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Psoriasis is a chronic inflammatory skin disease that forms a vicious cycle with psychological stress. Whether and how the hypothalamic-pituitary (HP) axis-mediated neuroendocrine system regulates psoriasis remains obscure. Here, we report elevated levels of the pituitary hormone prolactin (PRL) in both psoriasis patients and imiquimod (IMQ)-induced psoriasis mice. Mechanistically, PRL acts on dermal PRLR-expressing fibroblasts to promote the production of the chemokines CCL2 and CCL7, which then recruit monocytes/macrophages into psoriatic lesional skin, thereby activating local IL-17A-producing T cells. Accordingly, pharmacological targeting of PRL signaling inhibits the recruitment of monocytes/macrophages, decreases the frequency of IL-17A-producing T cells, and alleviates IMQ-induced psoriasis in mice. In summary, our results delineate a mechanism by which the neuroendocrine hormone PRL aggravates psoriasis and highlight a potential therapeutic strategy of inhibiting PRL-PRLR signaling, particularly in psoriasis patients experiencing psychological stress.Weiterlesen

Psoriasis is a chronic, complex immune-mediated inflammatory disorder with cutaneous and systemic manifestations in which keratinocytes, dendritic cells and T cells have central roles. UBE2L3 may be a protective biomarker that regulates the pathogenesis of psoriasis. Here, we identify the IL-17A signaling similarity between human psoriatic skin and Ube2l3 conditional knockout mouse skin in the epidermis rather than dermis. IL-17A is regulated by CXCR6+ Vγ2+ γδT cells in mouse while CXCR6+ CD8+ T cells in human. CXCL16 is the only chemokine that binds to and stimulates CXCR6. Ube2l3 reduction in keratinocytes activates IL-1β and then promotes CXCL16 expression through STAT3 signaling. Up-regulated CXCL16 in keratinocytes and cDC2/mDC then attracts Vγ2+ γδT17 or CD8+ T cells to secrete IL-17A and form a positive feedback loop in keratinocytes supporting psoriatic lesions. Thus, UBE2L3 is a keratinocyte-intrinsic suppressor of epidermal IL-17 production in Vγ2+ γδT cells in mouse and CD8+ T cells in human through the CXCL16/CXCR6 signaling pathway in psoriasis.Weiterlesen

Inflammatory monocytes are increasingly recognized as key amplifiers of psoriasis, yet the epigenetic drivers of their pathogenic signature remain unclear. Here, we demonstrate that the histone demethylase KDM6B is markedly upregulated and catalytically active in classical monocytes during the imiquimod (IMQ)-induced psoriasis model. This is associated with reduced levels of the repressive histone mark H3K27me3, an epigenetic modification linked to chromatin compaction and transcriptional silencing, at the Il1b, Tnf, Pgam1, Pgk1, and Aldoa promoters, together with an enhanced inflammatory and glycolytic gene signature. Pharmacological blockade of KDM6B after disease onset using GSK-J4, a cell-permeable prodrug that is intracellularly converted to the active KDM6B inhibitor GSK-J1, restores H3K27me3 at inflammatory and metabolic loci, suppresses Il1b/Tnf transcription, normalizes bioenergetic profiles, and reduces monocyte and neutrophil recruitment to the inflamed skin. Single-cell transcriptomic profiling further reveals that KDM6B inhibition represses cytokine-mediated signaling, glycolysis, and chemotaxis pathways in monocytes, yet enriches antigen presentation modules, consistent with a shift toward a homeostatic, antigen-presenting surveillance program in myeloid cells and a Treg-supportive milieu. Collectively, our data identify KDM6B as an epigenetic-metabolic switch that sustains monocyte-driven inflammation in the IMQ-induced psoriasis model. Importantly, we provide preclinical evidence that targeting KDM6B can reduce maladaptive inflammatory response even in progressed diseases. These findings propose KDM6B inhibitors as a promising adjunct to current biologics for psoriasis and other myeloid-driven autoinflammatory disorders.Weiterlesen

IntroductionPsoriatic arthritis (PsA) presents various imaging abnormalities in joints and diverse nail changes, but the link between nail and joint findings remains unclear. This study aimed to gain a better understanding of the relationships between nail manifestations and abnormal articular architectures by investigating the associations between nail abnormalities and articular findings in PsA-affected interphalangeal joints.MethodsA total of 106 nails adjacent to PsA-affected distal interphalangeal joints were examined in 29 patients who underwent comprehensive systemic evaluation and imaging for the diagnosis and treatment of PsA. Imaging studies, including X-ray, magnetic resonance imaging, and iodine-enhanced dual-energy computed tomography, were conducted to examine the acral joints.ResultsNail manifestations were observed in 81 among 106 fingers or toes (76.4%). Pitting, the most common nail finding (75/106, 70.8%), was observed in isolation on 22/75 nails (29.3%), while other nail manifestations were observed in isolation on ≤ 3/50 nails (6.0%). Among the 81 examined nail lesions, 49 (61.3%) preceded the onset of articular symptoms in the adjacent interphalangeal joints, 9 (11.2%) followed the joint symptoms, and 23 (28.8%) occurred simultaneously. Articular bone findings, such as bone erosion and bone proliferation, were positively associated with subungual hyperkeratosis, leukonychia, crumbling, and/or transverse grooves. In contrast, soft tissue findings, including tenosynovitis, synovitis, and periarthritis, were negatively associated with onycholysis, subungual hyperkeratosis, leukonychia, and/or pitting.ConclusionThe study suggests that nail manifestations may be positively associated with bone abnormalities and negatively associated with soft tissue inflammation in PsA. Nail examinations may help estimate articular conditions. Key points • More than 60% of nail manifestations precede the onset of articular symptoms in the adjacent interphalangeal joints. • Nail manifestations may be positively associated with bone abnormalities and negatively with soft tissue inflammation in PsA. • Nail examination may aid in estimating articular status, prompting appropriate evaluation and early treatment for the affected joints.Weiterlesen

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No abstract supplied.Weiterlesen

ObjectivesPsoriatic arthritis (PsA) increases cardiovascular disease risk. Emerging evidence suggests biologic Disease-Modifying Antirheumatic Drugs (DMARDs) may offer protective effects, though their advantage over conventional therapy remains under investigation.MethodsA retrospective cohort study was conducted using the Chang Gung Memorial Research Database in Taiwan. Patients with PsA were identified from 2001 to 2022. The study included 2,383 patients who had used at least one disease-modifying antirheumatic drugs (DMARDs), divided into two groups: 1,190 on bDMARDs and 1,193 on conventional DMARDs (cDMARDs). The primary outcome was defined as a major adverse cardiovascular event (MACE), including stroke, myocardial infarction, cardiovascular mortality or coronary revascularization. Potential confounding was mitigated using inverse probability of treatment weighting.ResultsThe average follow-up period was 5.1 years for the bDMARD group and 5.0 years for the cDMARD group. The incidence of MACE was 0.34 and 0.55 events per 100 person-years in the bDMARDs and cDMARDs groups, respectively. All-cause mortality occurred at rates of 0.73 and 1.86 per 100 person-years in the bDMARDs and cDMARDs groups, respectively. The results showed that the bDMARDs group had lower risks of MACE (hazard ratio [HR]: 0.65; 95% confidence interval [CI]: 0.43-0.96), all-cause mortality (HR: 0.44; 95% CI: 0.35-0.57) and cardiovascular mortality (HR: 0.54; 95% CI: 0.32-0.92), but a higher incidence of infection-related admission (subdistribution HR: 1.45; 95% CI: 1.18-1.78).ConclusionsbDMARDs may reduce cardiovascular events and mortality in PsA, but infection risks warrant close monitoring. Further research is needed to refine treatment strategies.Weiterlesen

IntroductionTargeted biologic therapies have transformed outcomes for individuals with psoriasis, a common immune-mediated inflammatory skin disease. The widespread use of these highly effective treatments has led to a growing number of individuals with clear or nearly clear skin remaining on continuous, long-term treatment. Personalised strategies to minimise drug exposure may sustain long-term disease control while reducing treatment burden, associated risks and healthcare costs. This study aims to evaluate the feasibility of a definitive pragmatic effectiveness trial of two personalised dose minimisation strategies compared with continuous treatment (standard care) in adults with well-controlled psoriasis receiving the exemplar biologic risankizumab.Methods and analysisThis is a multicentre, assessor-blind, parallel group, open-label randomised controlled feasibility trial in the UK, evaluating two personalised biologic dose minimisation strategies for psoriasis. 90 adults with both physician-assessed and patient-assessed clear or nearly clear skin on risankizumab monotherapy for ≥12 months will be randomised in a 1:1:1 ratio to (1) patient-led 'as-needed' treatment, where risankizumab is administered at the first sign of self-assessed psoriasis recurrence, (2) therapeutic drug monitoring-guided treatment, with personalised dosing intervals determined using a pharmacokinetic model or (3) continuous treatment as per standard care, for 12 months. Participants will be invited to submit self-reported outcomes and self-taken photographs every 3 months using a bespoke remote monitoring system (mySkin app) and will attend an in-person assessment at 12 months. They may also request additional patient-initiated follow-up appointments during the trial if needed. The primary outcome is the practicality and acceptability of the two personalised biologic dose minimisation strategies, assessed as a composite measure including recruitment and retention rates, adherence to the assigned strategies and acceptability to both patients and clinicians. The feasibility of collecting healthcare cost and resource utilisation data will also be evaluated to inform a future cost-effectiveness analysis. A nested qualitative study, involving semistructured interviews with patients and clinicians, will explore perspectives on the personalised biologic dose minimisation strategies. These findings will inform the design of a future definitive trial.Ethics and disseminationThis study received ethical approval from the Seasonal Research Ethics Committee (reference 24/LO/0089). Results will be disseminated through scientific conferences, peer-reviewed publications and patient/public engagement events. Lay summaries and infographics will be codeveloped with patient partners to ensure the findings are accessible for the wider public.Trial registration numberISRCTN17922845.Weiterlesen

ObjectivesThis is a protocol for a Cochrane Review (intervention). The objectives are as follows: To investigate the benefits and harms of dose reduction and discontinuation of conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) in adults with rheumatoid arthritis or psoriatic arthritis, who have been in sustained remission or low disease activity. This is a common review protocol, outlining the approach for two separate Cochrane reviews for people with rheumatoid arthritis or psoriatic arthritis. Dose reduction or discontinuation of csDMARDs in adults with rheumatoid arthritis, who have been in sustained remission or low disease activity Dose reduction or discontinuation of csDMARDs in adults with psoriatic arthritis, who have been in sustained remission or low disease activity.Weiterlesen

Background and objectivesImproved understanding of the immunopathogenesis of psoriasis has led to the development of effective targeted therapies, but patients who respond to treatment without total skin clearance have residual disease. The aim of this study was to demonstrate the existence of specific residual disease (or residual PASI) anatomical localizations related to different biologic agents.Methods and patientsThis retrospective, observational, multi-center study analyzed clinical data of patients affected by psoriasis who had received biologic treatments for at least 6 months. The data analysis focused on patients with residual PASI.ResultsA total of 228 of 1,000 patients showed residual disease despite achieving PASI 90 at weeks 24-28 of biologic treatment. The anatomical sites most frequently involved in residual disease were the lower limbs (44.3%). We observed differences among the biologic agents in terms of frequency and localization of residual disease. The localization of residual skin lesions to lower limbs was associated with treatment switching/interruption. The drugs with the highest and lowest proportion of patients with residual disease in the lower limbs were, respectively, secukinumab and risankizumab.ConclusionsTreatment with anti-IL-17 and anti-IL-23 drugs is characterized by the persistence of residual skin lesions with differences in terms of frequency and anatomical localizations.Weiterlesen

IntroductionDifficult-to-treat psoriatic arthritis (D2T-PsA) is increasingly recognized as a complex clinical entity characterized by persistent disease burden despite multiple targeted therapies. Its identification is essential to improve patient outcomes and to guide the development of new therapeutic strategies.Areas coveredIn this perspective article, we discuss the evolving concept of D2T-PsA, including its epidemiology, clinical characterization, and underlying pathophysiological mechanisms. We highlight the role of gender differences, psychosocial comorbidities, and central sensitization in shaping disease persistence and patient-reported impact. We also examine the limitations of current disease activity indices (DAPSA, PsAID, PASDAS) in capturing heterogeneity and the need for multidimensional frameworks. A structured literature search was conducted in PubMed/MEDLINE and Scopus databases (January 2020-June 2025), restricted to English-language publications, using combinations of the terms psoriatic arthritis, difficult-to-treat, refractory, and difficult-to-manage. Additional references were identified from conference abstracts and relevant bibliographies.Expert opinionRecognizing D2T-PsA as a distinct, multifactorial entity is critical to advancing personalized medicine. Future directions will involve harmonizing EULAR and GRAPPA frameworks, integrating biomarker discovery, digital tools, and adaptive trial designs, and embedding patient perspectives. This multidimensional approach is expected to transform treatment from empirical cycling toward precision care in psoriatic arthritis.Weiterlesen

BackgroundPsoriasis is associated with increased risk of depression. Although cognitive behavioral therapy (CBT) is an evidence-based treatment, access remains limited.ObjectivesTo evaluate the feasibility, acceptability, and preliminary efficacy of a smartphone-delivered, coach-led CBT program for depression among individuals with psoriasis.MethodsThis single-arm, 8-week pilot study (Mindset trial, NCT06216691) enrolled adults with psoriasis and at least mild depressive symptoms (PHQ-9 ≥5). Participants engaged in a smartphone-based CBT program guided by bachelor's-level lay coaches. Primary outcomes were feasibility as evaluated by module completion and acceptability as evaluated by the Client Satisfaction Questionnaire-8 (CSQ-8]) and User Version of the Mobile Application Rating Scale (uMARS). Secondary outcomes included changes in the Patient Health Questionnaire-9 (PHQ-9), General Anxiety Disorder-7 (GAD-7), Appearance Anxiety Inventory, Skindex-16, and Psoriasis Symptom Inventory.ResultsOf 30 participants, 63.3% completed ≥4/8 modules and 43.3% completed ≥6/8 modules. Mean CSQ-8 and uMARS scores were 27.2 (SD 4.5) and 4.0 (SD 0.7), respectively, supporting high satisfaction. Statistically and clinically significant improvements were observed in PHQ-9 (mean change -4.4; Cohen's d = 0.92), GAD-7 (-2.8; d = 0.63), and Skindex-16 symptoms (5.0; d = 0.78), emotions (10.0; d = 0.95), and functioning (6.4; Cohen's d = 0.71) subscales as well as the Psoriasis Symptom Inventory (3.1; d = 0.43).ConclusionsThis study supports the feasibility, acceptability, and preliminary efficacy of smartphone-delivered CBT for individuals with psoriasis and depressive symptoms. Given the scalability of this model, future randomized trials are warranted to assess broader effectiveness in dermatology care settings.Weiterlesen

BackgroundPsoriasis is a chronic inflammatory skin disease, and the risk of developing cancer has been postulated due to the presence of several plausible underlying mechanisms. Understanding the association between psoriasis and cancer is imperative to the provision of optimal psoriasis care.ObjectivesTo examine the risk of developing cancer in individuals with psoriasis.MethodsPopulation-based cohort studies were conducted in Denmark, England, Israel, and Taiwan through the use of linked electronic health records. Individuals aged at least 18 years of age with a diagnosis of psoriasis in the country-specific study period were matched to up to 6 comparators with no record of psoriasis prior to index date. Country-specific hazard ratios for the risk of cancer development overall and for 26 site-specific cancers between individuals with and without psoriasis were calculated through Cox regression. Country-specific estimates were pooled using random effects modelling.ResultsWe included 702,022 individuals with psoriasis and 4,185,342 matched comparators. In models implicitly controlled for age, sex and calendar time by matching, there was a small association between psoriasis and cancer overall (pooled HR [pHR]:1.08;95%CI, 1.04-1.13; I2= 92.4%). Adjustment for potential confounding factors resulted in a slight attenuation of risk (pHR:1.05; 95%CI, 1.01-1.09; I2=81.2%). When restricted to those with moderate-to-severe psoriasis, the risk of cancer overall was slightly higher (pHR:1.16;95%CI, 1.04-1.28; I2=92.8%) and confounder adjusted models (pHR: 1.09;95%CI, 1.03-1.15; I2=60.6%). Associations with psoriasis were present for oral cavity (pHR: 1.29; 95%CI, 1.12-1.47; I2=55.4%), pharynx (pHR:1.30;95%CI, 1.07-1.58; I2=58.4%), oesophagus (pHR:1.17;95%CI, 1.03-1.33; I2=56.6%), liver (pHR:1.53;95%CI, 1.33-1.77; I2=75.1%), pancreas (pHR:1.09;95%CI, 1.02-1.17; I2=0.0%), kidney (pHR:1.19;95%CI, 1.11-1.27; I2=0.0%), bladder (pHR: 1.13; 95%CI, 1.06-1.20; I2=28.7%), and keratinocyte cancers (pHR:1.37;95%CI, 1.16-1.63; I2=97.5%), Hodgkin lymphoma (pHR:1.56;95%CI, 1.16-2.11; I2=69.7%), non-Hodgkin lymphoma (pHR:1.16;95%CI, 1.07-1.26; I2=35.5%) and leukaemia (pHR:1.18; 95%CI, 1.08-1.29; I2=41.9%). Site-specific associations generally persisted, with slight risk exacerbations and additional associations for lung and ovarian cancers, when limited to people with moderate-to-severe psoriasis.ConclusionPsoriasis was associated with an increased risk of developing 14 of 26 investigated site-specific cancers, including cancers with poor prognosis, such as liver, lung, and oesophageal cancer. Our findings can be used to reinforce cancer prevention strategies in psoriasis care.Weiterlesen

No abstract supplied.Weiterlesen

Dysregulated copper homeostasis is implicated in inflammatory skin diseases such as psoriasis and atopic dermatitis (AD), but the role of cuproptosis remains poorly defined. This study aimed to elucidate the role and mechanism of cuproptosis in inflammatory skin diseases. Transcriptome analysis of patient lesions revealed significant alterations in cuproptosis-related genes correlating with disease-specific pathological features. These cuproptosis-related gene expression signatures demonstrated strong clinical relevance to therapeutic efficacy in both psoriasis and AD cohorts. Functional validation using disease models showed that pharmacologically inhibiting cuproptosis with the copper chelator tetrathiomolybdate (TTM), or genetically knocking down the copper importer SLC31A1, effectively alleviated chronic skin inflammation and hallmark pathological changes induced by imiquimod (IMQ) or calcipotriol (MC903). Mechanistically, we uncovered that SLC31A1-mediated cuproptosis promotes intracellular α-ketoglutarate (α-KG) accumulation, driving activation of the lysine demethylase KDM5B. Activated KDM5B specifically demethylates H3K4me3 marks at the promoter of the ferroptosis regulator ferritin heavy chain 1 (FTH1), suppressing its transcription and consequently sensitizing keratinocytes to ferroptotic cell death, thereby amplifying inflammatory tissue damage. Our findings establish a fundamental pathogenic SLC31A1/KDM5B/FTH1 molecular axis linking dysregulated copper metabolism and cuproptosis to ferroptosis execution in psoriasis and AD, providing significant mechanistic insights and pinpointing promising therapeutic targets for these refractory skin disorders.Weiterlesen

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No abstract supplied.Weiterlesen

BackgroundWhile clinical examination remains the diagnostic cornerstone for psoriasis, there is a relative lack of objective, quantitative biomarkers to complement clinical assessment for tracking disease severity and monitoring therapeutic response. We evaluated serum SCCA's utility in identifying psoriasis and assessing its severity across demographic (gender, age) and clinical (comorbidity) subgroups, and its association with therapeutic responses.MethodsA total of 181 adult (≥18 years old) patients with newly diagnosed psoriasis were included in the disease group; 385 patients with other skin-related diseases and 658 healthy adults were included as controls. Patients diagnosed with tumors or renal failure were excluded. Serum SCCA was determined using Roche Cobas e 801 analyzer (Roche, Basel, Switzerland). Dynamic analysis was performed to evaluate the significance of serum SCCA in monitoring psoriasis treatment response.ResultsSerum SCCA levels in psoriasis patients were mainly affected by gender and concomitant diseases. Notably, SCCA demonstrated high diagnostic accuracy (AUC: 0.89-0.90) in patients with comorbidities, with sex-specific cutoffs. The cutoff value of serum SCCA for identifying severe psoriasis was 2.64 ng/mL with an AUC greater than 0.9 and an NPV over 95 %. Serum SCCA levels were significantly correlated with the psoriasis area and severity index (PASI) and body surface area (BSA) both before and after treatment. The median decrease rate of serum SCCA was close to 50 % at >5 days post-treatment and 60 % at >10 days post-treatment.ConclusionsSerum SCCA shows promise as a reliable, complementary biomarker for the severity assessment and treatment monitoring of psoriasis. Its application for identification purposes should be stratified by sex and comorbidities.Weiterlesen

Celastrol(CE) has been investigated for its prophylactic and anti-inflammatory effects in various inflammatory and autoimmune diseases like psoriasis. However, poor water solubility, low bioavailability, and high toxicity, have limited its application The objective of this study is to design and synthesize a gelatin-based CE prodrug polymer which can self-assemble into nanoparticles, encapsulating CE to improve its aqueous solubility. Two gelatin derivatives with opposite charges were synthesized through a condensation reaction. CE prodrug nanoparticles were formed by coupling CE to these two gelatin derivatives using dynamic chemical bonding: C-S bonds and borate bonds. The resulting nanoparticles(G-C-G) had an average particle size of approximately 147.15 ± 8.25 nm, and a drug loading capacity (DL) of 1.52 ± 0.25%. The transdermal penetration of nanoparticles (G-C-G) was found to be improved compared to free CE in vitro. In a mouse model of psoriasis, nanoparticles G-C-G resulted in a reduction of erythema, scaly epidermal symptoms, spleen weight, and cytokine levels, including IL-17 and IL-23, indicating high therapeutic potential for psoriasis. In conclusion, CE prodrug nanoparticles (G-C-G) increase the water solubility and skin permeability of free CE, making it a potential therapeutic agent for psoriasis.Weiterlesen

BackgroundPsoriasis a chronic inflammatory skin disease, poses a substantial economic burden on healthcare systems globally. This study examines psoriasis consultations from the provider's perspective within a dermatology department, aiming to generate detailed cost data to support value-based care. Specifically, it investigates the drivers of consultation-level cost variability, explores opportunities for efficiency, and also estimates one-year treatment costs to inform the development of bundled payment models. The goal is to highlight the importance of patient cost transparency and improving cost structures in chronic disease settings.MethodsUsing Time-Driven Activity-Based Costing (TD-ABC), treatment costs associated with nurses, doctors, and total visits for 127 patients with mild and moderate forms of psoriasis were measured. Financial data was collected in collaboration with the hospital's financial department. During consultations, nurses and physicians recorded time and patient-related information. Additional or missing details were retrieved from patient medical files. Descriptive analyses assessed mean costs and variability by patient and disease characteristics.Independent variablestherapy type, patient status (new vs. returning), comorbidities, and treatment changes, were stratified to compare cost differences across groups.ResultsMean consultation costs were €55, with a minimum and maximum of €25 and €110. New patients incurred 40% higher costs than returning ones, mainly due to longer interactions with nurses and physicians. Key cost drivers for a total consultation included patient status, personality traits, nurse experience, and therapy switches. Physician consultations were particularly impacted by treatment changes and patient engagement levels. Annual treatment costs varied substantially by medication type: topical treatments averaged €325 per year, systemic treatments €1,353, and biological therapies €11,920, highlighting the significant impact of medication choice on overall expenses.ConclusionsThis study highlighted substantial variability in consultation and yearly treatment costs for psoriasis patients. These findings emphasized the critical need for detailed cost data to optimise departmental workflows, support efficient resource allocation, and inform the design of equitable bundled payment models. Improving cost transparency was shown to strengthen clinical and financial decision-making. Future research was recommended to explore the cost implications of comorbidities and to extend benchmarking efforts across dermatology settings to guide system-wide improvements in care delivery and sustainability.Weiterlesen

Forschende sind optimistisch: Eine dauerhafte Heilung der Psoriasis könnte bald möglich sein. Bisher wirken Antikörper-Therapien sehr gut, sie stoppen die Entzündung fast komplett. Das Problem ist, dass man diese Mittel lebenslang nehmen muss. Setzt man sie ab, kehrt die Schuppenflechte oft schnell zurück[1]. Es gibt aber Ausnahmen: Manche Menschen bleiben auch nach dem Absetzen jahrelang beschwerdefrei. Forschende hoffen, mit neuen Methoden genau das für viele zu erreichen. Besonders spannend ist, dass man gezielt Zellen beeinflussen kann, die sich das „Kranksein“ merken. Wird dieses Gedächtnis gelöscht, könnte die Haut gesund bleiben, auch ohne ständige Medikamente[1]. In den nächsten zehn Jahren könnte aus dieser Forschung tatsächlich eine richtige Heilung entstehen, meinen Expertinnen und Experten[1]. Originaltitel: A psoriasis cure could be in touching distance Link zur Quelle

In der INSPIRE 1-Studie wird untersucht, wie wirksam und sicher Tildrakizumab bei Erwachsenen mit aktiver Psoriasis-Arthritis ist, die bereits mit Anti-TNF-Medikamenten behandelt wurden, aber weiterhin Beschwerden haben. Die Studie ist eine große, internationale Phase-III-Studie, bei der die Teilnehmenden entweder Tildrakizumab oder ein Placebo als Injektion erhalten. Ziel ist es, nach 24 Wochen zu prüfen, wie viele Patientinnen und Patienten eine spürbare Verbesserung ihrer Gelenkbeschwerden erreichen (ACR20-Response). Die bisherigen Ergebnisse zeigen, dass Tildrakizumab die Symptome der Psoriasis-Arthritis im Vergleich zum Placebo deutlich verbessert und dabei ein bekanntes, gutes Sicherheitsprofil aufweist. Tildrakizumab ist ein sogenannter monoklonaler Antikörper, der gezielt den Botenstoff Interleukin-23 (IL-23) blockiert. IL-23 spielt eine wichtige Rolle bei Entzündungsprozessen im Körper, insbesondere bei Autoimmunerkrankungen wie Psoriasis und Psoriasis-Arthritis. Durch die Hemmung von IL-23 kann Tildrakizumab die Entzündung und die damit verbundenen Beschwerden wie Gelenkschmerzen und Hautveränderungen lindern. Das Medikament wird bereits zur Behandlung der Schuppenflechte (Plaque-Psoriasis) eingesetzt und wird als Fertigspritze unter die Haut gespritzt. Originaltitel: A Phase III, Randomized, Double-Blind, Placebo-Controlled Study to Demonstrate the Efficacy and Safety of Tildrakizumab in Anti-TNF Experienced Subjects with Active Psoriatic Arthritis I (INSPIRE 1) Erkrankung: Psoriasis-Arthritis Phase: III Firma: Sun Pharmaceutical Industries Limited Art der Verabreichung: Injektion (Fertigspritze, subkutan) https://euclinicaltrials.eu/search-for-clinical-trials/?lang=en&EUCT=2023-507415-35-00

## Kontinuierliche Behandlung mit Biologika Bei der Behandlung von Psoriasis wird eine kontinuierliche Therapie mit Biologika empfohlen. Diese Medikamente sind bei der Behandlung der Schuppenflechte sehr wirksam, da sie direkt auf das Immunsystem eingreifen und Entzündungen reduzieren[1][2]. Beliebte Biologika sind IL-17- (z.B. Ixekizumab, Secukinumab) und IL-23-Inhibitoren (z.B. Guselkumab, Risankizumab), die eine schnelle Symptomlinderung bieten[3]. ## Unterbrechungen in der Behandlung In der Praxis kommt es jedoch häufig zu Unterbrechungen der Behandlung. Diese können verschiedene Gründe haben und sind nicht immer medizinisch bedingt. Solche Unterbrechungen können zu schnellen Rezidiven der Psoriasis führen, was die Behandlung erschwert[3]. Es ist wichtig, dass Patienten mit ihrem Arzt besprechen, wie sie ihre Behandlung am besten fortsetzen können. ## Optimierung der Behandlung Um die Behandlung zu optimieren, ist es entscheidend, die richtigen Biologika für den individuellen Patienten auszuwählen. Neuere Studien zeigen, dass eine Anpassung der Therapie an die spezifischen Bedürfnisse des Patienten zu besseren Ergebnissen führt[2][5]. Originaltitel: Optimierung von Biologika bei chronischer Plaque‐Psoriasis: Einblicke zu nichtmedizinischen Unterbrechungen von IL‐17‐, IL‐12/23‐ und IL‐23‐Inhibitoren Link zur Quelle

Biologische Therapien bei Psoriasis haben bestimmte anatomische Unterschiede in der verbleibenden Krankheitsaktivität, die als residueller PASI-Wert bezeichnet wird. Eine Studie hat gezeigt, dass trotz erfolgreicher Behandlung mit biologischen Medikamenten bei 228 von 1000 Patienten nach 24 bis 28 Wochen noch Hauterkrankungen verblieben sind. Die unteren Gliedmaßen waren am häufigsten betroffen (44,3%). Es wurden Unterschiede in der Häufigkeit und dem Ort der verbleibenden Erscheinungen zwischen verschiedenen biologischen Medikamenten beobachtet. Secukinumab hatte den höchsten und Risankizumab den niedrigsten Anteil an Patienten mit verbleibender Krankheitsaktivität an den unteren Gliedmaßen. Dies führte häufig zu Behandlungswechseln oder -unterbrechungen. Originaltitel: Biologic treatments for psoriasis have different anatomical specificities in residual PASI. Link zur Quelle