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Psoriasis and psoriatic arthritis (PsA) are chronic immune-mediated inflammatory diseases associated with obesity, cardiometabolic disease, and mortality. The glucagon-like peptide-1 (GLP1) pathway has emerged as a key factor in the development of obesity and cardiometabolic disease. GLP1 receptor agonists demonstrably improve insulin resistance, dyslipidemia, obesity, and mortality, with emerging evidence suggesting potential benefit for psoriasis. To evaluate whether GLP1 biology influences psoriatic disease risk, we conducted a Mendelian randomization study. A 22-variant cis-eQTL genetic instrument for GLP1R expression in whole blood from the eQTLGen consortium was generated as a proxy for GLP1R pathway activity (n=31,684). Genetic proxies of GLP1R expression were associated with a lower risk of psoriasis (OR=0.723, 95% CI 0.678-0.771, p=1.08×10 −22 ) and PsA (OR=0.483, 95% CI 0.402-0.580, p=5.33×10 −15 ) in European-ancestry GWAS meta-analyses. Effects persisted after adjustment for genetic proxies of central adiposity, HbA1c, LDL cholesterol, and triglycerides, consistent with potential pathway effects on psoriatic disease, independent of metabolic effects. To determine the specificity of the observed effect, we conducted analyses of seven additional immune-mediated diseases (IMIDs). No protective effects were observed for other IMIDs, including acne and atopic dermatitis. In contrast, risk-increasing effects were observed for Crohn’s disease (OR=1.242, 95% CI 1.107-1.395, p=2.35×10 −4 ) and rheumatoid arthritis (OR=1.502, 95% CI 1.350-1.672, p=1.36×10 −13 ). These findings provide genetic evidence of disease-specific, potentially direct immunomodulatory effects of GLP1R signaling on psoriasis and PsA risk, and support further mechanistic and therapeutic evaluation in randomized trials.Weiterlesen

Objectives: To estimate the prevalence of psoriatic arthritis (PsA) and associated fac-tors in patients with moderate-to-severe psoriasis. Methods: Retrospective, single-center study of a cohort of psoriasis patients in stand-ard follow-up in a dermatology department from July 2008 to January 2024. Patients ≥18 years with moderate-to-severe psoriasis were included and classified into 3 groups according to the treatment received: group 1, biologics or small molecules with or without conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs); group 2, only csDMARDS; and group 3, non-pharmacological treatments. Demographic and clinical variables were collected. The prevalence of PsA was estimated with its 95% confidence interval (CI). The cumulative incidence of PsA was analyzed across groups, and logistic regression models were built. Results: The study population comprised 308 patients (67.2%, 22.7%, 10% in groups 1, 2, and 3, respectively). Dif-ferences between the groups were observed in severity of psoriasis, weight, smoking status, and dyslipidemia (p< 0.05). The prevalence of PsA was 11.7% (95% CI, 8.1-15.3), with most patients in group 1. This group had a high-er risk of PsA following diagnosis of psoriasis or initiation of treatment. Belonging to groups 2 and 3 had a smaller effect than belonging to group 1 in the development of PsA; nail involvement and obstructive sleep apnea (OSA) were associated with development of PsA (p< 0.05). Conclusions: The prevalence estimate was lower than previous estimates, probably owing to the increased use of biologics. Not requiring biologics for disease control had less effect on development of PsA. Nail involvement and OSA were associated with PsA.Weiterlesen

ObjectiveSecondary failure to biologic disease-modifying antirheumatic drugs (bDMARDs) is challenging and contributes to the complexity of managing psoriatic arthritis (PsA). We aimed to define the frequency and incidence of this phenomenon in PsA and identify the risk factors for its occurrence.MethodsWe retrieved data on patients with PsA from our single-center, specialized-care, prospective observational cohort who initiated and remained on bDMARDs for ≥ 1 year after clinic enrollment between 2000 and 2023. We defined response to therapy at the 1-year visit (baseline) as achievement of ≥ 40% reduction in the swollen joint count (SJC) and either ≥ 50% reduction in Psoriasis Area and Severity Index (PASI) or PASI ≤ 2. We defined secondary failure as the inability to maintain response criteria or as the clinician's judgment of loss of effectiveness. To examine factors associated with secondary failure, we fitted Cox regression models.ResultsOf 482 patients included in the study, 264 (54.8%) were responders at 1 year. Of these, 94 (35.6%) developed secondary failure at a median of 1.6 (IQR 0.7-3.8) years from response. In the multivariable model, higher SJC (hazard ratio [HR] 1.39, 95% CI 1.05-1.84) and PASI (HR 1.14, 95% CI 1.01-1.29) at baseline were associated with secondary failure. Tumor necrosis factor inhibitors (TNFi) vs other bDMARD use (HR 0.39, 95% CI 0.18-0.88), initiation as first-line bDMARD (HR 0.48, 95% CI 0.25-0.91), and treatment initiation during more recent calendar years (HR 0.34, 95% CI 0.12-0.98) were associated with less secondary failure.ConclusionSecondary failure to bDMARD is common in PsA and may be influenced by both disease- and therapy-related factors.Weiterlesen

BackgroundTo identify new targets for protein-based treatments in psoriasis and evaluate the possible negative impacts of these druggable proteins.MethodsWe carried out an extensive analysis of the entire set of proteins in the blood (proteome-wide) to determine if there are causal links between certain blood proteins and the likelihood of developing psoriasis. The proteins were selected from the UK Biobank Pharma Proteomics Project (UKBPPP) database, which includes genetic data for 2,940 different blood proteins. We obtained the cis-expression quantitative trait locus (cis-eQTL) of druggable genes from eQTLGen Consortium as exposure and the genome-wide association study (GWAS) of psoriasis.ResultsOur research discovered a strong genetic link between plasma APOF, ATP6V1G2, IFNLR1, CRELD1, PRSS8, and TNF proteins and a higher chance of having psoriasis. These proteins share genetic variations associated with psoriasis (PPH3+PPH4>0.8). The ROC curves derived from these protein quantity trait loci (pQTLs) demonstrate that they can distinguish between individuals with psoriasis and those without. The druggable gene analysis showed that simvastatin is related to TNF based on the Drug SIGnatures DataBase webtool.ConclusionOur study has explored the causal relationships between six blood proteins and psoriasis, offering a detailed insight into potential therapeutic targets. Among them, simvastatin might have an effect on psoriasis via TNF.Weiterlesen

No abstract supplied.Weiterlesen

BackgroundAlthough biologic and systemic therapies have advanced psoriasis management, real-world evidence guiding individualized treatment remains limited. In particular, the influence of body size and metabolic parameters on disease severity and treatment response is underexplored.ObjectiveTo investigate the associations of body mass index (BMI), basal metabolic rate (BMR), body surface area (BSA), and body weight with baseline psoriasis severity and therapeutic response across different treatment modalities.MethodsThis multicenter, prospective study included 1955 patients from the Shanghai Psoriasis Effectiveness Evaluation CoHort (SPEECH) and 1663 patients for longitudinal follow-up. Multivariable regression models were used to examine the associations between body size/metabolic parameters and the baseline psoriasis area and severity index (PASI) scores, as well as PASI-based treatment responses at Week 12 and Week 20. Stratified analyses by treatment type and receiver operating characteristic curve analysis were conducted to assess predictive performance.ResultsAll four parameters were positively associated with baseline PASI scores (FDR-adjusted P < 0.05). Prospectively, elevated BMI, BMR, BSA, and body weight were significantly associated with reduced likelihood of achieving PASI 75/90/100, and lower percentage reduction in PASI score at both time points. These associations were particularly pronounced in patients receiving biologic therapies. In the ustekinumab subgroup, body composition showed enhanced predictive accuracy for high-level PASI responses.ConclusionElevated BMI, BSA, body weight, and BMR are associated with more severe psoriasis and diminished treatment efficacy, especially those treated with biologics. These findings underscore the need for personalized dosing strategies in biologic therapy, especially for fixed-dose agents like ustekinumab.Weiterlesen

IL-17A spielt eine zentrale Rolle bei der Entzündung an den Sehnenansätzen (Enthesitis) bei Psoriasis-Arthritis. Eine Studie hat gezeigt: Bekamen Betroffene 24 Wochen lang ein Medikament, das IL-17A blockiert, so besserten sich bei 9 von 10 die Symptome deutlich. Es gab weniger „böse“ Entzündungszellen im Gewebe. Gleichzeitig vermehrten sich Zellen, die Entzündungen dämpfen. Auch Hinweise auf schädlichen Knochenumbau, wie er oft bei Psoriasis-Arthritis vorkommt, gingen zurück. Das zeigt: IL-17A-Hemmer können direkt an den betroffenen Stellen für mehr Ruhe sorgen und das Fortschreiten der Erkrankung bremsen[1][2][4]. Originaltitel: Entheseal tissue signature in response to IL-17A inhibition in psoriatic arthritis: results from the EBIO entheseal biopsy study. Link zur Quelle

Im Medizinstudium gibt es jetzt ein neues Seminar, das sich mit Stigmatisierung und psychosozialen Belastungen von Menschen mit sichtbaren Hauterkrankungen wie Psoriasis beschäftigt[1][2][4]. Hier unterrichten Ärztinnen, Psychologinnen und Expertinnen gemeinsam, damit die Studierenden von verschiedenen Blickwinkeln lernen[1][2]. Im Seminar reden sie nicht nur über Juckreiz und Hautprobleme, sondern auch darüber, wie es sich anfühlt, wenn andere negativ reagieren oder Vorurteile haben[1][2]. Die Studierenden üben, wie man Betroffenen besser hilft und sie beraten kann[2]. Fast alle Teilnehmer finden den Unterricht sinnvoll, weil er praktische Tipps liefert und einen offenen Umgang mit schwierigen Themen ermöglicht[2]. Es zeigt auch: Gute Behandlung braucht Wissen über Körper und Psyche. Das Seminar hilft dabei, das besser zu verstehen, und macht das Medizinstudium ein Stück menschlicher[1][2]. Originaltitel: Implementierung eines Team-Teaching-Seminars in der Regellehre des Medizinstudiums zur Stigmatisierung und zu psychosozialen Belastungen von Menschen mit sichtbaren Hauterkrankungen | Publisso Link zur Quelle

Viele Menschen mit rheumatoider Arthritis oder Psoriasis-Arthritis, die seit mindestens sechs Monaten eine stabile Remission oder nur eine geringe Krankheitsaktivität haben, fragen sich, ob sie ihre Medikamente (konventionelle synthetische DMARDs) reduzieren oder sogar ganz absetzen können. Experten empfehlen, eine vorsichtige und schrittweise Reduktion auszuprobieren[1][2]. Ein einfaches, abruptes Absetzen wird nicht empfohlen, da es das Risiko eines Krankheitsschubs erhöhen kann[1]. Es gibt bisher wenig sichere Daten, welche Strategie die beste ist und wie lange der Effekt anhält. Neue internationale Leitlinien raten dazu, gemeinsam mit dem Arzt eine individuelle Entscheidung zu treffen und die Erkrankung weiter engmaschig zu kontrollieren[1]. In etwa 10 bis 20 Prozent der Betroffenen gelingt es, nach und nach ganz auf DMARDs zu verzichten, ohne dass die Krankheit zurückkommt[3]. Doch jeder Körper reagiert anders, daher ist Teamarbeit mit dem Arzt wichtig, damit Beschwerden früh erkannt und behandelt werden können. Originaltitel: Dose reduction and discontinuation of conventional synthetic disease‐modifying anti‐rheumatic drugs (DMARDs) for people with rheumatoid arthritis or psoriatic arthritis in remission or low disease activity Link zur Quelle

Menschen mit **Psoriasis** haben ein etwas höheres Risiko, an bestimmten **Krebsarten** zu erkranken[1][4][3]. Gerade **Hautkrebs** kommt bei ihnen häufiger vor, aber auch das Risiko für **Lymphome** ist leicht erhöht[1][4]. Besonders betroffen sind Menschen mit schwerer Psoriasis oder solche, die bestimmte Therapien wie Lichtbehandlung mit PUVA bekommen[1]. Gleichzeitig haben viele Betroffene weitere bekannte Risikofaktoren wie Rauchen oder Übergewicht, die das Krebsrisiko ebenfalls steigern können[3]. Die Forschung zeigt: Nicht jede Studie findet das gleiche Ergebnis – manche zeigen ein klares Mehr an Krebs, andere bleiben unentschlossen[4]. Trotzdem sind sich viele Expertinnen und Experten einig, dass regelmäßige **Krebsvorsorge** bei Psoriasis sinnvoll ist[3]. Originaltitel: Psoriasis and the risk of 26 cancers: pooled population-based cohort studies from Denmark, England, Israel, and Taiwan Link zur Quelle

An neues Seminar für Medizinstudenten an der Uni Hamburg zeigt, wie wichtig das Thema **Stigmatisierung bei sichtbaren Hautkrankheiten wie Psoriasis** ist. Dermatologen, Psychologen und Experten haben sich zusammengetan und unterrichten gemeinsam. Die Studierenden lernen durch Vorträge, Übungen und Diskussionen, was Betroffene erleben und wie sie besser helfen können. Nach dem Seminar fühlen sich die meisten sicherer darin, Patientinnen und Patienten bei psychosozialen Problemen durch Ausgrenzung zu unterstützen. Fast alle finden das Seminar und die Teamarbeit richtig gut und hilfreich[1]. Originaltitel: Implementation of a team-teaching seminar on the stigmatization and psychosocial burdens of people with visible skin diseases in the standard curriculum of medical studies. Link zur Quelle

Viele Menschen mit **Psoriasis** oder **atopischer Dermatitis** kämpfen nicht nur mit ihrer Haut, sondern auch mit seelischem Stress. In einer aktuellen Studie zeigte sich: Jeder dritte Betroffene leidet im Laufe seines Lebens an **Scham-bedingten Störungen** wie **Körperbildstörung** oder **sozialer Angststörung**. Frauen und jüngere Menschen sind besonders oft betroffen. Die Krankheit erschwert ihnen den Alltag und senkt die Lebensqualität. Es gab keinen Unterschied zwischen den Erkrankungen. Ärztinnen und Ärzte sollten Scham-Gefühle ernst nehmen und in der Behandlung beachten[1][4]. Originaltitel: Shame-related disorders in patients with atopic dermatitis and psoriasis - An exploratory, cross-sectional interview study on the prevalence and correlates of body dysmorphic disorder and social anxiety disorder. Link zur Quelle

Forscher aus Deutschland haben mit künstlicher Intelligenz berechnet, wie gut die Behandlung mit Secukinumab bei Menschen mit Psoriasis-Arthritis oder axialer Spondyloarthritis wirkt. Sie haben Daten von fast 2000 Patientinnen und Patienten ausgewertet. Die wichtigsten Faktoren dafür, ob du nach vier Monaten wenig Krankheitsaktivität oder eine bessere Lebensqualität hast, hängen unter anderem davon ab, wie sehr du und dein Arzt deine Krankheit am Anfang einschätzen, wie viele Gelenke wehtun, dein Alter, dein Gewicht und ob du schon vorher mit Biologika behandelt wurdest. Die Methode könnte Ärzten helfen, den Behandlungserfolg besser vorherzusagen und Therapien individueller anzupassen. Originaltitel: Predicting treatment outcomes in patients with psoriatic arthritis or axial spondyloarthritis: An artificial intelligence-driven approach. Link zur Quelle

Biologika sind spezielle Medikamente gegen Psoriasis, die gezielt Teile des Immunsystems ausschalten[4][7][8]. Das ist anders als bei älteren Mitteln, die die Abwehr komplett bremsen. Je nach Biologikum werden zum Beispiel die Botenstoffe TNF-alpha, IL-17 oder IL-23 unterdrückt. Diese spielen eine wichtige Rolle bei der Entzündung und den Hautveränderungen[4][8]. Die neuen Wirkstoffe helfen oft schnell und stark, trotzdem bleibt manchmal an einigen Stellen noch etwas von der Krankheit sichtbar – das nennt man „residuales PASI“. Dabei fällt auf, dass bestimmte Biologika an verschiedenen Körperstellen besser wirken als an anderen[1]. Einige reduzieren die Entzündung besonders an der Kopfhaut, andere eher an den Nägeln oder Gelenken. Ärzte können dadurch gezielter behandeln, sodass jeder Patient die beste Therapie für seine Problemzonen bekommt[1][8]. Biologika werden meist als Spritzen alle paar Wochen verabreicht, je nach Wirkstoff[4][7]. Originaltitel: Biologic treatments for psoriasis have different anatomical specificities in residual PASI Link zur Quelle

**Psoriatische Arthritis und Uveitis: Wie hängen sie zusammen?** Psoriatische Arthritis (PsA) ist eine chronische Entzündungskrankheit, die oft mit Uveitis in Verbindung gebracht wird. Uveitis ist eine Entzündung im Auge, die Sehprobleme verursachen kann. Wissenschaftler haben nun herausgefunden, dass PsA das Risiko für Uveitis erhöht. **Die Studie: Was wurde entdeckt?** Eine Studie hat gezeigt, dass Menschen mit PsA fast doppelt so häufig Uveitis entwickeln wie andere. Der genaue Mechanismus wie diese Krankheiten miteinander zusammenhängen, ist noch nicht vollständig geklärt. Die Studie nutzte eine Methode namens Mendelian Randomization, um die kausale Beziehung zu untersuchen. Das Ergebnis: PsA führt zu einem erhöhten Risiko für Uveitis. **Was bedeutet das für Betroffene?** Für Menschen mit PsA ist es wichtig, regelmäßig Augenkontrollen durchführen zu lassen, um mögliche Augenprobleme frühzeitig zu erkennen. Die Forschung zu PsA und Uveitis hilft, die Verbindung zwischen diesen Krankheiten besser zu verstehen. Originaltitel: Integrative Mendelian randomization and transcriptomic analysis reveals the causal association between psoriatic arthritis and uveitis Link zur Quelle

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

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

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

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

No abstract supplied.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

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

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

No abstract supplied.Weiterlesen

No abstract supplied.Weiterlesen