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ObjectivesTo perform the cross-cultural adaptation of the Psoriasis Epidemiology Screening Tool (PEST) questionnaire into Spanish (PEST-S) and conduct a preliminary exploratory assessment of its discriminative ability to identify psoriatic arthritis (PsA) among patients with psoriasis (Ps), osteoarthritis (OA), or both.MethodsThe PEST questionnaire was translated and culturally adapted into Spanish following international guidelines. A cross-sectional study was conducted including adult patients with PsA, Ps, OA, and Ps+OA. The PEST-S was administered to all participants. PsA diagnosis was confirmed using CASPAR criteria. Diagnostic performance was evaluated using sensitivity, specificity, likelihood ratios, area under the ROC curve (AUC), and Cohen's kappa coefficient. Comparisons of individual PEST-S items were performed across diagnostic groups.ResultsA total of 124 patients were included: 32 with PsA, 31 with Ps, 33 with Ps+OA, and 28 with OA. The questionnaire required less than one min to complete. PEST-S scores ≥3 yielded a sensitivity of 100%, specificity of 94.2%, LR+ of 17.2, and LR- of 0. The AUC was 0.97 (95% CI: 0.95-0.99). Agreement between PEST-S and CASPAR classification was 93.2% (κ = 0.838). A statistically significant difference was found in the responses to all five PEST-S items between patients with PsA and those in the other diagnostic groups (p< 0.05).ConclusionThe Spanish version of the PEST questionnaire (PEST-S) demonstrated excellent diagnostic performance in distinguishing PsA from Ps and OA in a Spanish-speaking population. These findings support its clinical utility and justify further validation in a screening context among patients with psoriasis without prior rheumatologic evaluation.Weiterlesen

BackgroundPsoriasis is a chronic inflammatory skin disorder with unclear etiology. The roles of skin microbiome and metabolic dysregulation in psoriasis pathogenesis are not yet fully understood.MethodsWe conducted an integrated microbiome and untargeted metabolomic analyses on skin samples from 29 patients with psoriasis and 31 healthy controls. The skin microbiota was characterized using 16 S rRNA gene sequencing, and untargeted metabolomic profiling was performed using LC-MS/MS. Multivariate statistical analyses were used to identify differential microbes and metabolites, followed by correlation analyses to explore microbe-metabolite interactions.ResultsPsoriatic lesions exhibited significantly higher skin microbial alpha diversity compared to healthy controls. Principal component analysis revealed distinct microbial community structures between the two groups. At the genus level, Corynebacterium and Staphylococcus were significantly enriched in psoriatic lesions, while Cutibacterium was notably reduced. Metabolomic analysis identified 63 differential metabolites, with 39 upregulated and 24 downregulated in psoriatic lesions. These metabolites were primarily involved in lipid metabolism (particularly phospholipids and sphingolipids), amino acid metabolism, and inflammatory mediator pathways. Correlation analysis revealed significant associations between microbial alterations and metabolic dysregulation. Cutibacterium abundance was negatively correlated with inflammatory lipids and positively correlated with antioxidant metabolites, whereas Staphylococcus and Corynebacterium exhibited the opposite pattern. Notably, the abundance of Propionibacteriaceae strongly correlated with glutathione levels (r = 0.821, P < 0.001), indicating a potential role of microbiome-mediated oxidative stress in psoriasis.ConclusionsThis study highlights significant alterations in both the skin microbiome and metabolome in patients with psoriasis, revealing complex microbe-metabolite interaction networks. The findings suggest that microbial dysbiosis, particularly the decreased abundance of Cutibacterium and the increased abundance of Staphylococcus/Corynebacterium, may contribute to psoriasis pathogenesis by modulating lipid metabolism, inflammatory pathways, and oxidative stress responses.Weiterlesen

ObjectivesBiologic therapies for skin psoriasis (PsO) have been linked to a lower risk of developing psoriatic arthritis (PsA), but their efficacy across different mechanisms of action remains to be fully explored. This study aimed to compare PsA risk in PsO patients prescribed interleukin-23 inhibitors (IL23i) vs interleukin-17 inhibitors (IL17i).MethodsThis retrospective cohort study utilized the TriNetX database to categorize adult PsO patients into two cohorts: those newly prescribed IL23i (without IL17i exposure) and those newly prescribed IL17i (without IL23i exposure). Patients with a history of PsA or previous use of anti-tumor necrosis factor-α or anti-interleukin-12/23 agents were excluded. A total of 5,490 patients, matched 1:1 by propensity scores, were analyzed for PsA risk using hazard ratios (HR) from Cox regression.ResultsThe 5-year cumulative incidence of PsA was significantly lower in IL23i users compared with IL17i users (11.68% vs 19.94%; p <0.001). IL23i treatment was associated with a reduced PsA risk (HR 0.475, 95% CI 0.382-0.590). This reduced risk persisted across various subgroups defined by age, sex, race, PsO subtypes, obesity, and elevated inflammatory markers. Similar results were observed in individual drug comparisons, with lower risks for guselkumab vs secukinumab (0.480, 0.358-0.645) and ixekizumab (0.698, 0.509-0.956), risankizumab vs secukinumab (0.433, 0.306-0.612) and ixekizumab (0.504, 0.347-0.732), and tildrakizumab vs secukinumab (0.339, 0.131-0.875). The comparison of tildrakizumab vs ixekizumab (0.451, 0.171-1.191) also suggested a lower risk but was not statistically significant.ConclusionsPsO patients treated with IL23i had a lower subsequent PsA risk compared with those treated with IL17i.Weiterlesen

Background and objectivesAtopic dermatitis (AD) and psoriasis (Pso) are frequently associated with psychological distress. This study evaluated the prevalence and correlates of shame-related disorders (SRD), namely body dysmorphic disorder (BDD) and social anxiety disorder (SAD), in patients with AD and Pso.Patients and methodsA monocentric, cross-sectional study was conducted in adult patients from 07/2023 to 03/2024. A trained clinical psychologist assessed subjects for BDD and SAD. Additionally, subjects completed the DLQI. Objective severity of their disease was physician-rated using the EASI or PASI.ResultsOne hundred and fifty-one patients were included, n = 55 (36.4%) with AD and n = 96 (63.6%) with Pso. Among all study participants, the point and lifetime prevalence of SRD was 17.2% and 31.8%, respectively. Point and lifetime prevalence for BDD was 10.6% and 26.5%, and for SAD 12.6% and 17.2%. There were no differences in the point or lifetime prevalence of BDD or SAD between patients with AD or Pso. SRD were associated with younger age and female sex. DLQI was significantly reduced in those suffering from SRD.ConclusionsOur results indicate that SRD are prevalent in AD and Pso and should therefore be further investigated for their use in routine clinical practice.Weiterlesen

No abstract supplied.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

No abstract supplied.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

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

No abstract supplied.Weiterlesen

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