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No abstract supplied.Weiterlesen

Psoriasis is an inflammatory skin disease, and current treatments have their own limitations, including moderate treatment effectiveness, poor compliance, and potential safety risks, etc. Therefore, the primary focus of this study is to explore novel molecular targets and improve the diagnosis and treatment of psoriasis patients. In this study, comprehensive bioinformatics analysis was performed on the expression profiles of tissue samples from patients with psoriasis in the clinical trial of TYK2/JAK1 inhibitor treatment (NCT02310750). Weighted gene co-expression network analysis (WGCNA) and least absolute shrinkage and selection operator (LASSO) regression were performed to identify characteristic genes and construct the diagnostic models. Gene set enrichment analysis (GSEA) was used to identify the biological processes of psoriasis characteristic gene sets. GO and KEGG pathway analysis were combined to elucidate the potential biological significance of differentially expressed genes (DEGs). The accuracy of biomarker identification was further validated using immune cell infiltration and receiver operating characteristic (ROC) curves based on external data (GSE6710\GSE30999\GSE14905). A total of 5 genes (DEFB103A, OAS3, OASL, SAMD9, STAT1) were co-identified as characteristic genes in psoriasis progression and treatment. The feature of the immune cell infiltration was highly consistent with association of characteristic biomarkers with immune cells. A total of 14 up-regulated genes and 5 down-regulated genes were identified in respective modules (AUC NL/LS = 0.9783; AUC pre/post = 0.9395; AUC external = 0.9469). In addition, 8 genes (DEFB103A, OASL, HERC6, ISG15, MKI67, MX1, MXD1, SCO2) were considered to have statistically significant differences in sensitivity of short-term treatment for psoriasis. The research findings provide an understanding of the role of novel biomarkers and offer a perspective for further in-depth investigation into the progression and treatment of psoriasis.Weiterlesen

Psoriasis is a chronic inflammatory skin disease whose main manifestation is scaly and erythematous plaques. The pathogenesis is complex, including genetic and environmental factors. In recent years, epigenetic modifications, which means changing in gene expression instead of altering the DNA sequence, have been gradually studied by scholars as an important mechanism in psoriasis pathogenesis. The clinical application of epigenetics in psoriasis is promising with its potential as diagnostic biomarkers, predictors of disease progression, and targets for treatment. This review reveals the role of epigenetics in the pathogenesis of psoriasis and its contribution to clinical treatment for patients with psoriasis.Weiterlesen

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ObjectivePsoriatic arthritis (PsA) is a chronic inflammatory condition associated with psoriasis and characterised by heterogeneous clinical manifestations, including peripheral and axial arthritis, enthesitis and dactylitis. A subset of patients exhibits a 'difficult-to-treat' (D2T) phenotype, necessitating complex therapeutic strategies. Metabolic syndrome (MetS) is highly prevalent in PsA patients and has been implicated in increased disease activity.This study aimed to evaluate the impact of MetS on the development of D2T phenotype in PsA and its potential implications for disease management.MethodsA cross-sectional study was conducted on PsA patients recruited from the Rheumatology Clinic at Fondazione Policlinico Campus Bio-Medico of Rome. Patients fulfilling the Classification Criteria for Psoriatic Arthritis criteria were assessed for disease activity and the presence of MetS according to National Cholesterol Education Programme Adult Treatment Panel III criteria. D2T PsA was defined based on the Rheumatoid Arthritis European Alliance of Associations for Rheumatolog criteria revised for PsA by Perrotta et al. Statistical analyses, including logistic regression and path analysis, were performed to explore associations between MetS and D2T PsA.ResultsAmong 182 PsA patients, 42.94% met MetS criteria. The D2T subset (n=66) demonstrated a significantly higher prevalence of MetS (81.82% vs 29.37%, p<0.0001). Logistic regression revealed a strong association between MetS and D2T PsA (OR 7.56, 95% CI 2.53 to 22.56, p<0.0001), and path analysis confirmed MetS as an independent predictor of D2T phenotype.ConclusionsMetS is strongly associated with a D2T phenotype in PsA, suggesting that metabolic comorbidities contribute to disease severity and treatment resistance. Addressing metabolic dysfunction may be crucial in optimising therapeutic outcomes in PsA management.Weiterlesen

Background/objectivesThe mechanism of action of treatment drugs for psoriasis is based on anti-inflammation and the inhibition of epidermal proliferation, and retinoids and vitamin D3 derivatives are first-line therapy drugs for psoriasis. This meta-analysis aimed to comprehensively evaluate the efficacy and safety of calcipotriol-acitretin combination therapy for psoriasis and investigate its effect on serum inflammatory factors.MethodsA systematic search of PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Data, Chinese biomedical literature service system (SinoMed), and Chinese Biomedical Journal Database (VIP), from the earliest record until Dec.13, 2024, was conducted. The outcomes were overall effective rate, Psoriasis Area and Severity Index (PASI) scores, inflammatory factor level and side effects.ResultsA total of 13 studies with 1196 patients were included in this meta-analysis. The results of this study show that the calcipotriol-acitretin combination therapy could improve the total effective rate when compared with acitretin [RR = 1.25, 95% CI (1.18, 1.33)] or calcipotriol [RR = 1.36, 95% CI (1.20, 1.56)] monotherapy. The combined therapy could decrease the PASI score observably when compared with acitretin monotherapy [SMD =  - 2.26, 95% CI (-3.24, -1.28)] or calcipotriol monotherapy [SMD =  - 3.79, 95% CI (-5.78, -1.79)]. Calcipotriol-acitretin combination therapy remarkably reduced the levels of TNF-α, IL-23, IL-17, INF-γ and IL-6 in serum, while increasing the levels of IL-4 and IL-10 within the serum, compared to acitretin monotherapy. This combination therapy did not increase the risk of skin irritation & burning pain, dry skin and perioral dermatitis. Notably, the incidence of perioral dermatitis was lower in combination therapy than acitretin monotherapy [P = 0.04, RR = 0.24, 95% CI (0.06, 0.93)].ConclusionsThe calcipotriol-acitretin combination therapy could be a safe and effective therapeutic strategy in the treatment of psoriasis. However, the lack of PROSPERO registration and the high heterogeneity in this study limited the conclusion, and more high-quality RCTs were needed for further evaluation.Weiterlesen

Psoriasis, a chronic skin autoimmune disease characterized by abnormal immune responses, is influenced by genetic and environmental factors. Recent microbiota research has revealed that short-chain fatty acids (SCFAs), metabolites produced by gut microbiota, play a pivotal role in regulating immune function and inflammation. This review examines the current literature on the relationship between gut dysbiosis, SCFA production, and immune modulation in psoriasis, focusing on emerging evidence from microbiota and immunological studies. SCFAs have been shown to influence key immune pathways, including T-cell activation and cytokine production, which are critical in psoriasis pathogenesis. Reduced SCFA levels have been observed in psoriasis, highlighting the role of gut dysbiosis in disease progression. Understanding the gut-skin axis and the role of SCFAs offers novel insights into developing effective, safe, and accessible treatments for psoriasis. Restoring microbial balance and SCFA production may serve as a promising therapeutic approach for managing psoriasis.Weiterlesen

BackgroundPsoriasis is a chronic inflammatory skin disorder characterized by elevated levels of proinflammatory cytokines. Mesenchymal stem cells (MSCs) have demonstrated therapeutic potential, yet the specific mechanisms involved are not fully understood.ObjectiveTo investigated the effectiveness of extracellular vesicles (EVs) derived from MSCs that were genetically modified to overexpress miR-146a, in a mouse model of psoriasis.MethodsTo enhance miR-146a expression, MSCs were transfected, and their EVs were subsequently purified. Thirty mice were randomly assigned to three groups and induced with imiquimod cream to develop psoriasis-like skin lesions. The treatment groups included: (1) a control group administered PBS, (2) a group treated with EVs containing a control miRNA (miR-control EVs), and (3) a group receiving EVs enriched with miR-146a (miR-146a-EVs). EVs were administered intravenously and lesions were evaluated. Following intravenous administration of EVs, the severity of skin lesions was assessed. Concentrations of key cytokines, including IFN-γ, IL-17, TNF-α, IL-23, IL-6, IL-1β, TGF-β, IL-10, and IL-4, were quantified in both spleen and skin tissue lysates using ELISA and qRT-PCR techniques.ResultsThe experimental findings demonstrated that the administration of miR-146a-enriched EVs led to a significant improvement in clinical symptoms. There were substantial reductions observed in combined erythema, scaling, and skin thickness measurements compared to untreated controls. Additionally, levels of proinflammatory cytokines IFN-γ, IL-17, TNF-α, IL-23, IL-6, and IL-1β were significantly downregulated in the miR-146a-EV group, while anti-inflammatory TGF-β, IL-10 and IL-4 were upregulated. The same results were obtained in the spleens of mice.ConclusionEVs derived from miR-146a-modified MSCs effectively reduced psoriasis-like inflammation by modulating cytokine expression. This novel cell-free therapy holds promise for the treatment of psoriasis.Weiterlesen

IntroductionPsoriatic arthritis (PsA) is an immune-inflammatory disease involving skin and synovial-entheseal compartments. The understanding of IL-17 biological function has revolutionized the understanding of PsA pathogenesis and, consequently, its therapeutic approach.Areas coveredIn this review article, we have outlined the primary evidence regarding the biological functions of IL-17A in PsA, and summarized data from randomized controlled trials (RCTs) on PsA and psoriasis approved secukinumab, ixekizumab, bimekizumab, brodalumab, and emerging IL-17 inhibitors.Expert opinionThe biologic disease-modifying antirheumatic drugs (bDMARDs), secukinumab, and ixekizumab target interleukin-17A (IL-17A), and bimekizumab, which simultaneously neutralizes IL-17A and IL-17F, have demonstrated efficacy in treating both peripheral and axial articular manifestations of PsA, as well in improving skin involvement, enthesitis and dactylitis. Brodalumab, which inhibits the IL-17 receptor A (IL-17RA), represent an efficacious strategy for psoriasis.Continued research into the role of IL-17s in PsA pathogenesis is crucial for improving our understanding of the disease and developing more effective therapeutic strategies. Further research and advancements in biologic therapies will refine IL-17 inhibitory strategies, potentially improving outcomes for PsA patients, and other immune-mediated diseases.Weiterlesen

Background: Psoriasis is a chronic autoimmune condition characterized by recurrent episodes of skin inflammation. Despite progress in treatment, managing flare-ups of psoriasis remains a significant hurdle once the therapy is halted. This review aims to unravel the enigma of relapse by examining the interactions between epigenetics, metabolic reprogramming, and inflammatory memory.Methods and Results: Skin-resident memory T cells and keratinocytes with a history of inflammation play crucial roles in the metabolic and epigenetic alterations observed during relapse. This review explores epigenetic factors involved in the recurrence of psoriasis, such as histone alterations, chromatin restructuring, and non-coding RNAs. Furthermore, we explored environmental influences, metabolic reprogramming, and genetic predispositions that influence the persistence and recurrence of psoriasis. We also outline the function of the gut-brain-skin axis in this scenario. Finally, we discuss pharmacological strategies for managing psoriasis relapse, including targeted biologics.Conclusion: This review provides a comprehensive summary on the intricate epigenetic, molecular, metabolic and environmental cues that exacerbate or facilitate psoriasis relapse. In summary, it also provides an enticing update on the therapeutics currently employed to treat psoriasis relapse.Weiterlesen

Bei einem Patienten mit Asthma entwickelte sich nach einer Behandlung mit den Medikamenten Dupilumab und Tezepelumab eine sogenannte generalisierte pustulöse Psoriasis. Das ist eine Form von Schuppenflechte, bei der viele kleine Eiterbläschen auf der Haut entstehen. Dupilumab wird eigentlich häufig gegen Neurodermitis und Asthma eingesetzt, doch es gibt Berichte, dass manche Menschen dadurch eine pustulöse Psoriasis entwickeln können[1][3][4][5]. Diese Hautreaktion ist selten, aber möglich und zeigt, dass neue Medikamente manchmal unerwartete Nebenwirkungen haben können. Wer Veränderungen auf der Haut bemerkt, sollte das seinem Arzt melden. Originaltitel: Generalized pustular psoriasis in a patient with asthma following dupilumab and tezepelumab therapy. Link zur Quelle

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Introduction Paediatric psoriasis is often misdiagnosed, and the overlap condition of psoriasis and atopic dermatitis (AD), known as psoriasis-dermatitis, further complicates accurate identification. Research has shown that interleukin-36 gamma (IL-36γ) measurement via tape stripping can help diagnose complex cases of psoriasis in adults. However, there are no published studies evaluating the applicability of this method in children, especially for distinguishing psoriasis from AD and the overlap condition. We aimed to assess the utility of IL-36γ measurement via tape stripping for distinguishing psoriasis from AD and for predicting the evolution of psoriasis-dermatitis in children and adolescents. Methods We conducted a cross-sectional diagnostic accuracy study in consecutive cases of psoriasis, AD, and psoriasis-dermatitis, and in healthy controls. IL-36γ concentration was measured using tape stripping and enzyme-linked immunosorbent assay (ELISA). Expert paediatric dermatologists independently confirmed the clinical diagnoses (reference standard). Results We included 11 children with psoriasis, 11 with AD, 11 with psoriasis-dermatitis, and 10 healthy controls (mean age 8.7 years, 57% female). Mean IL-36γ levels in psoriasis lesions were significantly higher than in AD lesions (144 pg/mL versus 14.4 pg/mL, P = 0.033) and in healthy controls (144 pg/mL versus 10.4 pg/mL, P = 0.037). The IL-36γ tape stripping method demonstrated a sensitivity of 91% and specificity of 91% for distinguishing psoriasis from AD, with an area under the receiver operating characteristic (ROC) curve of 0.959. The IL-36γ concentrations in participants with psoriasis-dermatitis predicted the evolution to psoriasis or dermatitis in most cases (5 out of 6, 83.3%). Conclusion IL-36γ measurement via tape stripping offers a promising method for distinguishing psoriasis from AD in children. This non-invasive approach is practical for routine clinical application and demonstrates good sensitivity and specificity, which suggests it could improve early diagnosis and patient outcomes.Weiterlesen

IntroductionPsoriasis is a chronic immune-mediated skin disease with known physical and mental health comorbidities, such as cardiovascular disease, depression, and anxiety. Psoriasis also has a significant impact on quality of life and sleep due to factors like itch and pain. This study aims to assess the relationship between sleep quality, mental health, and psoriasis, and specifically investigate the impact of poor sleep quality on mental health outcomes within participants with psoriasis.MethodsIn this cross-sectional study, we enrolled 556 participants into two cohorts: 487 participants were enrolled into the psoriasis cohort, and 69 were enrolled into the healthy control cohort. The demographics, disease severity, family history, sleep quality (PROMIS 8a, PROMIS 8b, and Insomnia Severity Index), and mental health (Patient Health Questionnaire-8 and Generalized Anxiety Disorder-7) of participants were assessed. Descriptive analysis and logistic regression models were employed to examine sleep and mental health, adjusting for potential confounders like demographics and comorbidities.ResultsA comparison of patients with psoriasis and healthy controls revealed worsened sleep and mental health outcomes in patients with psoriasis. Among participants with psoriasis, greater sleep impairment (Patient-Reported Outcomes Measurement Information System (PROMIS) 8a), sleep disturbance (PROMIS 8b), and insomnia were significantly associated with anxiety (ORa 1.22; 95% confidence interval (CI) 1.16, 1.30; ORa 1.26; 95% CI 1.16, 1.80; ORa 5.13; 95% CI 2.91, 9.33; respectively) and depression (ORa 1.42; 95% CI 1.32, 1.56; ORa 1.16; 95% CI 1.08, 1.26; ORa 7.04; 95% CI 4.01, 12.77; respectively).ConclusionThese findings underscore the importance of recognizing how psoriasis can impact mental health and sleep. Building a collaborative relationship between patients with psoriasis and their providers is essential to improve overall sleep and life quality.Weiterlesen

BackgroundThe impact of traditional systemic drugs to treat psoriasis (ciclosporin, methotrexate, and acitretin) in a subsequent response to biologics has not been adequately addressed in the literature. In clinical practice, it is increasingly necessary to initiate, due to concomitant comorbidities, biologics in patients with psoriasis or psoriatic arthritis (PsA) who have not undergone prior treatment with systemics, i.e. full-naive.Objectives and methodsThis study analyzed the possible impact of non-biological systemic therapies on the effectiveness and drug survival of first-line biologic drug up to 12 months in bio-naive psoriatic and PsA patients consecutively enrolled from January 2017 to March 2021.ResultsNinety-five patients with severe psoriasis (13.5%) were full-naive. Being full-naive and having or not having undergone methotrexate or cyclosporine therapy did not impact response to subsequent years of biologic therapy. Only acitretin promotes faster response to subsequent biologic drugs with 59.6% and 74.2% of patients achieving Psoriasis Area Severity Index (PASI) 90 at 16 and 28 week, respectively, vs. 50.5% and 65% (p = 0.034 and 0.026). In multivariate analysis, the advantage given by acitretin was lost.ConclusionPrevious systemic therapy in bio-naive patients does not appear to result in a differential response to biologics during the first year of treatment.Weiterlesen

BackgroundPsoriasis is a chronic skin disease affected by genetic and autoimmunity. The traditional Chinese medicine, Compound Qingdai Capsule (CQC), has shown potential benefits in treating psoriasis in clinical settings. Despite its efficacy, the molecular mechanisms underpinning its therapeutic action remain unclear.PurposeThis study aimed to unravel the molecular mechanism of Compound Qingdai Capsule for psoriasis based on the psoriasis pathogenic pathway network, integrating multi-omics analysis, systems pharmacology, machine learning modeling, and animal experimentation.MethodsPsoriasis pathogenic pathway network was constructed through employing bioinformatics analysis and psoriasis-related multi-omics data mining. The ingredients of CQC were detected by UPLC-MS/MS, and target prediction was performed by systems pharmacology. Machine learning, including Lasso regression, Random Forest, and Support Vector Machine (SVM), were utilized to screen core targets of psoriasis. Molecular docking was employed to evaluate the binding affinity between ingredients and core targets. The expression levels of core targets were determined using qRT-PCR and ELISA.ResultsPsoriasis-related datasets GSE201827 and GSE174763 were comprehensively analyzed to obtain 635 psoriasis-related genes. These genes were further enriched to elucidate signaling pathways involved, leading to the construction of psoriasis pathogenic pathway network. Utilizing UPLC-MS/MS, 29 main ingredients of CQC were characterized. CQC ingredients-targets network was constructed using these ingredients and their targets. Screening of CQC anti-psoriasis core targets using machine learning algorithm. Molecular docking confirmed good binding affinity between these targets and ingredients. Imiquimod (IMQ) induced psoriasis-like rat validated the anti-psoriasis effect of CQC by alleviating symptoms, reducing spleen and thymus index, and modulating the expressions of core targets at mRNA and protein levels.ConclusionCQC effectively modulates the expression levels of AURKB, CCNB1, CCNB2, CCNE1, CDK1, and JAK3 through various ingredients, such as astilbin, salvianolic acid A, and engeletin, via multiple pathways, thereby alleviating psoriasis-like symptoms.Weiterlesen

Psoriasis is a chronic inflammatory skin disease driven by immune dysregulation. This study explores the role of B cells, particularly cytokine-producing subsets, in psoriasis pathogenesis. Although T cells, particularly Th17, have been well documented in psoriasis, recent evidence suggests that B cells contribute to the disease process. Flow cytometry analysis of 50 psoriasis patients and 20 healthy controls revealed a significant increase in IL-6-producing effector B cells (Beffs) and a decrease in IL-10-producing regulatory B cells (Bregs) in psoriasis patients. As IL-6 is pro-inflammatory and IL-10 is anti-inflammatory, this imbalance likely exacerbates inflammation in psoriasis. The study also examined the effects of guselkumab, an IL-23 inhibitor, on cytokine-producing B cells. The frequency of IL-6-producing Beffs in the blood was significantly (p < 0.05) elevated in patients with psoriasis compared with that in healthy controls. In contrast, the frequency of IL-10-producing Bregs in the blood was significantly (p < 0.05) decreased in patients with psoriasis compared with that in healthy controls. In 10 biologic-naïve psoriasis patients, guselkumab significantly reduced IL-6-producing Beffs 4 weeks posttreatment, corresponding with a marked decrease in the Psoriasis Area and Severity Index (PASI). However, IL-10-producing Bregs showed no significant change over this period, suggesting that regulatory B cell recovery may require a longer timeframe or additional stimuli. These findings highlight the potential of B cells as biomarkers for disease activity and therapeutic response in psoriasis. The observed cytokine imbalance suggests that targeting B cell-mediated inflammation could be a novel therapeutic avenue. Further research is needed to assess long-term Breg dynamics and their role in maintaining immune homeostasis in psoriasis. This study reinforces the importance of both effector and regulatory B cells in psoriasis and suggests that monitoring their balance may improve disease characterization and treatment strategies.Weiterlesen

IntroductionResearch findings show a substantial correlation between Crohn's disease and psoriasis. However, the exact cause or pathogenesis of the concurrent manifestations of these two conditions in the same individuals remains uncertain. This research aimed to scrutinize the important molecules and mechanisms responsible for the concomitance of Crohn's disease and Psoriasis by using quantitative bioinformatics utilizing a publicly available RNA sequencing repository.MethodsThe database Gene Expression Omnibus were assessed, specifically for Crohn's disease (GSE95095) and psoriasis (GSE13355). The 'limma' library of the R programming syntax is employed to identify differentially expressed genes. The Search Tool for Interacting Genes dataset was utilized to study the interaction between proteins networks. The Cytoscape software was utilized to efficiently view and analyse these Protein-Protein Interaction networks. The ctoHubba Cytoscape plugin helps in the selection of hub genes. These hub genes have been confirmed using data from GSE102133 for Crohn's disease and GSE14905 for psoriasis. The ROC curves were utilized in this study to assess the diagnostic value of the hub genes. Moreover, new research involving gene-set enriched studies and the study of immunological surveillance associated with these specific genes is attainable.ResultsAmong the identified common DEGs, 40 genes were downregulated and 37 were upregulated, totaling 77 genes. Crohn's disease and Psoriasis had a higher concentration of pathways associated with inflammation. After validation, functionality of hub genes was confirmed for S100A12, CXCL8, IL1RN, S100A9, CXCL10, MMP1, CXCL1, FPR1, CXCR2, and S100A8. The hub genes showed an increase in expression in response to neutrophil infiltration. The expression of S100A12, CXCL8, IL1RN, S100A9, CXCL10, MMP1, CXCL1, FPR1, CXCR2, and S100A8 was found to be significantly linked to immune processes such as neutrophil activation, neutrophil chemotaxis, and neutrophil migration associated with Crohn's and Psoriasis disease.ConclusionsThis bioinformatics study has elucidated S100A12, CXCL8, IL1RN, S100A9, CXCL10, MMP1, CXCL1, FPR1, CXCR2, and S100A8 as the central genes in the pathogenesis of CD and Psoriasis comorbidity. The significance of neutrophil infiltration in promoting inflammatory and immune-mediated dysfunction seems to be crucial in the etiology of concurrent Crohn's and Psoriasis, offering an avenue for diagnostic and therapeutic methods.Weiterlesen

Few studies have examined the features of patients with IgA nephropathy secondary to psoriasis (IgAN-Pso); leaving the long-term renal outcomes and risk factors for this group unclear. A total of ninety patients with IgAN without evidence of a secondary cause other than psoriasis were enrolled in this retrospective study. The participants were categorized into two groups: the mild-to-moderate psoriasis group (n = 74) and the severe psoriasis group (n = 16). A comparative analysis was conducted on the clinicopathological attributes and renal outcomes between the two groups. Additionally, prognostic risk factors for end-stage renal disease (ESRD) were assessed. The patients within the severe psoriasis cohort exhibited a heightened prevalence of eGFR < 60 ml/min/1.73 m2 and urinary protein levels exceeding 1.49 g/d, alongside more pronounced T lesions and an increased incidence of C2 lesions (crescent > 25%) compared to their mild-to-moderate psoriasis counterparts. During a median follow-up period of 34.8 months, 11 patients (5 [35.7%] with severe psoriasis and 6 [8.2%] with mild-moderate psoriasis, P < 0.05) progressed to ESRD. At the time of biopsy, eGFR, CRP > 21.2 mg/l, immunoglobulin G > 8.05 g/l, low C3 and time-average proteinuria emerged as independent predictors of future ESRD. Pathological parameters could not independently predict ESRD when considering the baseline clinical features. Our study indicates that severe psoriasis is associated with worse renal impairment observed at biopsy and a greater likelihood of developing ESRD afterwards.Weiterlesen

IntroductionPalmoplantar pustulosis (PPP) is a chronic inflammatory skin condition characterized by pustules on the palms and soles. Patients with PPP may be at an increased risk of developing psoriatic arthritis (PsA). The Psoriatic Arthritis Screening and Evaluation (PASE) questionnaire is a tool designed to screen for PsA in at-risk populations. The objective of this study was to identify potential risk factors influencing PASE scores in patients with PPP.MethodsThe EPPPIK study was a cross-sectional, multicenter, noninterventional study conducted at 20 sites in Korea, in which patients (≥ 19 years of age) with a confirmed PPP diagnosis were reviewed. In a post hoc analysis of EPPPIK data, PASE outcomes were evaluated for two groups of patients with PPP stratified on the basis of a cutoff score of 37 points.ResultsIn total, 375 patients with PPP (mean age, 51.3 years; 38.9% male) were included. At enrollment, 175 (46.7%) patients had a PASE score ≥ 37, and 200 (53.3%) patients had a PASE score < 37. Significant differences between the groups were demonstrated for sex, age of menarche, presence of arthritis or psoriatic arthropathy, Physician's Global Assessment score, Palmo-Plantar Pustulosis Area and Severity Index (PPPASI) score, and hand PPPASI score (p ≤ 0.05). Quality-of-life (QoL) measurements and patient-reported outcomes were significantly worse in patients with PASE ≥ 37 (p ≤ 0.05). Multivariable linear regression analysis revealed that a PASE score ≥ 37 was positively associated with female sex (β = 7.19; p < 0.001) and high hand PPPASI score (β = 0.22; p = 0.0243).ConclusionsIn patients with PPP, PASE score ≥ 37 correlated with increased presence of any arthritis or psoriatic arthropathy, more severe PPP, worse QoL outcomes, female sex, and higher hand PPPASI scores. Therefore, PASE may serve as a useful tool for initial screening and appropriate treatment selection, management, and ongoing monitoring of patients with PPP.Weiterlesen

PurposePsoriasis is a common chronic inflammatory skin disease. Acupoint injection is reported to be used for the treatment of psoriasis, however its mechanism is not yet clear. The study aimed to investigate the efficiency of combined treatment including acupoint injection in the treatment of psoriasis.Patients and methodsHere, we compared the efficacy of multiple immune intervention therapy (MII, acupoint injection with BCG-PSN combined with thymosin enteric-coated tablets, levamisole, intramuscular injection with BCG-PSN) to NB-UVB and acitretin for psoriasis. One thousand two hundred patients with moderate-severe psoriasis vulgaris were randomly treated with MII, NB-UVB or acitretin. For another 53 patients treated with MII, the T cell subsets and TCR repertoire analysis were investigated with sequencing and flow cytometry.ResultsThe effective rate in MII treated group was similar to acitretin-treated group in 3 months (P > 0.05), though lower than in subjected treated with NB-UVB (P < 0.05). MII treatments maintained a longer remission of both PASI25 and PASI75 in comparison to the treatment with either NB-UVB or acitretin in following 5-year follow-up. Moreover, the relapse rate was lower in MII treatment than in either NB-UVB (P < 0.0001) or acitretin treatment (P < 0.0001), accompanied with longer remission duration (MII vs both NB-UVB and acitretin, P < 0.0001). Meanwhile, MII treatments markedly increased Treg cells (P = 0.04), while decreasing the number of both Th1 (P < 0.001) and Th17 cell (P = 0.01), along with decreased secretion of IFN-γ (P = 0.03) and IL-17 (P = 0.02). Multivariable Cox regression analysis demonstrated that MII significantly reduced psoriasis relapse risk versus NB-UVB (58.7% reduction; HR = 0.413, 95% CI: 0.329-0.517, P < 0.001) and acitretin (65.3% reduction; HR = 0.347, 95% CI: 0.276-0.435, P<0.001).ConclusionAcupoint injection combined with BCG-PSN, thymosin enteric-coated tablets and levamisole treat psoriasis and prevent relapse of psoriasis, via modulation of Treg/Th1/Th17.Weiterlesen

In dieser Studie wird untersucht, wie wirksam, sicher und verträglich das Medikament Risankizumab bei Kindern mit aktiver juveniler Psoriasis-Arthritis ist. Dabei wird Risankizumab mit dem bereits zugelassenen Medikament Adalimumab verglichen. Beide Medikamente werden als Injektion unter die Haut (subkutan) verabreicht und sollen Entzündungen sowie Schmerzen in den Gelenken lindern. Die Kinder, die an der Studie teilnehmen, haben mindestens drei betroffene Gelenke und sprechen nicht ausreichend auf andere Therapien wie Methotrexat an. Die untersuchte Substanz Risankizumab ist ein sogenannter monoklonaler Antikörper. Das bedeutet: Es handelt sich um einen gentechnisch hergestellten Eiweißstoff, der gezielt einen bestimmten Botenstoff im Immunsystem blockiert – Interleukin-23 (IL-23). IL-23 spielt eine wichtige Rolle bei Entzündungsprozessen im Körper und trägt zur Entwicklung von Autoimmunerkrankungen wie Psoriasis-Arthritis bei. Durch die Blockade dieses Botenstoffs kann Risankizumab dazu beitragen, Entzündungssymptome zu verringern und das Fortschreiten der Erkrankung zu bremsen. Originaltitel: Open-label, randomized, assessor-blinded, efficacy, safety, tolerability, and pharmacokinetics study of subcutaneous risankizumab with an adalimumab reference arm in children with active juvenile psoriatic arthritis Erkrankung: Juvenile Psoriasis-Arthritis Phase: Phase III (therapeutisch-bestätigend) Firma: AbbVie Deutschland GmbH & Co. KG Art der Verabreichung: Injektion (subkutan) https://euclinicaltrials.eu/search-for-clinical-trials/?lang=en&EUCT=2023-506026-36-00

Mastzellen spielen eine größere Rolle bei Schuppenflechte, als viele denken: Sie bilden in den betroffenen Hautstellen die Entzündungsstoffe IL17A, IL17F und RORC[5]. Vor einer Therapie sind sie besonders aktiv. Auch nach erfolgreicher Behandlung, zum Beispiel mit Antikörpern oder UVB-Licht, bleiben viele dieser Mastzellen erhalten – dann aber eher in einer „ruhigen“ Variante, die trotzdem weiter IL-17A ausschüttet[5]. Auffällig: Je mehr dieser Mastzellen nach der Therapie übrigbleiben, desto schneller kehrt die Schuppenflechte zurück. Mastzellen und T-Zellen arbeiten dabei eng zusammen und steuern das Entzündungsgeschehen über die sogenannte IL-23/IL-17-Achse[5]. Originaltitel: Mast cells express IL17A, IL17F and RORC in lesional psoriatic skin, are activated before therapy and persist in high numbers in a resting state with IL-17A positivity after treatment. Link zur Quelle

In dieser Studie wird untersucht, wie wirksam und sicher Zasocitinib (TAK-279) bei Erwachsenen mit aktiver Psoriasis-Arthritis ist. Besonderes Augenmerk liegt darauf, ob die Patientinnen und Patienten zuvor bereits biologische Medikamente erhalten haben oder nicht. Die Teilnehmenden werden nach dem Zufallsprinzip entweder mit Zasocitinib in unterschiedlichen Dosierungen oder einem Placebo behandelt. Ziel ist es herauszufinden, wie viele der Behandelten nach 16 Wochen eine spürbare Verbesserung ihrer Gelenkbeschwerden (ACR20-Ansprechen) erreichen. Zusätzlich werden weitere Aspekte wie Hautbeteiligung, Lebensqualität und Fatigue bewertet. Zasocitinib ist ein sogenannter TYK2-Inhibitor – das heißt, er blockiert gezielt das Enzym Tyrosin-Kinase 2 im Körper. Dieses Enzym spielt eine wichtige Rolle bei Entzündungsprozessen des Immunsystems, die für Erkrankungen wie Psoriasis-Arthritis typisch sind. Durch die Hemmung von TYK2 kann Zasocitinib dazu beitragen, Entzündungen zu verringern und Symptome sowohl an den Gelenken als auch an der Haut zu lindern. Das Medikament wird als Tablette eingenommen. Originaltitel: A Multi-Center, Randomized, Double-Blind, and Placebo-Controlled Phase 3 Study to Evaluate the Efficacy and Safety of Zasocitinib (TAK-279) in Subjects with Active Psoriatic Arthritis Stratified by Prior Biologic Use (LATITUDE-PsA-3002) Erkrankung: Aktive Psoriasis-Arthritis Phase: III Firma: Takeda Development Center Americas Inc. Art der Verabreichung: Tablette https://euclinicaltrials.eu/search-for-clinical-trials/?lang=en&EUCT=2024-513112-99-00