley Online Library Link zur Quelle