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BackgroundHyperkeratotic psoriasis is a rare variant that includes forms such as elephantiasis, considered the rarest. It is characterized by thick, persistent plaques, resembling elephant skin, located mainly on the extremities and buttocks. Early detection and appropriate treatment, including systemic therapies, are essential for its management.Clinical caseA 58-year-old male patient presented in 2018 with dermatosis on his forehead, right elbow, and the backs of both hands. He was initially diagnosed with seborrheic dermatitis and chronic lichen simplex and received multiple topical therapies without improvement. In 2024, he developed new, disseminated lesions on his elbows, hands, and both legs, characterized by hyperkeratotic plaques and excoriations. A biopsy confirmed the diagnosis of elephantiasis variant hyperkeratotic psoriasis. Treatment with ustekinumab was initiated, resulting in significant improvement of the lesions.ConclusionsElephantine psoriasis is a rare and difficult-to-treat variant, with few reported cases, which hinders the standardization of its management. Biologic therapies represent an effective alternative for improving prognosis, reducing complications, and preventing progression to other associated pathologies. Disseminating these cases is essential to expanding knowledge of this variant and optimizing available therapeutic options, for the benefit of patients.Weiterlesen

Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and immune activation. The single nucleotide polymorphism (SNP) rs610604 within the TNFAIP3 locus is associated with increased psoriasis susceptibility and response to TNF-targeted therapies, yet its functional mechanism remained unclear. In this study, we identify, to our knowledge, previously unreported regulatory axis linking IKKα to TNFAIP3 in keratinocytes and demonstrate how genetic variation at rs610604 modulates inflammatory signaling. Genome-wide chromatin profiling revealed nuclear IKKα predominantly occupies transcriptionally inactive regions and acts as a chromatin-associated repressor. Among its targets, TNFAIP3 emerged as a key locus containing an IKKα-binding region overlapping the rs610604 variant. Functional analyses showed allele-specific recruitment of IKKα, with the psoriasis-risk G allele displaying stronger and more persistent binding compared with the protective T allele. This interaction promotes transcriptional repression of TNFAIP3, a negative regulator of NF-κB, MAPK, and IL-17 pathways, thereby sustaining pro-inflammatory signaling; consistently in psoriatic lesions nuclear IKKα is reduced. These findings identify a nuclear IKKα-TNFAIP3 axis linking genetic susceptibility to inflammatory signaling, providing a potential explanation for the paradox of chronic inflammation without frequent malignant transformation in psoriatic skin, and highlighting IKKα as a potential therapeutic target in psoriasis and related inflammatory disorders.Weiterlesen

Ethnopharmacological relevanceXiegan-Liangxue-Jiedu decoction (XLJD) is an ethnopharmacological empirical prescription inherited from Gu's Surgery, a national intangible cultural heritage of Chinese ethnomedicine. Developed based on the classic TCM theory of Liver governing emotion, XLJD has been clinically used for centuries to treat psoriasis (PsO) via the principle of the TCM principle of "treating PsO from the Liver perspective", and has shown favorable efficacy in alleviating psychiatric comorbidities in psoriasis (PCP) by soothing the Liver and relieving emotional discomfort.Aim of the studyTo determine the therapeutic efficacy of XLJD and its potential mechanisms of action in PCP mice, and to reveal the modern pharmacological mechanism of the TCM theory of Liver governing emotion in the treatment of PCP.Materials and methodsMass spectrometry were used to elucidate XLJD's phytochemical profile and blood-absorbed components. The murine PCP model was established by exposure to CUMS and imiquimod. The efficacy of treating PsO was evaluated using PASI, HE staining, lymphocyte proliferation levels, cytokine levels, etc. Mental disorders were evaluated using the open field, elevated plus maze, and tail suspension tests. RNA-seq was performed to detect transcriptional changes in skin tissues, while lipidomics was applied to analyze serum lipids. Key genes and protein were validated using qPCR and Western-blotting, respectively. Acid sphingomyelinase (ASM) and M1/M2 microglia in the hippocampus were determined via immunofluorescence staining.ResultsAmong the 142 compounds identified in XLJD, 21 were detected in the blood. XLJD significantly alleviated the severity of PsO-related indicators in PCP mice while ameliorating behavioral abnormalities and mitigating HPA axis hyperactivity. XLJD downregulated the transcription of genes involved in lipid metabolism and ameliorated abnormal sphingolipid (SP) metabolism. It inhibited lesions mediated by sphingosine-1-phosphate signaling in lesioned skin. In the hippocampus, XLJD reduced the proportion of M1 microglia and exerted potential neuroprotective effects by inhibiting ASM expression and activity.ConclusionsBased on the TCM theory of Liver governing emotion, XLJD alleviated PsO severity and improved associated mental dysfunctions concomitantly in PCP mice by regulating SP metabolism. This study verifies the scientific connotation of the ethnopharmacological principle of treating PsO from the Liver perspective and provides a new ethnopharmacological strategy for the clinical management of PCP.Weiterlesen

PurposeEmerging evidence suggests the involvement of the renin-angiotensin system (RAS) in the pathogenesis and progression of autoimmune dermatological diseases. In a small exploratory study, we investigated angiotensin-converting enzyme (ACE) activity in blood obtained from male probands with psoriasis vulgaris (n = 4) and atopic dermatitis (AD, n = 5).MethodsThe degradation capacity of dabsylated synthetic bradykinin (DBK) with and without inhibition was determined using a thin-layer chromatography (TLC)-based neuropeptide reporter assay.ResultsWe observed a significantly reduced capacity for cleavage of DBK in psoriasis patients compared with that in AD patients and controls. In patient samples, the variation in the measured values was generally greater than that in healthy controls. We could not confirm the increased ACE activity in the circulation in psoriasis patients reported by others, likely because of different study designs and detection methods. We did not include samples of female patients and focused on younger men to avoid hormonal effects and minimize age-related factors.ConclusionThis preliminary study of the hypothesis-generating nature lacks power, but it certainly adds a question to the current view of the role of ACE in psoriasis. Treatments targeting specific components of the RAS could ameliorate inflammatory responses; thus, research in this area is becoming increasingly important.Weiterlesen

PurposeWhile dietary factors are known to be associated with the development and progression of psoriasis, their effect on treatment efficacy remains unclear. Therefore, this study aimed to elucidate the influence of tea consumption, sugar drinks, and high-fat foods on the treatment response in psoriasis.Patients and methodsWe undertook a prospective cohort study comprising 559 patients with psoriasis from Shanghai Skin Disease Hospital between 2022 and 2024. Data on demographics, lifestyle (including tea, sugary drinks, and high-fat food consumption), and disease severity (PASI, BSA, PGA) were collected via structured questionnaires at baseline, week 4, and week 8. The primary endpoints were the proportions of patients achieving PASI 50 responses at week 8. Multivariable logistic regression was used to estimate odds ratios with 95% confidence intervals, adjusting for age, sex, BMI, smoking, alcohol, and treatment regimen. Data were analyzed using SAS 9.4 software.ResultsIn the psoriasis cohort (mean age 48.5 years; 73.2% male), 37.1% and 68.7% of patients consumed sugar drinks and high-fat foods ≥2 times/week, respectively. Frequent sugar drinks consumption (≥4 times/week) was independently associated with significantly reduced odds of achieving PASI 50 (adjusted OR=0.24, 95% CI: 0.08-0.75) and PASI 75 (adjusted OR=0.27, 95% CI: 0.07-1.00) at week 8. Moderate intake of high-fat foods (2-3 times/week) showed an inverse, borderline significant association with PASI 50 at week 4 (adjusted OR=0.68, 95% CI: 0.45-1.00). Tea consumption showed a non-significant association with treatment response (e.g, week 8 PASI 50 adjusted OR=1.44, 95% CI: 0.88-2.35), warranting further investigation in larger cohorts.ConclusionThis study demonstrates that high consumption of sugar drinks and high-fat foods is associated with suboptimal treatment response in psoriasis. Tea consumption was not significantly associated with treatment outcomes, although further investigation with larger cohorts may be warranted. These findings highlight the importance of integrating dietary assessment and counseling into comprehensive psoriasis management.Weiterlesen

BackgroundLangerhans cells (LCs) play a crucial role in sensing and processing stimuli from the skin and the external environment. They are implicated in various skin disorders, acting either as pro-inflammatory agents or as regulatory elements. However, the exact function of LCs in the pathogenesis of psoriasis remains unclear. Psoriasis is characterized by a significant Th17/Treg immune imbalance. To elucidate the independent effect of Treg dysfunction on psoriatic inflammation, we established a Treg-inhibited psoriasis group using the Foxp3 inhibitor CMD178, in conjunction with LC depletion models to investigate the LC-Th17/Treg regulatory axis METHODS: Psoriasis models were established through the topical application of IMQ. Female C57BL/6 N mice were divided into three groups: control, IMQ-induced psoriasis, and Treg-depleted psoriasis. LCswere depleted using diphtheria toxin in Langerin-DTR mice, while Tregs were inhibited by CMD178. Inflammation was assessed through measurements of ear thickness, histopathology, apoptosis, and cytokine production. Additionally, RT-qPCR was utilized to detect the expression of S100A7, S100A8, and MMP2. Flow cytometry was employed to analyze the functional status of lymphocytes and T cell phenotypes.ResultsIMQ-induced psoriasis-like lesions exhibit activated LCs, an increase in Th17 cells, a decrease in Tregs, elevated levels of IL-17A and IL-22, and reduced levels of TGF-β and PD-L1. Depletion of LCs alleviated the lesions and restored the Th17/Treg balance, whereas depletion of Tregs exacerbated the inflammation.ConclusionLCs play a central regulatory role in the psoriatic skin environment by influencing the Th17/Treg.Weiterlesen

Skin psoriasis involves the activation of skin dendritic cells (DCs) by external triggers. Activated DCs then secrete interleukin 23 (IL-23), which acts as a connector between innate and adaptive immunity and promotes the differentiation of T helper 17 (Th17) cells. This process leads to an elevated production of interleukin 17 (IL-17) and excessive keratinocyte production, creating an autoimmune loop in the development of psoriasis. Dihydrotanshinone 1 (DIH), a flavonoid recognized for its antitumor effects, was assessed for its impact on imiquimod (IMQ)-induced psoriatic plaques in mice. In this investigation, our team used IMQ-induced mouse models to study how DIH affects keratinocytes and skin immunity. At first, we noticed that psoriasis-like lesions were significantly more severe in mice treated with DIH. However, after giving DIH to IMQ-induced mice, we observed a reduction in hyperproliferative keratinocytes, cytokine release, and the accumulation of DCs and Th17 cells. Further exploration showed that DIH relieved psoriasis-like skin conditions and inhibited the abnormal proliferation of HaCaT cells and Th17 cell differentiation. In particular, we found that DIH achieved these outcomes by modulating the STAT3 signaling pathway, which in turn suppressed DCs/Th17 cell responses and keratinocyte proliferation. Hence, DIH may affect the recruitment and function of immune cells in the skin and alter keratinocyte proliferation and differentiation in the context of psoriasis.Weiterlesen

Single-cell RNA sequencing has rapidly expanded the scale of skin transcriptomic data, yet these datasets remain fragmented across studies spanning different species, diseases and experimental manipulations. An up-to-date, comprehensive, and queryable single-cell cross-species repository for skin is still lacking. Here, we present scSAID (skin-scsaid.com), a single-cell database with an interactive web portal offering a broad suite of in-depth analyses for human and mouse skin. It integrates more than 1.2 million high-quality cells collected from 252 samples, establishing a unified reference for cell-type annotation, cross-species comparison and pathological studies. Using psoriasis as a case study, we demonstrate how scSAID can be used to evaluate how faithfully mouse models reproduce human pathology. Systematic comparison with the imiquimod-induced mouse model revealed numerous species-specific molecular signatures of psoriasis, including human-specific NFKB1 activation and STAT1 involvement, indicating that the current mouse model captures only limited aspects of the disease. We further introduce psoSpotter, a disease-biomarker-selection algorithm that, coupled with in silico perturbation using scSAID data, uncovers PPIA as a novel psoriasis drug target, illustrating the potential of scSAID for identifying therapeutic approaches. Overall, scSAID delivers a large-scale, cross-species skin single-cell resource and analysis platform, opening new opportunities for the discovery of disease-relevant targets in skin diseases.Weiterlesen

**Nierensicherheit von Biologika bei Psoriasis** Die TriNetX‑Studie wertet Versorgungsdaten von vielen Psoriasis‑Betroffenen aus und vergleicht Personen mit und ohne moderne Systemtherapien wie Biologika oder Apremilast.[11] Andere große Auswertungen zeigen, dass Biologika die Nierenfunktion in der Regel nicht verschlechtern.[1][2] Das Risiko für akutes oder chronisches Nierenversagen bleibt niedrig und ist vergleichbar mit klassischen Systemtherapien.[1][7] Unterschiede zwischen den einzelnen Biologika‑Klassen sind gering.[1][5] Für Euch bedeutet das: Die Entscheidung für ein Biologikum geht meist nicht mit einem zusätzlichen Nierenrisiko einher.[1][5] Gleichzeitig bleibt das durch Psoriasis erhöhte Grundrisiko für Nierenschäden bestehen, besonders bei Diabetes oder bereits eingeschränkter Nierenfunktion.[1][4][9] Im Alltag sind regelmäßige Blut‑ und Urinkontrollen, guter Blutdruck‑ und Blutzucker‑Einstellung und ausreichende Flüssigkeitszufuhr wichtig.[1][4][5] Sprecht mit Eurem Behandlungsteam, welches Medikament zu Eurer Gesamtsituation passt und welche Laborwerte überwacht werden sollen.[1][5] So könnt Ihr von der Wirkung der Biologika profitieren und Eure Nieren bestmöglich schützen.[1][5] Originaltitel: 0334 Renal safety in psoriasis patients treated with biologics: Evidence from TriNetX Link zur Quelle

Trial number: 2023-503859-10-00 Overall trial status: Ongoing, recruitment ended Trial title: A MULTICENTER, RANDOMIZED, PARALLEL-GROUP, DOUBLE-BLIND, ACTIVE-CONTROLLED STUDY TO EVALUATE THE EFFICACY AND SAFETY OF BIMEKIZUMAB COMPARED TO USTEKINUMAB IN CHILDREN AND ADOLESCENT FROM 6 YEARS TO LESS THAN 18 YEARS OF AGE WITH MODERATE TO SEVERE PLAQUE PSORIASIS Medical conditions: Moderate to Severe Plaque Psoriasis Status in each country: Germany:Ongoing, recruitment ended, Belgium:Ongoing, recruitment ended, Czechia:Ongoing, recruitment ended, Spain:Ongoing, recruitment ended, Italy:Ongoing, recruitment ended, France:Ended, Hungary:Ongoing, recruitment ended, Poland:Ongoing, recruitment ended Trial phase: Therapeutic confirmatory (Phase III) Therapeutic Areas: Diseases [C] - Immune System Diseases [C20] Primary end point: Psoriasis Area Severity Index 90 (PASI90) response at Week 16, Investigator´s Global Assessment (IGA) 0/1 response at Week 16 Secondary end point: PASI75 response at Week 4, PASI100 response at Week 16, PASI90 response at Week 48, IGA 0/1 response at Week 48, PASI100 response at Week 48, IGA 0 response at Week 16, IGA 0 response at Week 48, Treatment-emergent adverse events (TEAE)s, Serious TEAEs, TEAEs leading to discontinuation of investigational medicinal product (IMP), TEAEs leading to withdrawal from the study, Selected safety topics of interest (including infection [serious, opportunistic, fungal, and tuberculosis (TB)], inflammatory bowel disease (IBD), and injection site reactions) with onset occurring from day of first dose through 20 weeks after final dose of IMP adjusted by duration of study participant exposure to IMP, Change from Baseline in vital signs, Change from Baseline in physical examination findings, Change from Baseline in height (growth assessment), Change from Baseline in weight (growth assessment), Change from Baseline in laboratory analyses (chemistry and hematology), Change from Baseline in Children’s Dermatology Life Quality Index (CDLQI) total score at Week 16, Change from Baseline in CDLQI total score at Week 48, Change from Baseline in Childhood Health Assessment Questionnaire (CHAQ) disability index at Week 16 for study participants with juvenile psoriatic arthritis (PsA) prior to Baseline, Change from Baseline in Peak Pruritus numerical rating scale (NRS) score at Week 16, Plasma bimekizumab concentrations prior to and following IMP administration over the Initial Treatment Period, over the Maintenance Period, and over the OLE Period, Plasma anti-bimekizumab antibodies prior to and following IMP administration over the Initial Treatment Period, over the Maintenance Period, and over the OLE Period Age of participants: 0-17 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 122 Sponsor: UCB Biopharma Sponsor type: Pharmaceutical company Trial product: Placebo matching test and comparator. 0.9% sodium chloride solution for injection (unauthorized), ustekinumab, Placebo matching test and comparator. 0.9% sodium chloride solution for injection (authorized - MA number: 6697366.00.00), bimekizumab Results posted: No Overall decision date: 15/07/2024 Countries decision date: CZ: 17/07/2024, FR: 15/07/2024, HU: 17/07/2024, ES: 16/07/2024, IT: 13/09/2024, BE: 22/07/2024, PL: 22/07/2024, DE: 17/07/2024 Last updated date: 27/02/2026Den kompletten Artikel zeigen

Trial number: 2024-512207-39-00 Overall trial status: Ended Trial title: A Phase 2, Multicenter, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group, Dose-Ranging Study of LY4100511 (DC-853) for the Treatment of Adult Participants with Moderate-to-Severe Plaque Psoriasis Medical conditions: Plaque Psoriasis Status in each country: Hungary:Ended, Poland:Ended, Czechia:Ended, Germany:Ended Trial phase: Therapeutic exploratory (Phase II) Therapeutic Areas: Diseases [C] - Skin and Connective Tissue Diseases [C17] Primary end point: Proportion of participants achieving PASI 75 at Week 12 Secondary end point: 1. Proportion of participants achieving: • an sPGA score of 0 or 1 with ≥2 grade improvement from baseline at Week 12 • ≥50%, ≥75%, ≥90%, and 100% reduction in PASI score at all scheduled timepoints • an sPGA score of 0 or 1 at all scheduled timepoints • Mean change and percent change from baseline in PASI score at all scheduled timepoints • Mean change and percent change from baseline in the percentage of BSA affected at all scheduled timepoints, 2. Summary of safety data, including number and proportion of: • TEAEs • SAEs • discontinuations due to TEAEs, 3. Measurement of plasma concentration of LY4100511 at scheduled timepoints to evaluate steady state maximum concentration (Cmax,ss) and trough concentration (Ctrough,ss) and associated intra-individual variability Age of participants: 65+ years, 18-64 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 134 Sponsor: Dice Therapeutics Inc. Sponsor type: Pharmaceutical company Trial product: Placebo tablets will be the same size, shape, and color as the active tablets and will consist of the compendial excipients present in the active tablets. Placebo tablets are supplied in the same packaging configuration as the active tablets. Results posted: Yes Overall decision date: 23/01/2025 Countries decision date: PL: 27/01/2025, HU: 24/01/2025, DE: 24/01/2025, CZ: 23/01/2025 Last updated date: 06/10/2025Den kompletten Artikel zeigen

Trial number: 2023-505121-14-00 Overall trial status: Authorised, recruiting Trial title: A Phase 3 Multicenter, Randomized, Double-blind, Placebo-controlled and Deucravacitinib Active Comparator-controlled Study to Evaluate the Efficacy and Safety of JNJ-77242113 for the Treatment of Participants With Moderate to Severe Plaque Psoriasis Medical conditions: Moderate to Severe Plaque Psoriasis Status in each country: Italy:Not authorised, Hungary:Ongoing, recruitment ended, Poland:Ongoing, recruitment ended, Germany:Ongoing, recruitment ended, France:Not authorised, Spain:Ongoing, recruitment ended Trial phase: Therapeutic confirmatory (Phase III) Therapeutic Areas: Diseases [C] - Immune System Diseases [C20] Primary end point: IGA score of 0 or 1 and a ≥2-grade improvement from baseline at Week 16., PASI 90 at Week 16. Secondary end point: N/A Age of participants: 18-64 years, 65+ years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 320 Sponsor: Janssen - Cilag International Sponsor type: Pharmaceutical company Trial product: JNJ-77242113, DEUCRAVACITINIB, Film-Coated Tablet without JNJ-77242113, Film-Coated Tablet without Deucravacitinib Results posted: No Overall decision date: 17/01/2024 Countries decision date: FR: 22/01/2024, IT: 22/01/2024, DE: 28/05/2024, HU: 22/01/2024, PL: 07/02/2024, ES: 29/05/2024 Last updated date: 16/07/2026Den kompletten Artikel zeigen

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

### Psoriasis und Risiko für trockene Netzhautschäden Die Studie zeigt: Menschen mit Psoriasis haben ein erhöhtes Risiko für eine altersbedingte Makuladegeneration, vor allem für die trockene Form.[4][3][1] Über zehn Jahre war das AMD‑Risiko um 56 Prozent höher als in einer Vergleichsgruppe mit Depression, für die trockene AMD um 13 Prozent.[4][3][10] Die Forschenden vermuten, dass Entzündung und eine Störung der Blutfette eine Rolle spielen.[1][3][2] Für Euch heißt das: Achtet neben Haut und Gelenken auch auf Eure Augen. Besonders ab 55 Jahren sind regelmäßige Kontrollen beim Augenarzt sinnvoll. Ein wichtiges Zeichen für die Zukunft: In der Studie hatten Menschen mit Psoriasis, die Biologika erhielten, etwa 27 Prozent weniger AMD‑Risiko als nur mit Kortison‑Salben.[3][7][10] Ihr könnt selbst beitragen: nicht rauchen, Euch regelmäßig bewegen, auf ausgewogene Ernährung achten und Begleiterkrankungen wie Diabetes gut behandeln. Diese Maßnahmen schützen Herz und Gefäße und damit auch die Augen. Originaltitel: Psoriasis is associated with increased risk of non-exudative age-related macular degeneration Link zur Quelle

Trial number: 2023-509668-11-00 Overall trial status: Ended Trial title: Adjustable brodalumab dosage regimen compared with standard brodalumab treatment for 52 weeks in subjects with moderate-to-severe plaque psoriasis and ≥120 kg body weight; ADJUST - Phase 4 – efficacy, A randomised, double-blind, controlled, parallel group, multi-centre trial Medical conditions: Moderate-to-severe plaque psoriasis and a body weight ≥120 kg. Status in each country: Czechia:Ended, Hungary:Ended, Italy:Ended, Germany:Ended, Belgium:Ended, Spain:Ended, Greece:Ended, Poland:Ended, France:Ended Trial phase: Therapeutic use (Phase IV) Therapeutic Areas: Diseases [C] - Skin and Connective Tissue Diseases [C17], Diseases [C] - Immune System Diseases [C20] Primary end point: Having at least 90% lower Psoriasis Area and Severity Index (PASI) score relative to baseline (PASI 90 response) at Week 40. Secondary end point: Having static Physician’s Global Assessment (sPGA) score of 0 or 1 at Week 40., Having PASI 90 response at Week 52., Having sPGA score of 0 or 1 at Week 52., Having sPGA of genitalia (sPGA-G) of 0 or 1 at both Weeks 40 and 52., Having sPGA-G score of 0 or 1 at Week 40., Having sPGA-G score of 0 or 1 at Week 52., Having PASI 100 response at Week 40., Having PASI 100 response at Week 52., Change from baseline at Weeks 40 and 52 in PASI score., Change from baseline at Weeks 40 and 52 in affected body surface area (BSA)., Having Dermatology Life Quality Index (DLQI) total score of 0 or 1 at Week 40., Having DLQI total score of 0 or 1 at Week 52., Change from baseline at Weeks 40 and 52 in DLQI total score. Age of participants: 65+ years, 18-64 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 352 Sponsor: Leo Pharma A/S Sponsor type: Pharmaceutical company Trial product: Brodalumab 70 mg, The placebo presentation is a pre-filled syringe containing the same excipients in the same amounts as the IMP, without the active substance., Kyntheum 210 mg solution for injection in pre-filled syringe Results posted: Yes Overall decision date: 06/06/2024 Countries decision date: FR: 18/06/2024, PL: 21/06/2024, IT: 12/06/2024, GR: 22/07/2024, ES: 06/06/2024, BE: 06/06/2024, CZ: 10/06/2024, DE: 07/06/2024, HU: 06/06/2024 Last updated date: 21/11/2025Den kompletten Artikel zeigen

Viele Menschen nutzen Biologika bei Psoriasis oder Gelenkproblemen, doch die Mittel können selten die Haut neu reizen[1][2]. Ein 42 Jahre alter Arbeiter mit Spondylitis bekam lange Adalimumab, erst nach vier Jahren traten Rötungen und Pusteln an Händen und Füßen auf. Ärztinnen stellten palmoplantare Pustelpsoriasis und Psoriasis vulgaris fest. Sie wechselten auf Secukinumab, die Haut wurde etwas ruhiger. Solche Fälle zeigen, dass Biologika auch nach langer Zeit plötzlich Psoriasis auslösen oder verschlimmern können[1][2]. Wer neue Flecken oder Pusteln unter der Spritzentherapie bemerkt, sollte früh mit dem Hautarzt reden. Originaltitel: [Cutaneous side effects of biologics: an important topic also in occupational dermatology]. Link zur Quelle

Viele Menschen mit Psoriasis fragen sich, ob sie später eine Psoriasis Arthritis entwickeln. In einer neuen Studie wurden Blut und Haut von Betroffenen genau angesehen. Bei Menschen mit Psoriasis Arthritis war ein Schutzstoff namens Elafin schwächer, dazu war das Enzym neutrophile Elastase stärker. Das Gleichgewicht dieser Stoffe war also verschoben. Das spricht dafür, dass Abwehrzellen bei Psoriasis Arthritis weniger gebremst werden. Solche Unterschiede könnten helfen zu erkennen wer ein höheres Risiko für Gelenkbeschwerden hat. Originaltitel: Psoriasis patients with psoriatic arthritis demonstrate a reduced regulatory capacity for neutrophil elastase. Link zur Quelle

Originaltitel: Safety and pharmacokinetics of anumigilimab for hidradenitis suppurativa or palmoplantar pustulosis: A phase 1b study. Link zur Quelle

Trial number: 2023-509216-28-00 Overall trial status: Ongoing, recruitment ended Trial title: EffisayilTM ON: An open-label, long term extension study to assess the safety and efficacy of spesolimab treatment in patients with Generalized Pustular Psoriasis (GPP) Medical conditions: Generalized Pustular Psoriasis Status in each country: France:Ongoing, recruitment ended, Italy:Ongoing, recruitment ended, Germany:Ongoing, recruitment ended, Belgium:Ongoing, recruitment ended, Spain:Ongoing, recruitment ended Trial phase: Therapeutic exploratory (Phase II) Therapeutic Areas: Diseases [C] - Skin and Connective Tissue Diseases [C17] Primary end point: Occurrence of treatment emergent adverse events (TEAEs) up to week 252 of maintenance treatment Secondary end point: The reoccurrence of a GPP flare defined by GPPGA, Time to first achievement of a GPPGA score of 0 or 1 in patients who received flare rescue treatment, A GPPGA pustulation sub-score of 0 indicating no visible pustules, by visit in patients who received flare rescue treatment, Change from baseline in Psoriasis Symptom Scale (PSS) score, by visit in patients who received flare rescue treatment Age of participants: 65+ years, 0-17 years, 18-64 years Gender of participants: Female, Male Trial region: In both EEA and non-EEA Planned number of participants: 25 Sponsor: Boehringer Ingelheim International GmbH, Boehringer Ingelheim Espana S.A. Sponsor type: Pharmaceutical company, Pharmaceutical company Trial product: Spesolimab Results posted: No Overall decision date: 12/02/2024 Countries decision date: FR: 13/02/2024, DE: 13/02/2024, BE: 19/02/2024, ES: 12/02/2024, IT: 18/03/2024 Last updated date: 20/07/2026Den kompletten Artikel zeigen

In der Studie wird gezeigt, dass ein höheres Körpergewicht die Chance verringert, einen Zustand mit **minimaler Krankheitsaktivität** zu erreichen.[2][4] Das gilt besonders für Psoriasis‑Arthritis‑Patienten, die mit **TNF‑Blockern** behandelt werden, andere moderne Medikamente sind davon weniger betroffen.[2] Vor allem die Beschwerden, die Ihr selbst angebt, wie Schmerzen und allgemeines Befinden, sind bei höherem Gewicht stärker.[2] ## Was bedeutet das für Euch? Für Euch heißt das: Gewicht spielt eine Rolle dafür, wie gut eine Therapie wirken kann, aber es ist nicht der einzige Faktor.[2][6] Auch Alter, Rauchen, Schäden an den Gelenken und Begleiterkrankungen haben einen Einfluss.[2] Es gibt verschiedene Wirkstoffklassen, bei denen ein höherer BMI die Wirkung offenbar weniger einschränkt, darüber könnt Ihr mit Euren Ärztinnen und Ärzten sprechen.[2][4] Im Alltag kann es helfen, schrittweise Gewicht zu reduzieren, zum Beispiel durch mehr Bewegung und eine angepasste Ernährung.[6][8] Studien zeigen, dass Gewichtsabnahme die Krankheitsaktivität bei Psoriasis‑Arthritis deutlich verbessern kann, besonders in Kombination mit einer laufenden Therapie.[6][8] Wichtig ist, dass Ihr Euch Unterstützung holt und Euch nicht selbst die Schuld gebt, sondern Gewicht als einen beeinflussbaren Baustein der Behandlung seht. Originaltitel: Body mass index and achievement of minimal disease activity in psoriatic arthritis across different classes of advanced therapy | Rheumatology | Oxford Academic Link zur Quelle

Psoriasis ist eine chronische Entzündung der Haut, dabei greifen angeborene und erworbene Abwehr eng ineinander.[2][13] Im Mittelpunkt steht ein Signalweg mit den Botenstoffen IL‑23 und IL‑17.[5][8] Zwei Arten von Abwehrzellen treiben diesen Weg an, Th17 Zellen aus dem trainierten Immunsystem und ILC3 Zellen aus der angeborenen Abwehr.[4][6] Beide Zellen geben IL‑17 und IL‑22 ab, diese Stoffe bringen Hautzellen dazu stark zu wachsen und weiter Entzündung zu machen.[4][7][8] Th17 Zellen halten den Prozess lange in Gang, ILC3 Zellen reagieren früh und schnell auf IL‑23.[4][6] Bei manchen Menschen überwiegen eher Th17 Zellen, bei anderen eher ILC3 Zellen das könnte erklären warum Formen von Psoriasis und die Wirkung von Therapien sich unterscheiden.[2][5] Forschende hoffen dass dieses Wissen hilft Behandlungen besser auf einzelne Patienten zuzuschneiden.[5][9] Originaltitel: T helper 17 cells and group 3 innate lymphoid cells define a spectrum of psoriasis endotypes. Link zur Quelle

Infliximab gibt es nicht nur als Infusion, sondern auch als Spritze unter die Haut. Eine kleine Studie aus einem Kinderzentrum hat 20 Kinder und Jugendliche mit chronisch entzündetem Darm beobachtet. Darunter waren auch jüngere Kinder mit geringem Gewicht, die von Infusion auf Spritze gewechselt sind. Nach gut zehn Monaten blieben 16 Kinder bei der Spritze und die Entzündung blieb ruhig. Die Blutspiegel des Wirkstoffs stiegen deutlich an und störende Antikörper verschwanden. Schwerwiegende Nebenwirkungen traten nicht auf, zwei Kinder bekamen aber stärkeres paradoxes Psoriasis und stoppten deshalb. Für Kinder mit Bedarf an Anti TNF Therapie wirkt die Spritze wie eine bequeme Option, größere Studien laufen noch. Originaltitel: Subcutaneous infliximab as a maintenance option in pediatric IBD: a real-world cohort including younger and lower-weight children. Link zur Quelle

Forscher in Bochum testen, wie sich Psoriasis Arthritis besser für jeden einzelnen behandeln lässt.[1] Sie beobachten 100 Menschen mit aktiver Psoriasis Arthritis, bei denen Methotrexat nicht gut wirkt.[1] Ärzte geben dann eines von drei Biologika mit Wirkung gegen TNF, IL‑17 oder IL‑23.[1] Nach 16 Wochen prüfen sie, ob die Krankheit fast ruhig ist.[1] Dazu sehen sie sich Haut, Gelenke und Nägel genau an und nehmen Blut und kleine Hautproben.[1] Mit Methoden der künstlichen Intelligenz suchen sie Muster, die zeigen, welches Medikament wem hilft.[1] Die Studie läuft bis Juli 2026, die Forschenden wollen die Ergebnisse später in Fachzeitschriften teilen.[1] Originaltitel: Development of a predictive marker panel for the individualised bDMARD therapy of psoriatic arthritis: protocol for a prospective observational study (Integrate-PsA). Link zur Quelle

Bei manchen Krankheiten hängen Haut und Knochen eng zusammen, dazu zählt auch die Psoriasisarthritis[1]. Dieses Zusammenspiel heißt SKIBO, also skin bone interaction[1]. Ursache sind vererbbare Anlagen und Entzündungen im Immunsystem[1]. Die Haut zeigt Warnzeichen, während Röntgenbild oder MRT Veränderungen am Knochen zeigen[1]. Radiologinnen und Radiologen sollen darum immer auch die Haut ansehen, wenn sie nach Schäden an Gelenken und Knochen suchen[1]. So lassen sich Krankheiten wie Psoriasisarthritis oder SAPHO früher erkennen und besser behandeln[1]. Für Betroffene erklärt SKIBO, warum Haut und Gelenke oft gleichzeitig Probleme machen[1]. Originaltitel: [Cutaneous and skeletal manifestations of systemic diseases: SKIBO]. Link zur Quelle

PsA ist eine chronische Gelenkkrankheit und sie kann das Leben stark einschränken[2][11]. Viele Betroffene haben Übergewicht und sie tragen öfter Herz und Stoffwechselprobleme mit sich[2][11]. Extra Kilos verstärken die Entzündung im Körper und sie drücken auf die Gelenke und dadurch werden Schmerzen und Steifigkeit stärker und Therapien wirken schlechter[2][3][5]. Biologika helfen dann oft weniger gut und Ziele wie niedrige Aktivität sind schwerer zu erreichen[5][12]. Studien zeigen dass Abnehmen Beschwerden mindern kann und Medikamente dann besser greifen[5][12][14]. Fachleute raten deshalb zu einem Plan der Gelenke Haut Gewicht Bewegung und Herz gemeinsam im Blick hat[2][5][11]. Originaltitel: Psoriatic arthritis and obesity: a review of clinical burden and considerations for comprehensive care. Link zur Quelle