Redaktion

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Abstract Background: Psoriasis vulgaris, particularly when manifesting in highly visible regions such as the face and hands, can profoundly impair self-perception and social functioning. Despite a growing interest in psychodermatology, the specific impact of visible psoriatic lesions on social appearance anxiety remains insufficiently explored. Objective: To assess the severity of social appearance anxiety in patients with visible psoriasis vulgaris lesions compared to healthy controls, and to examine its associations with general anxiety, depression, perceived disease severity, and dermatology-related quality of life. Methods: A cross-sectional case-control study was conducted involving 178 patients diagnosed with psoriasis vulgaris exhibiting visible skin lesions and 196 age- and sex-matched healthy controls. All participants completed the Social Appearance Anxiety Scale (SAAS) and the Hospital Anxiety and Depression Scale (HADS). Patients additionally completed the Dermatology Life Quality Index (DLQI) and a Visual Analog Scale (VAS) to evaluate subjective disease severity. Statistical analyses included group comparisons and Pearson correlations between psychological and clinical parameters. Results: SAAS scores were significantly elevated in the patient group (mean = 60.32 ± 8.10) compared to controls (mean = 22.15 ± 9.05; p < 0.001), indicating a large effect size. In psoriasis patients, social appearance anxiety showed a moderate positive correlation with perceived disease severity (r = 0.293, p < 0.01), while correlations with DLQI and depression scores were not statistically significant. General anxiety levels (HADS-A) demonstrated a moderate correlation with SAAS (r = 0.484, p < 0.01). Conclusion: Visible lesions in psoriasis vulgaris contribute substantially to social appearance anxiety, independent of general psychopathology. These findings underscore the psychological vulnerability of patients with visible psoriatic involvement and highlight the need for integrated psychosocial interventions as part of comprehensive dermatological care.Weiterlesen

Psoriasis is a chronic skin disorder with significant individual and societal impacts. Current therapies often lack efficacy, are costly, or cause side effects, necessitating new treatments. This study explores regenerative therapies-exosomes, mesenchymal stem cells (MSCs), epigallocatechin-3-gallate nanoparticles (EGN), and EGN-loaded exosomes (EGN-Exo)-in regulating psoriasis-related markers (IL-6, IL-4, Bcl-2, Bax, NF-κB, CDC25B). An imiquimod-induced psoriasis model in Wistar rats was used, with six groups: negative control, positive control, and treatments (MSCs, exosomes, EGN, EGN-Exo). After seven days, ELISA revealed EGN-Exo most effectively reduced pro-inflammatory IL-6 and pro-apoptotic Bax while increasing anti-inflammatory IL-4 and anti-apoptotic Bcl-2. EGN-Exo also significantly lowered NF-κB and CDC25B, demonstrating superior anti-inflammatory effects. Apoptosis profiling showed EGN-Exo reduced late apoptotic cells, highlighting cytoprotective abilities. EGN had a moderate effect, while MSCs and exosomes showed modest improvements. Histopathological and immunohistochemical analyses confirmed EGN-Exo's efficacy, notably reducing TGF-β expression. These findings suggest EGN-Exo combines EGCG's antioxidant and anti-inflammatory properties with exosomes' targeted delivery, offering a promising advanced therapy for psoriasis.Weiterlesen

Psoriasis is an autoimmune inflammatory condition that often intersects with orthopaedic care due to its connection to psoriatic arthritis. However, not all psoriasis patients develop psoriatic arthritis. Psoriasis patients may undergo hip or knee arthroplasties for reasons unrelated to psoriasis. This condition, marked by inflamed, scaly skin caused by an overactive immune system, may pose challenges for orthopaedic surgeries. This systematic review evaluated outcomes for psoriasis patients after total hip arthroplasty (THA) or total knee arthroplasty (TKA), focusing on postsurgical impact to inform additional considerations for patients. Following PRISMA guidelines, a systematic search was conducted in Medline, Embase, Web of Science, and Cochrane (up to October 2024). Studies involving patients with psoriasis undergoing THA or TKA were analyzed for postoperative outcomes. 359 studies were screened, 7 met inclusion criteria. Two studies focused on THA, three on TKA, and two examined both procedures. Patients with psoriasis undergoing THA showed increased risk of infections compared to non-psoriasis patients. For TKA, results were mixed in whether psoriasis led to higher infection rates. Psoriasis did not lead to increased revisions in both THA and TKA. Additionally, two studies found no significant differences in wound complications in TKA patients. This systematic review underscores the importance of considering post-surgical complications in psoriasis patients undergoing either a THA or TKA. However, lack of research makes it difficult to generalize findings. Psoriasis is an important factor to consider for surgical outcomes, but further research is needed to clarify risks and optimize care for patients.Weiterlesen

Psoriasis is a chronic immune-mediated skin disorder characterized by excessive keratinocyte proliferation, inflammation, and oxidative stress. This study investigates the role of the JNK/c-Jun cascade in psoriasis pathogenesis, focusing on its impact on keratinocyte proliferation and inflammatory responses. An in vitro psoriasis model was established using M5-stimulated HaCaT keratinocytes, while an in vivo model was created with imiquimod-treated Wistar rats. The results indicated that M5 stimulation significantly enhanced keratinocyte viability and proliferation, as demonstrated by increased optical density, EdU incorporation, and Ki-67 expression. M5 treatment also elevated pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, while inducing oxidative stress through increased ROS production, lipid peroxidation, and mitochondrial membrane potential (MMP) disruption. Blocking the JNK/c-Jun cascade with the SP600125 inhibitor effectively reduced keratinocyte hyperproliferation, cytokine secretion, and oxidative stress, while restoring mitochondrial integrity. In addition, knockdown of Nrf2 suppressed M5-induced ROS generation, inflammatory signaling, and antioxidant enzyme activity. In psoriasis rats, JNK/c-Jun inhibition significantly alleviated skin tissue damage, reducing inflammatory cell infiltration, epidermal hyperkeratosis, and phosphorylation of key inflammatory markers. Correspondingly, serum pro-inflammatory cytokines were decreased, and oxidative stress indices improved. These findings suggest that the JNK/c-Jun cascade plays a central role in psoriasis pathogenesis by regulating keratinocyte proliferation, inflammation, and oxidative stress. Targeting this pathway presents a promising therapeutic strategy for psoriasis treatment. Further studies are warranted to explore upstream regulators and downstream effectors of the JNK/c-Jun signaling pathway.Weiterlesen

BackgroundPsoriasis is a chronic inflammatory disease associated with multiple comorbidities, including metabolic syndrome and cardiovascular disease. Although specific dietary interventions, such as intermittent fasting and caloric restriction, have been shown to ameliorate inflammation and promote weight loss, the effect of these interventions independent of weight loss remains unclear. Time-restricted eating (TRE), a type of intermittent fasting, limits the daily eating window to a fixed number of hours. Recent studies suggest TRE may improve immune function in individuals with metabolic syndrome and cardiovascular risk factors. A crucial advantage of TRE over other investigated dietary restriction strategies is its reported high adherence rate, making it a more feasible intervention for long-term use. Therefore, exploring the effects of TRE on metabolic and immunological parameters in psoriasis is warranted.ObjectiveThis study was designed to evaluate the effects of short-term, isocaloric TRE, independent of weight loss, on immune cell function and serum metabolite profiles of volunteers with mild-to-moderate psoriasis compared to healthy individuals.MethodsThis case-control, prospective study was performed on 10 healthy male participants and 10 age-, BMI-, and sex-matched individuals with mild-to-moderate psoriasis. All individuals with psoriasis had stable disease and were being treated with topical therapies without any exposure to immunomodulatory biologics. This study was conducted at the National Institutes of Health Clinical Center. Immune profiles, glucose handling, energy expenditure, and participants' weights were assessed at baseline and after 3 days of TRE following a daily 6-hour eating window and 18-hour fast.ResultsThe trial commenced in June 2021 and was completed in February 2023. A total of 20 participants were enrolled-10 with mild-to-moderate psoriasis and 10 age-, BMI-, and sex-matched healthy individuals. As of the time of manuscript submission, data processing is ongoing. Multiomic datasets, including gene expression, surface and intracellular protein levels, and metabolite profiles, are being generated from peripheral blood mononuclear cells, CD4+-enriched T-cells, and serum samples. The integrated bioinformatics analyses will be reported once the data analysis is completed.ConclusionsThis clinical protocol was designed to characterize the effects of short term (3-day) TRE on psoriasis, independent of weight loss, by comparing immune cell regulatory responses between healthy individuals and those with psoriasis. More specifically, we aim to map the molecular pathways activated by TRE and assess how they affect immune cell composition, activation, and metabolism. Additionally, components of the metabolic response to isocaloric TRE are being explored. Insights into how dietary interventions impact metabolism and the immune system will enhance our understanding of the pathogenesis of psoriasis and may reveal new therapeutic avenues for managing this inflammatory condition.Trial registrationClinicalTrials.gov NCT04728165; https://clinicaltrials.gov/study/NCT04728165.Weiterlesen

BackgroundPsoriasis is a persistent inflammatory skin condition. Several studies have revealed that obesity significantly contributes to both the initiation and advancement of psoriasis. The metabolic score for visceral fat (METS-VF) represents an innovative measure designed to forecast visceral obesity, integrating factors such as insulin resistance metabolic score, waist-to-hip ratio (WHR), age, and gender. The present study aimed to investigate the association between METS-VF and psoriasis prevalence, using information gathered from the National Health and Nutrition Examination Survey (NHANES).MethodsThis study utilized the data from a nationally representative cohort of 8023 adults from NHANES from 2003-2006 to 2009-2014, of which 234 declared a psoriasis history. Multivariate logistic regression analysis and restricted cubic spline (RCS) analyses were used to investigate the association between METS-VF and psoriasis, followed by subgroup analysis to identify populations that may exhibit higher sensitivity.ResultsAfter adjusting for confounding variables, the results of the multivariate logistic regression analysis showed a significant positive association between METS-VF and the risk of psoriasis. One-unit increasement in METS-VF corresponded to a 47% rise in psoriasis risk (odds ratio [OR] = 1.47, 95% confidence interval [CI] = 1.10-1.96). Finally, the results were uniform across all subgroups (P for interaction > 0.05). The results from the RCS analysis indicated a notable linear association.ConclusionThis research indicated that elevated levels of METS-VF are linked to a higher occurrence of psoriasis, suggesting the potential of METS-VF as a predictive anthropometric index for assessing the risk of developing psoriasis.Weiterlesen

Ixekizumab is a monoclonal antibody used in the treatment of moderate-to-severe psoriasis and psoriatic arthritis by targeting interleukin-17 A (IL-17 A). It has demonstrated efficacy in controlling inflammation in autoimmune diseases, though adverse reactions can arise. This case study reports a case of 25-year-old female with psoriatic arthritis undergoing treatment with ixekizumab, who developed acute enlargement and inflammation of a pre-existing sebaceous cyst located posterior to the left auricle, occurring two days after the administration of a routine ixekizumab dose. The present study investigates the potential association between the inflammatory process observed within the cyst and the immunomodulatory mechanisms of ixekizumab. Literature review revealed no prior reports directly linking ixekizumab with sebaceous cyst inflammation. However, related adverse effects, including paradoxical inflammation, infectious complications, and immune dysregulation have been described in patients treated with IL-17 A inhibitors. These include IBD exacerbation, eczematous eruptions, paradoxical psoriasis, and rare systemic complications, suggesting broader immunological effects of IL-17 blockade.Weiterlesen

Psoriasis is a chronic inflammatory skin disease driven by immune dysregulation and often exacerbated by metabolic comorbidities. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), initially developed for type 2 diabetes mellitus (T2DM) and weight management, have emerged as a promising treatment due to their anti-inflammatory and immunomodulatory properties. This review evaluates the clinical efficacy, mechanisms of action, and limitations of GLP-1RAs, such as liraglutide, exenatide, and semaglutide, in the management of psoriasis. A comprehensive literature review was conducted, including evidence from case reports, randomized controlled trials, prospective cohorts, and experimental studies, to assess the role of GLP-1RAs in psoriasis treatment. Evidence suggests that GLP-1RAs mitigate psoriasis severity through systemic effects, including weight loss and improved glycemic control, and local immunomodulation, such as the regulation of invariant natural killer T (iNKT) cells and AMPK activation in psoriatic plaques. These benefits are particularly notable in patients with coexisting metabolic conditions. However, the existing evidence is limited by small cohort sizes, heterogeneous patient populations, and confounding effects of concurrent therapies, limiting its generalizability. GLP-1RAs offer a novel integrative approach to managing psoriasis by targeting both inflammatory and metabolic pathways. Larger, long-term randomized controlled trials are needed to validate their efficacy, optimize dosing, and determine their role as standalone or adjunctive therapies, particularly in patients without metabolic comorbidities.Weiterlesen

BackgroundThere are only limited histomorphological data on the response of psoriatic skin lesions to topical dithranol. In vivo reflectance confocal microscopy (RCM) in psoriatic skin is highly correlated with histopathological findings and allows non-invasive monitoring of treatment effects on a cellular level.Patients and methodsProspective, single-center pilot study at a university-based clinic of dermatology between January 1st and August 30th, 2016. Psoriatic lesions of 20 patients receiving dithranol treatment were assessed by RCM at baseline, day 4 and 8 of treatment.ResultsRCM measurements of psoriatic lesions receiving dithranol treatment revealed epidermal histomorphological changes with a strong median reduction of baseline hyperkeratosis by 45.0% (p < 0.001), acanthosis by 38.2% (p < 0.001), and epidermal thickness by 66.5% (p < 0.001) from baseline until day 8. Moreover, semiquantitative measurements of parakeratosis also showed a significant reduction until day 8 (p < 0.001). Correspondingly, RCM revealed dermal histomorphological changes with a decrease in diameter of dermal papillae by 32.1% (p < 0.001), decrease in diameter of papillary vessels by 16.9% (p = 0.002) and a strong semiquantitative reduction of the inflammatory infiltrate (p < 0.001).ConclusionsResults from our pilot study indicate that topical dithranol treatment of psoriatic lesions may induce a rapid and marked reduction of pathologic epidermal and dermal RCM features.Weiterlesen

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BackgroundThe pathogenesis of nummular eczema (NE) remains unclear, and no targeted therapy has been approved. Apremilast is a small molecule inhibitor targeting phosphodiesterase-4.Patients and methodsA phase IIb randomized, double-blind, placebo-controlled study evaluating the effects of apremilast or placebo in patients with NE. Patients received apremilast (30 mg BID) or placebo until week 16 followed by an open label phase in which all patients were treated with apremilast until week 32. The primary endpoint was the number of patients achieving an improvement in Physician's Global Assessment (PGA) by two or more points or an absolute PGA of 0 or 1 at week 16. Secondary endpoints included changes in skin physiology, life quality, or dermato-pathology.Results33 patients were enrolled, of whom 31 were randomized to apremilast (n = 15) or placebo (n = 16). 1/15 (6.7%) patients in the apremilast group and 4/16 (25.0%) in the placebo group reached the primary endpoint (p = 0.369). There was no difference between placebo and apremilast with regard to all secondary endpoints at week 16 and week 32. The safety profile was in accordance with the known safety profile of apremilast.ConclusionPhosphodiesterase-4 inhibition by apremilast showed no beneficial effects for the treatment of NE.Weiterlesen

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Background/purposeWhile biologics and small-molecule inhibitors are first-line systemic treatments for psoriasis, phototherapy remains an alternative for patients unable to access these treatments because of medical or financial constraints. Narrow-band ultraviolet B (NB-UVB) is effective for localized psoriasis but less so for extensive disease. To address this limitation, bathwater delivery of psoralen plus ultraviolet A (bath-PUVA) was introduced in 2004. This study evaluates the efficacy, safety, and patient characteristics associated with bath-PUVA therapy in a large cohort.MethodsThis retrospective analysis included 229 patients (180 males, 49 females) treated with bath-PUVA from 2004 to September 2021. Baseline characteristics and treatment outcomes were assessed using the psoriasis area and severity index (PASI). Statistical analyses examined relationships between treatment outcomes and factors, including baseline PASI, body mass index (BMI), and smoking status.ResultsThe mean baseline PASI score was 24.9. Bath-PUVA achieved PASI 75 in 80.4% of patients, PASI 90 in 44.1%, and PASI 100 in 2.6%, with efficacy comparable to biologics. Patients achieving PASI 90 had significantly higher baseline PASI scores (p = 0.005), while the number of irradiations required did not differ (p = 0.692). Higher baseline PASI scores correlated with elevated BMI (p = 0.002), but BMI did not influence improvement rates (p = 0.094). Smokers had significantly higher baseline PASI scores (p = 0.004) compared with non-smokers, yet smoking status did not affect improvement rates (p = 0.862).ConclusionBath-PUVA demonstrates efficacy comparable with biologics for psoriasis, regardless of BMI or smoking status. This analysis supports its use as an effective and accessible treatment option for patients with extensive disease.Weiterlesen

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Psoriasis is a common chronic inflammatory skin disease that significantly affects patients'quality of life. There is no cure for psoriasis, and available treatments are not completely effective. We have previously found that hydroxytyrosol (HT) has anti-psoriatic effects in vitro. In the present study, we aimed to investigate the therapeutic effects of HT on psoriasis in vivo and to explore the underlying mechanisms. We explored the effects and molecular mechanisms of HT on imiquimod (IMQ)-induced psoriasis-like dermatitis in mice and an M5-induced in vitro cell model using real-time PCR, western blotting, hematoxylin-eosin staining, immunohistochemistry, and enzyme-linked immunosorbent assay. HT (10 mg/kg/d or 50 mg/kg/d, by gavage) ameliorated IMQ-induced clinical manifestations in mice. Moreover, HT ameliorated the histopathological changes and decreased the spleen index and levels of pro-inflammatory cytokines, such as interleukin (IL)-17 A, IL-23, and IL-22, in mouse serum or skin. Mechanistically, HT application inhibited the activation of ERK and NF-кB signaling in the skin samples. Consistently, in vitro analysis showed that HT significantly inhibited inflammation via ERK and NF-κB signaling in a cellular model of psoriasis. Our results indicate that HT alleviates IMQ-induced psoriasis-like dermatitis by inhibiting the ERK and NF-κB signaling pathways, suggesting that HT has a promising therapeutic application in psoriasis treatment.Weiterlesen

BackgroundGenetic susceptibility to psoriasis involves multiple loci, including TYK2 (Tyrosine Kinase 2), which is associated with various autoimmune diseases. However, its specific role and mechanisms in psoriasis remain unclear. This study aimed to identify psoriasis-associated proteins using Summary-based Mendelian Randomization (SMR) and to explore their regulatory mechanisms.MethodsSMR analysis integrating pQTL data was conducted to identify proteins linked to psoriasis, revealing ICAM1 (Intercellular Adhesion Molecule 1) as a potential pathogenic factor. A key SNP, rs34536443 (P1104A), located in TYK2, was found to regulate ICAM1. To assess its function, THP-1 cells carrying the TYK2-P1104A mutation were generated, and ICAM1 and cytokine expression were analyzed following LPS stimulation. The effect of the TYK2 inhibitor Deucravacitinib was tested in an imiquimod (IMQ)-induced psoriasis mouse model.ResultsSMR identified ICAM1 as a causal protein for psoriasis, regulated by the TYK2 SNP rs34536443. In TYK2-P1104A mutant THP-1 cells, LPS-induced ICAM1 expression was significantly reduced, with ICAM5 unaffected. The mutation also suppressed IL-1β, TNF-α, IL-6, and IL-18 expression, suggesting anti-inflammatory effects. Single-cell RNA-seq revealed enrichment of TYK2, ICAM1, and ICAM5 in dendritic cells and monocytes. In vivo, Deucravacitinib significantly downregulated ICAM1 in the IMQ-induced psoriasis model, with minimal effect on ICAM5.ConclusionThis study identifies ICAM1 as a key mediator in psoriasis via SMR analysis and implicates the TYK2 SNP rs34536443 in its regulation. The TYK2-P1104A variant attenuates ICAM1 and cytokine expression, and Deucravacitinib downregulates ICAM1 in vivo. These findings provide mechanistic insights into the TYK2-ICAM1 axis and support the therapeutic potential of TYK2 inhibitors for psoriasis.Weiterlesen

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Psoriasis and psoriatic arthritis are chronic autoimmune diseases characterized by dysregulated immune responses, particularly involving Th17 cells. Immune checkpoint molecules such as programmed death-1 (PD-1) and its ligands (PD-L1/PD-L2) are critical for maintaining immune tolerance. Disruptions in these pathways contribute to psoriatic disease pathogenesis. Notably, immune checkpoint inhibitors used in cancer therapy have been linked to the development of psoriasis or its exacerbation. This highlights the complex role of checkpoint pathways in psoriatic diseases. Thus, immune checkpoint agonists could be a therapeutic strategy aimed at restoring immune balance without widespread immunosuppression. Preclinical studies demonstrate that PD-1 agonists can mitigate inflammation by enhancing inhibitory signaling. Additionally, early-phase clinical trials in autoimmune diseases such as rheumatoid arthritis and ulcerative colitis suggest potential benefits of PD-1 modulation in psoriasis. This review explores immune checkpoint agonists in psoriatic disease as a promising alternative to conventional immunosuppressants by selectively suppressing pathogenic T-cell activity.Weiterlesen