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ObjectivesSeveral studies have reported weight gain with tumor necrosis factor inhibitors (TNFi) in psoriatic disease. However, such analyses have not accounted for the natural propensity for weight gain over time. We aimed to investigate whether therapy with TNFi in psoriatic arthritis (PsA) patients is associated with a change in the rate of weight gain post-treatment initiation.MethodsWe included patients with at least two weight measurements prior to, and after commencing TNFi and used change point analysis to assess the differences in the rate of weight gain based on the mean slope before and after TNFi initiation, adjusting for clinically relevant variables.ResultsOf 234 patients eligible for inclusion, 62.8% were males. At the first clinic visit, the mean (standard deviation) age was 41.8 (12.2) years, while the mean disease duration was 5.1 (6.8) years. The mean weight immediately prior to TNFi use was 83.8 (17.2) kg, while that at the last available visit on TNFi was 86.4 (18.6) kg (p = 0.39), over an average period of 7.9 (5.8) years. The mean values of the pre- and post-TNFi slopes were 0.52 (95% confidence interval [CI] 0.18-0.87) and 0.28 (95% CI - 0.05-0.61), respectively (p = 0.09); thus, there was a trend towards lower rate of weight gain followed the initiation of TNFi therapy.ConclusionsTNFi treatment is not associated with an increase in weight above the expected gain in PsA. Prior trajectory of weight gain with age must be considered while studying the impact of treatment on weight.Key points• TNFi are commonly used in the management of psoriatic disease and may influence body weight. • TNFi treatment is not associated with a significant increase in body weight when accounting for the trend of weight gain with time. • The trends in weight change may differ between etanercept and monoclonal antibody TNFi agents.Weiterlesen

Background: Psoriasis is a systemic inflammatory disease associated with metabolic dysregulation. Understanding these metabolic changes may reveal biomarkers to elucidate disease mechanisms and predict comorbidities. While previous studies have identified psoriasis-associated metabolites, findings are often limited by sample sizes and lack validation. Objectives: We aimed to identify circulating metabolites associated with psoriasis, including cutaneous activity, severity, and psoriatic arthritis. Further, we investigated whether the signature was disease-specific compared to other immune-mediated inflammatory diseases (IMIDs). Methods: We performed a cross-sectional analysis of 270,848 White/European individuals from the UK Biobank (n=253,924) and HUNT (n=16,924). Both cohorts used nuclear magnetic resonance spectroscopy to quantify metabolite levels, covering lipoprotein fractions and subfractions, fatty acids, and small-molecular metabolites. For each metabolite, we performed multivariable linear regression adjusting for age, sex, BMI, smoking status, and use of lipid-lowering medications. Results: The metabolomic profile of psoriasis was largely consistent across cohorts. In the model adjusted for age and sex, 116 metabolic measures were associated with psoriasis in both cohorts. After full adjustment, only Glycoprotein acetyls (GlycA) remained associated with psoriasis (coefficient [95% CI]: 0.09 [0.07-0.11] in UK Biobank and 0.11 [0.06-0.17] in HUNT). Despite more substantial metabolic alterations in cutaneous-active psoriasis, GlycA was also elevated in HUNT participants reporting no active psoriasis rash (coefficient [95% CI]: 0.12 [0.04-0.20] in non-cutaneous-active and 0.11 [0.03-0.19] in cutaneous-active psoriasis). In HUNT, severe psoriasis exhibited more pronounced metabolic alterations compared to non-severe psoriasis. Across both cohorts, phenylalanine levels were highly elevated in psoriatic arthritis compared to cutaneous psoriasis (coefficient [95% CI]: 0.41 [0.20-0.62] in UK Biobank and 0.47 [0.28-0.67] in HUNT). All IMIDs showed elevated GlycA and reduced albumin, with milder changes in atopic dermatitis. Psoriasis in the HUNT cohort exhibited a distinct lipoprotein profile compared to other IMIDs. Conclusions: This large-scale, cross-cohort study confirms metabolic alterations in individuals with psoriasis and highlights elevated GlycA levels regardless of cutaneous activity. The distinct metabolomic profile of psoriasis relative to other IMIDs suggests a potentially unique systemic profile. These findings offer a foundation for advancing biomarker research and mechanistic studies for psoriasis.Weiterlesen

BackgroundPsoriatic arthritis (PsA) and juvenile PsA (jPsA) are chronic inflammatory diseases with similar features that differ by age and sequence of symptom onset. PsA and psoriasis (PsO) share comparable pathology across ages, with interleukin (IL)-23 as a key mediator. Prior to the recent US FDA approval of guselkumab for treatment of pediatric plaque PsO and active jPsA, no approved pediatric treatment selectively targeted IL-23 signaling. Guselkumab (a fully human, dual-acting, IL-23p19 subunit inhibitor) was shown to be safe and effective in adult PsO and PsA, with consistent clinical benefits and safety in pediatric PsO. As jPsA shares features, including clinical characteristics and pathogenesis, with PsO and PsA, findings were extrapolated to jPsA using a similar approach previously applied to support ustekinumab and golimumab use in jPsA, which served as precedents for these analyses with guselkumab.AimsThe aim of this study was to demonstrate the similarity of serum guselkumab concentrations, clinical response, and safety among children and adults with PsO and/or PsA in guselkumab randomized controlled trials.MethodsOne-year data from participants receiving guselkumab at Week (W)0, W4, then every 8 weeks in VOYAGE 1/2 (adult PsO; N = 1221), DISCOVER-1/-2 (adult PsA; N = 375), and PROTOSTAR (pediatric PsO; N = 92; n = 3 with concurrent jPsA) were included. Serum guselkumab concentrations, Investigator Global Assessment of clear/minimal (IGA 0/1) and Psoriasis Area and Severity Index (PASI) 75/90/100 response rates and safety outcomes were summarized.ResultsSerum guselkumab concentrations over 1 year were similar between pediatric (max median: 3.2 µg/mL) and adult PsO (3.7 µg/mL), adult PsO and PsA (4.2 µg/mL), and pediatric PsO and adult PsA. IGA 0/1 response rates at W16 were approximately similar in guselkumab-treated participants with pediatric PsO (66%), adult PsO (84%), and adult PsA (77%). W16 PASI 75/90/100 response rates were comparable across guselkumab-treated participants with pediatric PsO without jPsA (PASI 75: 77%; PASI 90: 56%; PASI 100: 33%), pediatric PsO with jPsA (1 of 2 participants achieved all PASI improvement levels), and adult PsA (77%; 55%; 22%). Guselkumab safety outcomes were similar across ages and diseases.ConclusionComparable pharmacokinetic and clinical findings with guselkumab in children with PsO (3 with concurrent jPsA) and adults with PsO and PsA support the extrapolation of efficacy and safety data from adults to children with jPsA, supporting guselkumab use in jPsA.Clinical trials registrationThe clinical trials included in this analysis are registered at www.Clinicaltrialsgov with the identifiers: NCT02207231 (VOYAGE 1), NCT02207244 (VOYAGE 2), NCT03162796 (DISCOVER-1), NCT03158285 (DISCOVER-2), and NCT03451851 (PROTOSTAR).Weiterlesen

ObjectiveTo investigate the distribution characteristics of peripheral blood lymphocyte subsets in elderly psoriasis patients and analyze the interactions between immunosenescence and psoriasis and their impact on immune cell subpopulations.MethodsThis cross-sectional study enrolled 318 psoriasis patients and 167 healthy controls, stratified by age into elderly (≥ 65 years) and non-elderly (18-64 years) groups. Peripheral blood lymphocyte subsets, including CD3+ T cells, CD4+ T cells, CD8+ T cells, B cells, and NK cells, were analyzed using four-color flow cytometry. Generalized linear models were employed to analyze associations between PASI scores and lymphocyte subsets, and correlation network analysis was constructed to evaluate interaction patterns among immune cell populations.ResultsThe elderly psoriasis group demonstrated significantly reduced CD8+ T cell percentage compared to controls (24.52% vs. 28.62%, P < 0.001), accompanied by an elevated Th/Ts ratio (1.57 vs. 1.27, P < 0.001) and significantly increased NK cell percentage and absolute count. Generalized linear modeling revealed a significant negative interaction effect between psoriasis and age on CD8+ T cell percentage (β = -3.979, P = 0.019), while the Th/Ts ratio exhibited a significant positive interaction effect (β = 0.230, P = 0.010). B cell absolute count showed a positive correlation with PASI score (r = 0.180, P = 0.001), with this correlation being more pronounced in elderly patients (r = 0.308, P = 0.014). Network analysis demonstrated reduced connectivity density among immune cell subpopulations in elderly patients.ConclusionsElderly psoriasis patients exhibit age-related alterations in peripheral blood lymphocyte subset distribution, characterized by decreased CD8+ T cells, elevated Th/Ts ratio, and increased NK cells. B cells may serve as potential biomarkers for assessing disease severity in elderly psoriasis patients.Weiterlesen

Background: Managing psoriasis in patients with a history of lymphoma presents a unique clinical challenge. Psoriasis is associated with significant comorbidities such as cardiovascular disease and inflammatory arthritis, making optimal treatment vital. Systemic treatments like biologic agents may help mitigate these sequelae of systemic inflammation. However, concerns about immunosuppression in the context of lymphoma recurrence and progression complicate therapeutic decisions. Purpose: This review aims to examine the role of IL-12, IL-17, IL-23, and TNF-α in psoriasis and explores the safety of biologic therapies in this population, with a focus on impact on lymphoma recurrence and progression. Research Design: A narrative review of the current medical literature was conducted. Study Sample: The analysis synthesizes evidence from preclinical studies, clinical trials, post-marketing surveillance registries, retrospetive cohort studies, and case reports concerning the use of biologic agents in psoriasis. Data Collection: Relevant literature was identified an analyzed to compare the mechanisms of action, degree of immunosuppression, and available safety data of different biologic agent classes. Results: Based on current evidence, we propose that IL-17 and IL-23 inhibitors as preferred options due to their targeted mechanisms and favorable safety profiles. In contrast, TNF-α inhibitors are less favored due to their comparatively greater immunosuppressive effects and potential association with lymphoma risk. IL-12/23 inhibitors are questionable given their potential impact on tumor immunosurveillance. Conclusion: For psoriasis patients with a history of lymphoma, IL-17 and IL-23 inhibitors represent the most suitable biologic options, while TNF-α inhibitors and IL-12/23 inhibitors should be used with caution. Clinical data overall remains limited, however, as lymphoma patients are routinely excluded from clinical trials. Further research is needed to clarify long-term safety and optimize treatment strategies for this high-risk population.Weiterlesen

In this commentary, we discuss the role of pharmacy benefit managers (PBMs) on access to biologics for patients with psoriasis. We highlight structural and system level barriers to biologics access, as well as how PBMs work as intermediaries between insurers, pharmacies, and drug manufactures to influence prescription formularies and generate health savings. We also discuss how controversial PBM practices such as step therapy, prior authorizations, and spread pricing may limit access to biologics and potentially increase cost for patients. Finally, we highlight how dermatologists and national organizations such as the National Psoriasis Foundation can collaborate and advocate for legislative reforms to increase transparency among PBMs.Weiterlesen

Diabetes and psoriasis are known to increase the risk of each other, yet their combined impact on long-term mortality remains unclear. This prospective cohort study examined the associations between the coexistence of diabetes and psoriasis and all-cause and cause-specific mortality in a nationally representative sample of U.S. adults. Data were obtained from 16,852 participants in the National Health and Nutrition Examination Surveys (NHANES). Survival was assessed using the Kaplan-Meier method, and a weighted Cox proportional hazards model was employed. In fully adjusted models (adjusted for age, sex, race, BMI, smoking status, and comorbidities), individuals with both diabetes and psoriasis demonstrated significantly increased risks of all-cause mortality (hazard ratio [HR]: 1.76, 95% confidence interval [CI]: 1.04-3.00) and cancer-specific mortality (HR: 2.90, 95% CI: 1.28-6.54), but not cardiovascular mortality (HR: 0.87, 95% CI: 0.18-4.35). Comorbidity was significantly associated with elevated risks of all-cause and cancer mortality (P < 0.05). These findings suggest a notable association between the coexistence of these two chronic conditions and elevated overall and cancer mortality risks, while no significant effect was found on cardiovascular mortality. Exploratory analyses also indicated a possible dose-response relationship between psoriasis severity and cardiovascular mortality, warranting further investigation.Weiterlesen

Once hailed as a breakthrough in psoriasis research, the imiquimod (IMQ) mouse model is now overused, inconsistently applied, and increasingly disconnected from human disease. Nearly a decade after our initial critique, the field remains reliant on a tool that models acute, innate inflammation rather than chronic, adaptive immunity. In this paper, we revisit the limitations of the IMQ model, highlighting methodological drift, poor transcriptomic overlap with psoriasis, and the illusion of mechanistic discovery. We argue that progress in psoriasis research now depends on moving beyond this model toward more faithful systems that reflect the complexity of human disease.Weiterlesen

Plaque psoriasis is a chronic skin disorder involving dysregulated inflammation. While numerous biologic therapies targeting inflammatory mediators have been approved for moderate-to-severe psoriasis, their safety profiles may include an increased risk of adverse events (AEs), such as infections, cardiovascular diseases, and malignancies. Because patients with psoriasis also have increased incidence of comorbidities, long-term real-world AE monitoring is critical to further evaluate the safety of biologic therapies postapproval. Brodalumab is a recombinant, fully human interleukin-17 receptor A antagonist indicated for the treatment of moderate-to-severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and have failed to respond or have lost response to other systemic therapies. The safety profile of brodalumab has been established in clinical trials and industry-sponsored US pharmacovigilance reports. Herein, we summarize AEs reported in nonsponsored open-label and real-world studies of brodalumab. Across all studies, most common AEs were similar to those listed in the brodalumab package insert. While AEs of special interest were not reported comprehensively, their rates were generally low, with 3 cases of major adverse cardiac events, 2 cases of malignancy, 11 cases of depression, and no completed suicides in the overall safety population (N = 1701). There were 6 cases of serious infection and no serious fungal infections. Studies evaluating AEs of interest for brodalumab showed no causal link to suicide and no increase in risk of cardiac events or serious infection compared with other biologics. Together, these studies support a consistent safety profile of brodalumab in real-world use.Weiterlesen

BackgroundThe pathogenesis of psoriasis is characterized by dysregulated post-translational modifications, with particular emphasis on fucosylation-a glycosylation process mediated by fucosyltransferases (FUTs). Keratin 17 (K17), overexpressed in psoriatic keratinocytes, drives inflammation and proliferation, but its interplay with fucosylation remains unclear. This study aimed to elucidate the role of fucosylation in psoriasis, specifically focusing on the regulation of K17 stability by FUT11.MethodsTo investigate fucosylation dynamics, we employed single-cell RNA sequencing (scRNA-seq) to analyze N-glycan biosynthesis activity in psoriatic versus healthy keratinocytes. Fucosylation levels were assessed in human and murine psoriatic lesions, as well as in cytokine-stimulated keratinocytes, using Aleuria aurantia lectin (AAL). An imiquimod (IMQ)-induced psoriasis-like mouse model and primary keratinocytes treated with psoriasis-associated cytokines (Pso-Mix) (IL-17, TNF-α, IL-1α, OSM and IL-22) were utilized to evaluate the effects of 2-fluorofucose (2-FF) and FUT11 siRNA. We further explored the mechanisms regulating K17 stability through immunoprecipitation, ubiquitination assays, and cycloheximide chase experiments.ResultsOur findings revealed that psoriatic keratinocytes exhibited elevated levels of fucosylation, which correlated with upregulation of FUT11. Administration of 2-FF or silencing FUT11 significantly attenuated IMQ-induced inflammation, as evidenced by reductions in epidermal thickness, immune cell infiltration, and the expression of pro-inflammatory mediators such as IL-17A and CCL20. We demonstrated that FUT11 mediates α-1,3-fucosylation of K17, stabilizing it through K63-linked ubiquitination facilitated. Notably, silencing FUT11 disrupted the interaction between ubiquitination and fucosylation, leading to accelerated K17 degradation and a subsequent decrease in keratinocyte proliferation.ConclusionsOur results indicate that FUT11-driven fucosylation is integral to the stabilization of K17 via K63 ubiquitination, thereby perpetuating psoriatic inflammation. Targeting FUT11 or inhibiting fucosylation with 2-FF presents a novel therapeutic strategy for psoriasis management. This study highlights the critical interplay between glycosylation and ubiquitination in the pathophysiology of psoriasis, positioning FUT11 and K17 as pivotal targets for intervention.Weiterlesen

Epidemiological association between psoriasis and T2DM suggests shared pathophysiology that are to be explored. Microarray expression profiles for psoriasis and T2DM were obtained from the Gene Expression Omnibus (GEO) database. The "limma" package in R software was used to screen the differentially expressed genes (DEG). GO and KEGG enrichment analysis were further conducted to explore the functions of co-DEGs. By intesecting genes of the key disease-related modules from WGCNA with co-DEGs, candidate co-driver genes were identified and their PPI network was constructed. Hub genes with good diagnostic potential were obtained by ROC analysis and their expression was further compared in validation datasets as well as clinical samples. The crucial co-driver genes, identified by a consistently differential expression pattern, were further subjected to a series of analyses, including Gene Set Enrichment Analysis (GSEA), immune cell infiltration analysis, gene-chemistry networks analysis, gene-transcription factors (TF) network analysis, and gene-miRNA regulatory network analysis. In our study, 71 co-DEGs were identifed from psoriasis and T2DM training datasets. KEGG analysis revealed enrichment of pathways including toll-like receptor signaling pathway, cytokine-cytokine receptor interactions, chemokine signaling pathway, NOD-like receptor signaling pathway and cytosolic DNA-sensing pathway. By intersecting the critical WCGNA modules with co-DEGs, 33 candidate co-driver genes were obtained. 11 of them showed interactions with others on PPI network and 7 revealed good diagnostic value with AUC > 0.7 by ROC analysis. 4 genes, namely BEX5, EPHX2, GPRASP1, and RBP4 were finally identified as crucial co-driver genes with a consistent differential expression pattern in both training and validation datasets as well as validation experiments using clinical samples. GSEA analysis revealed that these crucial co-driver genes were involved in cytokine receptor interaction, proteasome, ribosome, apoptosis and so on. Immune cell infiltration and correlation analyses highlighted their roles in the immune microenvironment. Lastly, these genes targeted 76 skin and metabolic diseases and 135 chemicals were predicted to exert an modulatory effect of their expression. 13 TFs and 79 miRNAs were identified to modulate their expression. The integrated bioinformatics analysis conducted in our study identified co-DEGs and enriched immune-inflammatory pathways, providing novel insights into the pathogenesis underlying the comorbidity of psoriasis and T2DM. The crucial co-driver genes warrants further experimental validation and exploration to unveal the common pathophysiology.Weiterlesen

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Dithranol hilft bei Schuppenflechte schon nach kurzer Zeit. Eine neue Pilotstudie hat gezeigt, dass sich die Haut nach acht Tagen Behandlung deutlich verbessert hat. Die obere Hautschicht wird um etwa zwei Drittel dünner, Verhornungen gehen fast zur Hälfte zurück, und auch Entzündungen nehmen messbar ab[1]. Dabei wurden die Hautveränderungen mithilfe eines speziellen Lasers (in vivo konfokale Laserscanmikroskopie) untersucht, der die Zellen der Haut sichtbar macht – ganz ohne Gewebeproben. Dithranol hemmt das übermäßige Wachstum der Hautzellen und bremst Entzündungen[2]. Nebenwirkungen wie Hautreizungen sind möglich, verschwinden aber mit der Zeit oft wieder. Dithranol ist eine alte, aber immer noch wirksame Salbe gegen Psoriasis, besonders für Stellen, wo moderne Mittel nicht helfen. Originaltitel: Dithranoltherapie bei Psoriasis: eine Pilotstudie zur in vivo konfokalen Laserscanmikroskopie Link zur Quelle

Viele Menschen mit Psoriasis oder Neurodermitis schämen sich für ihre Haut, manchmal sogar mehr, als sie unter den Symptomen selbst leiden[1][2]. Besonders Frauen und Jüngere fühlen diese Scham stärker[1]. Wer stark an Depressionen leidet oder sein Leben als wenig lebenswert empfindet, empfindet meist auch mehr Scham wegen der Haut[1]. Ob jemand Psoriasis oder Neurodermitis hat, macht dabei kaum einen Unterschied; in beiden Gruppen ist die „Haut-Scham“ ähnlich verbreitet[1]. Je schwerer die Erkrankung, desto intensiver ist oft die Scham[1][5]. Diese Scham kann das Selbstbewusstsein und das Wohlbefinden deutlich verschlechtern und sogar wichtiger für die Lebensqualität sein als Depression oder Angst[1][2]. Es hilft, über die Scham zu sprechen und sich Unterstützung zu holen. Psychosoziale Hilfe kann wichtig sein, um die Lebensqualität zu verbessern[1]. 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

Viele Menschen mit Psoriasis-Arthritis haben eine schlechtere Ausdauer als gesunde Gleichaltrige[1][3]. In einer Studie mit 80 Betroffenen hatten 41 Prozent eine eingeschränkte Herz-Lungen-Fitness[1]. Das wurde durch einen Belastungstest gemessen. Die Forscher fanden heraus: Je aktiver die Erkrankung und je ungünstiger das Verhältnis von Taille zu Hüfte, desto niedriger war die Ausdauer[1]. Wer sich im Alltag viel bewegt, schneidet beim Test besser ab. Auch das persönliche Belastungserleben beeinflusst die Fitness[1]. Die Ergebnisse zeigen: Es ist wichtig, sich regelmäßig zu bewegen und auf das Gewicht zu achten. Das hilft nicht nur der Ausdauer, sondern auch dem allgemeinen Wohlbefinden. Originaltitel: Impaired cardiorespiratory fitness in psoriatic arthritis: insights from cardiopulmonary exercise testing Link zur Quelle

Forscher haben untersucht, wie chinesische Heilpflanzen bei Krankheiten wie Psoriasis wirken können[2][1]. Viele dieser Krankheiten entstehen durch eine fehlgeleitete Abwehr im Körper. Die bisherige Behandlung wirkt oft nicht gut und kann starke Nebenwirkungen haben[2][1]. BESTIMMTE Pflanzenstoffe wie **Curcumin**, **Resveratrol** oder **Berberin** können die Entzündung senken und das Immunsystem regulieren. Sie steuern dabei wichtige Signalwege im Körper[2][1]. Neue Mischungen aus mehreren Pflanzenstoffen helfen, den Schutz der Haut wiederherzustellen oder Immunzellen ins Gleichgewicht zu bringen[2][1]. Damit die Wirkstoffe besser im Körper ankommen, werden sie oft in winzige Teilchen verpackt[2]. Das verbessert die Wirkung und Stabilität. Erste Studien zeigen, dass die Stoffe auch bei Vitiligo oder Sjögren-Syndrom hilfreich sein könnten. Chinesische Heilmittel liefern also neue Ideen für sanfte Therapien. Noch sind weitere Tests am Menschen nötig, aber die Forschung geht voran[2][1]. Originaltitel: Frontiers | Research progress on traditional Chinese medicine compounds in autoimmune-related skin diseases Link zur Quelle

Bariatrische Operationen helfen vielen stark übergewichtigen Menschen, schnell viel Gewicht zu verlieren[1][2][3]. Das kann aber nicht nur die allgemeine Gesundheit verbessern, sondern hat auch Auswirkungen auf die Haut[1][2][3]. Nach der OP berichten viele Patienten, dass sich ihre Psoriasis, Akne oder andere Hautprobleme bessern[1][3]. Besonders Psoriasis und Hidradenitis suppurativa gehen oft zurück[1][3]. Gleichzeitig treten neue Hautprobleme auf, zum Beispiel große Hautlappen, Trockenheit, Juckreiz oder Haarausfall, weil die Haut mit dem raschen Gewichtsverlust nicht klarkommt und wichtige Nährstoffe manchmal fehlen[1][2][3]. Über 75 Prozent aller Operierten zeigen nach der OP irgendeine Veränderung der Haut[1]. Wichtig ist deshalb, regelmäßig die Haut zu kontrollieren und bei Problemen früh einen Hautarzt aufzusuchen[1][3]. Auch Cremes, gesunde Ernährung und in manchen Fällen eine Hautstraffung helfen, die Lebensqualität zu verbessern[1][3]. Originaltitel: The Impact of Bariatric Surgery on the Development and Progression of Dermatologic Diseases: A Narrative Review - Dermatology and Therapy Link zur Quelle

Menschen mit Schuppenflechte haben ein erhöhtes Risiko, auch eine Psoriasis-Arthritis zu bekommen. Neue Studien zeigen, dass Medikamente, die auf den Botenstoff **Interleukin-23 (IL-23)** wirken, dieses Risiko senken können. Wer stattdessen einen Blocker gegen **Interleukin-17 (IL-17)** bekommt, hat ein höheres Risiko, an Psoriasis-Arthritis zu erkranken[1][2][4]. Im Vergleich: Nach fünf Jahren erkrankten rund 12 Prozent der IL-23-Behandelten an Psoriasis-Arthritis, aber 20 Prozent der IL-17-Behandelten[1]. Die Forscher haben verschiedene Medikamente miteinander verglichen. IL-23-Blocker wie Guselkumab, Risankizumab und Tildrakizumab schnitten deutlich besser ab als IL-17-Blocker wie Secukinumab und Ixekizumab[1]. Das geringere Risiko trat bei verschiedenen Altersgruppen, Frauen, Männern und auch bei unterschiedlichen Hauttypen auf[2]. Aber: Ob IL-23-Blocker die Entwicklung von Psoriasis-Arthritis wirklich verhindern, ist noch nicht endgültig bewiesen[4]. Originaltitel: Psoriatic arthritis risk in psoriasis patients receiving anti-IL-23 vs anti-IL-17: comparison of drug classes and individual agents Link zur Quelle

Risankizumab hilft vielen Menschen mit Psoriasis-Arthritis gut, auch wenn sie vorher keine Biologika bekommen haben[1]. Die meisten Patientinnen und Patienten berichten schon nach der Behandlung über weniger Gelenkschmerzen und weniger Müdigkeit[1]. Wenn man Dactylitis oder Entzündungen an den Sehnenansätzen hatte, waren sie oft nach der Behandlung verschwunden (Dactylitis bei 82 %, Enthesitis bei 90 %)[1]. Außerdem hat sich die betroffene Hautfläche deutlich verringert (durchschnittlich um 10 %)[1]. Sowohl die Patientinnen und Patienten als auch ihre Ärztinnen und Ärzte waren sehr zufrieden mit dem Ergebnis[1]. Originaltitel: Real-World Effectiveness and Satisfaction with Risankizumab for the Treatment of Psoriatic Arthritis in Biologic-Naïve Patients: A Population Survey in the United States and Europe. Link zur Quelle

Curcumin, der gelbe Stoff aus der Kurkuma-Wurzel, wird seit Jahrhunderten als Gewürz und Naturheilmittel in Asien genutzt[1]. Studien zeigen, dass Curcumin Entzündungen im Körper hemmen kann, zum Beispiel bei Krankheiten wie Psoriasis, Arthritis, Asthma oder Darmproblemen[1][2]. Es kann dazu beitragen, typische Entzündungswerte zu senken und Beschwerden zu lindern[2]. Curcumin wirkt, indem es wichtige Botenstoffe der Entzündung hemmt und so das Gleichgewicht im Immunsystem wiederherstellt[2][3]. Allerdings: Viele dieser Ergebnisse stammen aus Labortests oder kleinen Studien. Die Forschung braucht noch mehr große Untersuchungen, bevor Ärztinnen und Ärzte Curcumin klar empfehlen können[1][3]. Trotzdem zeigt Curcumin als Nahrungsergänzung oder Zusatz zur Therapie schon jetzt vielversprechende Ansätze[2]. Originaltitel: Curcumin in Inflammatory Complications: Therapeutic Applications and Clinical Evidence Link zur Quelle

GLP-1-Rezeptor-Agonisten, ursprünglich zur Behandlung von Typ-2-Diabetes und Adipositas entwickelt, wirken nicht nur auf den Blutzucker und das Gewicht[2][5]. Neuere Studien zeigen, dass diese Medikamente auch das Immunsystem beeinflussen und Entzündungen im Körper dämpfen können[1][4]. Besonders interessant: GLP-1 wirkt im Gehirn und aktiviert dort eine Art "Bremse" für überschießende Entzündungen[1]. Auch bestimmte Immunzellen im Darm werden durch GLP-1-Rezeptor-Agonisten reguliert, was hilft, Entzündungen in Darm und anderen Organen zu verringern[3]. Das ist spannend für Menschen mit Autoimmun- oder Entzündungskrankheiten wie Psoriasis, Rheuma oder chronisch-entzündlichen Darmerkrankungen. Ob und wie stark diese Medikamente auch bei Psoriasis helfen, ist noch in der Forschung. Die Richtung ist aber klar: GLP-1-Rezeptor-Agonisten könnten zukünftig mehr sein als nur Blutzucker-Senker – möglicherweise auch eine neue Option für weniger Entzündungen und geregeltes Immunsystem[1][3]. Originaltitel: Roles of glucagon-like peptide 1 receptor agonists in immune cell biology and autoimmune/autoinflammatory diseases Link zur Quelle

Beliebte Diäten wie vegetarisch, glutenfrei oder kalorienreduziert wirken sich unterschiedlich auf entzündliche Hautkrankheiten wie Psoriasis oder Psoriasis-Arthritis aus. Eine aktuelle Studie zeigt: Eine streng kalorienreduzierte Ernährung kann das Risiko für Psoriasis-Arthritis leicht erhöhen, während vegetarische oder glutenfreie Diäten keinen klaren Einfluss auf diese Krankheiten zeigen[2]. Die Mittelmeerdiät kann dagegen hilfreich sein. Sie setzt auf viel Gemüse, Obst, Vollkorn und gesunde Fette und bringt viele antioxidative und entzündungshemmende Stoffe mit. Menschen, die sich so ernähren, berichten oft über weniger schwere Symptome bei Psoriasis und anderen entzündlichen Hautleiden[3]. Fazit: Spezielle Diäten sind kein Wundermittel gegen Psoriasis, aber ausgewogen und eher mediterran zu essen, kann Entzündungen abmildern und das Wohlbefinden unterstützen[3][5]. Originaltitel: Associations between Popular Diets and Inflammatory Skin Diseases: A M | CCID Link zur Quelle