Background:Psoriasis is widely recognized as a systemic inflammatory condition associated with numerous comorbidities. Among these, eating disorders (ED) and ED-related behavior, defined as restrictive or dysfunctional attitudes toward food, have been increasingly reported in patients with psoriasis. Aim of our study was to evaluate the prevalence of ED-related symptoms in psoriasis patients with excess body weight and to explore their association with body mass index (BMI) across the overweight and obese ranges. Methods:A multicenter, cross-sectional study was conducted on adult patients with psoriasis and BMI ≥25 kg/m2. ED-related symptoms were assessed using the Binge Eating Scale (BES ≥17) and Eating Attitudes Test-26 (EAT-26). Screening positivity required a positive result in at least one questionnaire. Patients were stratified into four BMI categories. Variables were compared using standard non-parametric tests, and logistic regression assessed predictors of screening positivity. Results:A total of 104 patients were included. Overall, 13 patients (12.5%) tested positive in at least one questionnaire. No statistically significant differences in the proportion of screening-positive patients were observed across the BMI categories or between the overweight and obese groups. Similarly, the mean BES and EAT-26 scores did not differ significantly between groups. Logistic regression analysis confirmed that BMI was not a significant predictor of ED-related screening positivity (OR = 0.942, 95% CI: 0.813-1.091). Spearman's analysis showed no significant correlation between BMI and BES scores (ρ = 0.031, p = 0.753) but a weak negative correlation between BMI and EAT-26 scores (ρ = -0.211, p = 0.032). Conclusion:Approximately one in eight psoriasis patients with excess body weight screened positive for ED-related symptoms. BMI category was not a predictor of ED-screening positivity. The weak negative correlation between BMI and restrictive eating attitudes indicates that dysfunctional eating behaviors may be more pronounced in patients with milder excess weight.
Background:Psoriasis is associated with increased epicardial adipose tissue (EAT), a metabolically active fat depot in direct contact with the myocardium, and a mediator of coronary artery disease and atrial fibrillation. The effects of psoriasis treatments on EAT are largely unknown. We conducted a post hoc analysis of the Vascular Inflammation in Psoriasis (VIP) trial (NCT01553058, NCT01866592). Methods:VIP compared, in a 1:1:1 randomized manner, placebo (n=27), adalimumab (n=31), and phototherapy (n=28) from baseline to week 12, with all subjects then receiving adalimumab for 52 weeks. EAT volume was quantified from CT imaging at baseline, week 12, and week 52, with concurrent assessment of clinical variables and metabolic and inflammatory biomarkers. Results:At baseline (N=86), EAT volume was positively correlated with age (r = 0.51, p= 2.44 × 10-), body mass index (r = 0.48, p= 2.01×10-6), and weight (r = 0.52, p= 3.17 × 10-), and with inflammatory biomarkers GlycA (r = 0.27, p= 9.48×10-3), C-reactive protein (r = 0.25, p= 9.94×10-3), and IL-6 (r = 0.23, p= 0.02). Over 12 weeks, adalimumab treatment reduced EAT volume (mean change -11.9 cm3, p=0.04; baseline mean EAT 183.1 cm3), with no improvement observed in the placebo or phototherapy groups. When compared with the placebo and phototherapy arms combined, adalimumab was associated with a greater reduction in EAT at week 12 (between-group difference -13.9 cm3, p=0.03). The reduction in EAT was not significantly associated with changes in weight or PASI. No additional reduction in EAT was observed after 52 weeks of adalimumab treatment. Conclusion:Adalimumab was associated with an early reduction in EAT that was not significantly correlated with changes in weight or psoriasis activity. These findings indicate treatment-specific effects on a high-risk cardiac fat depot and suggest that TNF inhibition may influence cardiac adiposity relevant to cardiovascular disease.
Background:Psoriasis is a chronic disease with a multidimensional impact that extends beyond skin symptoms, affecting physical, emotional, social well-being and satisfaction with care. This study aims to explore the perceived self-reported impact of psoriasis on patients' well-being across different life stages and to identify risk and protective factors associated with well-being over time. Methods:A cross-sectional observational study was conducted using an electronic questionnaire administered to adult patients with psoriasis and healthcare professionals involved in psoriasis management. Patients retrospectively self-reported the perceived impact of psoriasis on overall well-being and its physical, emotional, social, and treatment-related domains across consecutive 10-year life stages. Both patients and healthcare professionals evaluated perceived risk and protective factors for well-being. Results:A total of 53 patients and 54 healthcare professionals completed the questionnaire. Most patients (90.6%) reported psoriasis had negatively affected their general well-being at some point during the disease course, with the physical (90.6%) and emotional (88.7%) domains being the most impacted. The highest perceived burden was reported between 31 and 40 years of age. Better reported symptom control was associated with lower perceived impairment in well-being. Key risk factors included affected body areas (95.3%), comorbidities (93.5%), and disease severity (89.7%), whereas appropriate treatment (96.3%), adequate medical care (93.5%), and a positive physician-patient relationship (89.7%) were identified as protective factors. Conclusion:These exploratory findings suggest that the self-reported perceived impact of psoriasis on well-being varies across life stages and is strongly influenced by symptom control and holistic disease management. These findings support a longitudinal, patient-centered approach to optimize long-term well-being.
Purpose:While 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 methods:We 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. Results:In 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. Conclusion:This 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.
Jiankun Song,1,* Yue Luo,2,* Rui Zhang,3,* Xiangjin Gao,3 Fanlingzi Shen,3 Ruiqi Cai,4 Jinrong Lu,4 Haotian Xu,1 Xin Ma,2 Bin Li,2 Wencheng Jiang,2 Ruiping Wang31Central Laboratory, Shanghai Skin Disease Hospital, Institute of Dermatology, School of Medicine, Tongji University, Shanghai, 200443, People’s Republic of China; 2Traditional Chinese Medicine Dermatology Department, Shanghai Skin Disease Hospital, School of Medicine, Tongji University, Shanghai, 200443, People’s Republic of China; 3Clinical Research Center, Shanghai Skin Diseases Hospital, School of Medicine, Tongji University, Shanghai, 200443, People’s Republic of China; 4School of Public Health, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ruiping Wang, Clinical Research Center, Shanghai Skin Diseases Hospital, School of Medicine, Tongji University, 1278 Baode Road, Jing’an District, Shanghai, 200443, People’s Republic of China, Email w19830901@126.com Wencheng Jiang, Traditional Chinese Medicine Dermatology Department, Shanghai Skin Disease Hospital, School of Medicine, Tongji University, 1278 Baode Road, Jing’an District, Shanghai, 200443, People’s Republic of China, Email drjiangwencheng@163.comPurpose: While 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 methods: We 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.Results: In 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.Conclusion: This 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.Keywords: psoriasis, tea consumption, sugar drinks, high-fat foods, treatment outcome
Purpose:To explore genotype-phenotype associations of IL36RN variants and clinical outcomes of spesolimab treatment in acrodermatitis continua of Hallopeau (ACH). Patients and methods:This multicenter retrospective study included 14 ACH patients with IL36RN genotyping from 2019 to 2025. Clinical features were compared across all genotypes. Medical records of individuals who received spesolimab were reviewed to describe treatment responses, with a follow-up observation period up to 56 weeks. Results:Compared with monoallelic or wild-type genotypes, biallelic IL36RN variants were associated with earlier disease onset age (23 vs 48 and 47 years, P <0.05) and higher baseline disease severity (median GPPGA score, 4 vs 3 and 2, P <0.001). Among 6 patients with biallelic, refractory ACH who received spesolimab, including 3 isolated cases that were administered at a 450-mg dose, overall percentage improvement across disease activity and patient-reported measures occurred rapidly, reaching 54% at week 1 and 74% at week 4. Relapse occurred in 4 patients between weeks 31 and 44, with disease activity remaining lower than baseline and improvement observed after re-treatment. Conclusion:Spesolimab was associated with clinical improvement in refractory ACH with biallelic IL36RN mutations, including isolated ACH treated with a 450-mg dose, supporting further evaluation of dose individualization below the approved 900-mg regimen for GPP flares.
Tom M Hillary Department of Dermatology, University Hospital Leuven, Leuven, BelgiumCorrespondence: Tom M Hillary, Department of Dermatology, University Hospital Leuven, Herestraat 49, Leuven, Vlaams-Brabant, 3000, Belgium, Tel +3216337950, Email tom.hillary@uzleuven.beBackground: Biologic therapies targeting IL‑17 and IL‑23 have revolutionized psoriasis management, enabling rapid and durable disease control. Yet treatment selection still follows a trial‑and‑error approach, and clinically validated biomarkers for personalization remain absent.Objective: To outline current challenges in biomarker development for psoriasis and describe the design and aims of the PICASSO prospective cohort as a platform for future personalized medicine.Current Challenges: Despite evidence that IL‑17/IL‑23 inhibitors may induce disease modification through effects on effector, memory, and regulatory immune cells, reliable predictive or prognostic biomarkers have not emerged. Barriers include complex pathogenesis, universally high biologic efficacy reducing need for stratification, inconsistent findings from genetic or transcriptomic studies, and the multifactorial nature of comorbidities.Methods (Picasso (ProspectIve Cohort psoriASiS FOllow-Up)): PICASSO is a 10‑year prospective biobank/registry enrolling patients within three years of disease onset. Biological samples are longitudinally linked to clinical and epidemiological data, with follow‑ups every 2.5 years. The ultimate aim is to identify biomarkers predicting disease trajectory.Conclusion: Personalized psoriasis care requires biomarkers predicting progression and comorbidity risk. PICASSO represents a step toward disease‑modifying, preventive precision medicine.Keywords: personalized treatment, research, dermatology, disease modification
Background:Biologic therapies targeting IL‑17 and IL‑23 have revolutionized psoriasis management, enabling rapid and durable disease control. Yet treatment selection still follows a trial‑and‑error approach, and clinically validated biomarkers for personalization remain absent. Objective:To outline current challenges in biomarker development for psoriasis and describe the design and aims of the PICASSO prospective cohort as a platform for future personalized medicine. Current Challenges:Despite evidence that IL‑17/IL‑23 inhibitors may induce disease modification through effects on effector, memory, and regulatory immune cells, reliable predictive or prognostic biomarkers have not emerged. Barriers include complex pathogenesis, universally high biologic efficacy reducing need for stratification, inconsistent findings from genetic or transcriptomic studies, and the multifactorial nature of comorbidities. Methods Picasso ProspectIve Cohort psoriASiS FOllow-Up:PICASSO is a 10‑year prospective biobank/registry enrolling patients within three years of disease onset. Biological samples are longitudinally linked to clinical and epidemiological data, with follow‑ups every 2.5 years. The ultimate aim is to identify biomarkers predicting disease trajectory. Conclusion:Personalized psoriasis care requires biomarkers predicting progression and comorbidity risk. PICASSO represents a step toward disease‑modifying, preventive precision medicine.
Background:Psoriasis is a chronic inflammatory skin disease associated with systemic inflammation, abnormal hemorheology, and coagulation dysfunction, all of which contribute to the development of atherosclerosis (AS). Inflammation and coagulation are closely intertwined processes; however, studies on the specific profiles of hemorheological and coagulation indices and their synergistic mechanisms remain limited. Objective:To compare differences in hemorheological and coagulation parameters and preliminarily elucidate the regulatory mechanism of the inflammation-hemorheology-coagulation axis. Methods:A total of 439 patients with psoriasis and 198 controls were enrolled; after PSM, 206 cases and 126 controls were included. All participants underwent vascular ultrasonography between May 2014 and February 2025. Patients were divided into the case group (psoriasis with AS) and control group (psoriasis without AS) based on vascular ultrasound and clinical assessment by specialized clinicians. PSM was used to balance baseline confounders, and sample sizes varied due to missing data. Statistical analyses included Spearman correlation and multivariate logistic regression. Results:The case group had higher fibrinogen (FIB) levels (3.54 vs. 3.11, P = 0.005, Cohen's d = 0.163) and shorter activated partial thromboplastin time (APTT) (26.40 vs. 27.60 s, P = 0.002, Cohen's d = 0.181). FIB showed the strongest association, with a correlation coefficient of 0.56 (P < 0.001) for systemic immune inflammation index (SII) and 0.39 (P < 0.001) for neutrophil-to-lymphocyte ratio (NLR) in the case group, and there was a strong positive correlation between SII and FIB (r = 0.56, P < 0.001). Psoriasis inflammation directly promoted vascular inflammation with a large effect size (β = 0.45, P < 0.001). Multivariate logistic regression analysis showed WBV (whole blood viscosity) (1 mPa·s) was the strongest predictor, with an OR of 1.752 (95% confidence interval [CI]: 1.314-2.651, P < 0.001). Limitations:Selection and recall biases of retrospective single-center studies. Conclusion:Patients with psoriasis, particularly those with severe disease, long disease duration, or complications from other thrombotic factors, should be closely monitored for hemorheological and coagulation parameters to prevent cardiovascular disease occurrence.
Psoriasis is a common chronic dermatological disease, affecting approximately 1-3% of the global population, and is associated with numerous comorbidities, impaired quality of life, and reduced life expectancy compared with the general population. The pathogenesis of psoriasis is complex and multifactorial, involving genetic susceptibility, external environmental factors, and immune system dysregulation. Psoriasis is perceived as a systemic disorder associated with a systemic inflammatory condition. In psoriasis, a chronically activated immune response results in the expression of numerous pro-inflammatory mediators, which enhance and sustain the inflammatory feedback loop, thereby exacerbating cell senescence. Senescent cells adopt a hypersecretory state called senescence-associated secretory phenotype (SASP). Multiple SASP-related mediators are dysregulated in psoriasis, including pro-inflammatory cytokines, chemokines, growth factors, proteases and regulators, soluble or shed receptors and ligands, some of which may serve as biomarkers or therapeutic targets. Therefore, psoriasis is closely associated with immune dysregulation and inflammaging, which refers to a chronic, low-grade inflammatory state with exacerbated cellular senescence. The relationship between psoriasis, inflammation, and cellular senescence is multidirectional, and might be considered in two hypothetical scenarios of cause-and-effect relationship. A persistent pro-inflammatory state might promote cellular senescence and SASP upregulation, which in turn may trigger immunological alterations characteristic of psoriasis, or psoriasis and associated dysregulation of the immune system leading to systemic inflammation and thereby senescence. Hence, it is essential to clarify the mechanisms of inflammaging and the role of SASP in psoriasis. It may support the development of the therapeutic strategies that take into consideration comorbidities and their shared inflammatory background with psoriasis, enabling more precise assessment of the disease.
Psoriasis is a chronic systemic inflammatory disease that is increasingly seen in older patients. As the immune system ages, the mechanisms that normally keep immune responses in balance become less precise. The adaptive immune system is reshaped both quantitatively and structurally, whereas innate immunity becomes less well regulated rather than simply less active. Age-related changes in the skin microenvironment may also help sustain local inflammatory signaling. In older patients with psoriasis, these age-related immune changes intersect with the pathways already known to drive disease. Th17 and cytotoxic CD8⁺ T (Tc17) responses remain prominent, control of antigen-presenting cells (APCs) is less tightly regulated, and natural killer (NK) cell function is also altered. These changes help sustain inflammation and further compromise the epidermal barrier. Treatment decisions are made more complex by common comorbidities, especially cardiovascular disease and metabolic syndrome. Biologic agents targeting TNF-α, IL-12/23, IL-23, IL-17, and IL-36 have markedly expanded the therapeutic options for psoriasis. Direct evidence in older patients with psoriasis remains limited, but the studies available so far suggest that treatment efficacy is broadly comparable to that seen in younger populations. Even so, immune aging may still affect both susceptibility to infection and the likelihood of remaining on treatment over time. TNF inhibitors remain particularly useful in patients with systemic inflammatory comorbidities, although infection risk requires close attention. IL-12/23 inhibitors offer the advantage of dual cytokine blockade. Selective IL-23 inhibitors allow more focused control of Th17-driven inflammation while leaving Th1 function relatively preserved. IL-17 inhibitors are often associated with rapid clinical improvement, whereas IL-36 inhibitors may be particularly promising in pustular disease. Clarifying how immunosenescence shapes disease behavior and treatment response in older patients should make it easier to individualize therapy.
Background:Psoriasis is a chronic inflammatory skin disease. Narrow-band ultraviolet B (NB-UVB) phototherapy is an effective, cost-efficient, and safe treatment for plaque psoriasis; however, predictors of treatment response remain limited. Objective:To develop predictive models for the efficacy and safety of NB-UVB phototherapy in patients with plaque psoriasis. Methods:A total of 252 patients with plaque psoriasis were enrolled and received 12 weeks of NB-UVB phototherapy. Baseline clinical data and blood samples for genetic analysis were collected. A genome-wide association study (GWAS) was performed to identify single-nucleotide polymorphisms (SNPs) associated with treatment response and adverse events (AEs). Results:Using a suggestive genome-wide significance threshold (P < 1×10-5), the SLC7A13 rs35314286 TA allele and DYNC1H1 rs941636 A allele showed suggestive associations with better efficacy after 4 weeks of NB-UVB treatment. Seven ATP2B2 SNPs and ten PSMB7 SNPs showed suggestive associations with achievement of Psoriasis area and severity index (PASI) 75 at week 12. Two KCNA2 SNPs, seven THSD7B SNPs, and one TENM4 SNP were identified as candidate markers for the occurrence of AEs. Conclusion:Predictive models of NB-UVB treatment response in psoriasis were subsequently established and achieved area under the curve (AUC) values ranging from 0.80 to 0.85. Further validation in independent external cohorts is needed before clinical application.
Paraneoplastic papuloerythroderma of Ofuji (PEO) is a rare cause of exfoliative erythroderma characterized by intensely pruritic, generalized erythema and scale with relative sparing of the skin folds (deck-chair sign) and is frequently associated with underlying malignancy, most commonly cutaneous T-cell lymphoma (CTCL). We present a unique case of paraneoplastic PEO in a patient with a history of plaque psoriasis whose rash suddenly began to worsen despite treatments for psoriasis. He developed diffuse brightly erythematous plaques with sparing fo the skin folds and hyperkeratotic, fissured plaques on the palms and soles. This ultimately led to hospitalization for erythroderma. Upon further work up, he was found to have squamous cell carcinoma of the lung by computed tomography. This case underscores that abrupt erythrodermic worsening in a patient with known psoriasis should prompt evaluation for an underlying paraneoplastic process rather than being attributed to psoriasis progression alone.
Purpose:Psoriasis extends beyond skin manifestations and significantly impacts patients' psychological health, social interactions, and daily functioning. The main objective was to assess the 2-year effect of tildrakizumab, an interleukin-23p19 inhibitor, on the skin, the psychological well-being and the health-related quality of life (HRQoL) of people with psoriatic disease in real-world. Patients and Methods:The POSITIVE study is a 24-month, prospective observational multinational study enrolling adults with moderate-to-severe plaque psoriasis treated with tildrakizumab according to clinical practice. Outcome measurements included the 5-item WHO Well-being Index (WHO-5), Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index-Relevant (DLQI-R). Results:785 patients were included. The mean (95% CI) WHO-5 score increased from 53.7 (52.2, 55.3) at baseline to 63.2 (61.5, 64.8) at W16 and continued improving over time: 65.9 (64.0, 67.9) at W52 and 70.4 (68.1, 72.7) at W104. The mean (95% CI) PASI decreased from 12.9 (12.3, 13.5) at baseline to 2.4 (2.2, 2.7) at W16 and was maintained until W104 [1.3 (1.1, 1.5)]. At W104, 87.9/79.0/65.1% of patients maintained PASI ≤3/≤2/≤1. Drug survival due to lack of effectiveness or adverse events (AE) was 87.8% and 96.3% after 2 years. The mean (95% CI) DLQI-R score decreased from 12.0 (11.4, 12.6) at baseline to 3.1 (2.6, 3.6) W52 and 2.1 (1.7, 2.5) at W104. At the final analysis, 11.1% of patients had ≥1 related AE. Conclusion:Treatment with tildrakizumab delivered sustained and holistic long-term health for moderate to severe psoriasis over 2 years by consistently improving patients' psychological well-being, life and clinical outcomes with a favourable safety profile. ClinicalTrialsgov ID:NCT04823247.
Introduction:Psoriatic arthritis (PsA) involves intricate immune-mediated pathways that extend beyond the well-characterized IL-23/IL-17 axis. Given that many patients show inadequate responses to current therapies, identifying novel immune drivers is essential. To clarify how specific immune cell populations influence PsA susceptibility, we performed a bidirectional two-sample Mendelian randomization (MR) study. Methods:We used genetic instruments for immune traits from a GWAS of 3,757 European individuals and PsA summary data from the IEU database (5,065 cases and 21,286 controls). Applying inverse variance weighting as our principal method. Results:At a nominal significance level (P < 0.05), we detected 14 immune phenotypes linked to heightened risk and 12 associated with reduced risk. Among the risk-associated phenotypes, activated B cells-particularly those expressing CD25 and BAFF-R on IgD+CD24+ subsets-emerged as prominent markers, a finding that shifts focus toward humoral involvement alongside the conventional emphasis on T cells alone. We also identified pathogenic contributions from specific T cell subsets, notably CCR7+naïve CD4+T cells and CD127+CD45RA+CD4+T cells. Conversely, certain natural killer T cell phenotypes appeared protective, hinting at a regulatory role for these populations. Reverse MR indicated that PsA liability itself may drive changes in 23 immune phenotypes, including depletion of circulating plasmacytoid dendritic cells and alterations in myeloid compartments-patterns likely reflecting cellular migration into inflamed synovial tissue. Importantly, none of these associations survived false discovery rate correction, indicating that these findings are exploratory. Conclusion:Our findings map the genetic underpinnings of immune dysregulation in PsA and provide a hypothesis-generating resource for therapeutic strategies targeting B cell stimulation. The preliminary nature and uncertainty of these associations necessitates further investigation and validation in independent, larger cohorts alongside current cytokine-directed approaches.
Scalp psoriasis affects up to 80% of patients with psoriasis and possesses a significant challenge as a difficult-to-treat area. A comprehensive literature search was conducted in PubMed using relevant keywords to identify recent studies focusing on scalp psoriasis diagnosis and treatment. The diagnosis is mainly based on clinical evaluation and trichoscopy. Other diagnostic tools, such as histopathology, optical coherence tomography, reflectance confocal microscopy (RCM) and line-field confocal optical coherence tomography (LC-OCT) may offer valuable insights in doubtful cases. Topical therapies (glucocorticosteroids, a betamethasone-calcipotriol combination or calcineurin inhibitors) remain the first-line therapy for mild to moderate cases. Patients with severe scalp psoriasis and those who do not respond to topical treatment are candidates for systemic therapy, including targeted therapy (interleukin-17 inhibitors, interleukin-23 inhibitors, tumor necrosis alpha inhibitors) or classic treatment (methotrexate, cyclosporine) Recent studies have demonstrated promising outcomes with novel treatments including Janus kinase (JAK) inhibitors and other new small molecules. This review provides updated information focused on diagnostic methods and targeted treatment of scalp psoriasis with relevance to clinical management of patients.
Purpose:Psoriasis is a chronic inflammatory skin disease characterized by abnormal keratinocyte proliferation and differentiation, affecting approximately 2% of the global population. Patients and Methods:This study explored the role of specific molecular biomarkers in the pathogenesis of psoriasis through integrative bioinformatics analysis, aiming to improve diagnostic precision and uncover therapeutic targets. Four independent transcriptomic datasets (GSE34248, GSE41662, GSE50790, and GSE6710) were analyzed using bioinformatics tools to identify consistently dysregulated genes in psoriatic lesions. Subsequently, we constructed a protein-protein interaction (PPI) network using the STRING database and analyzed key gene modules and hub genes involved in disease pathways. Results:This integrative approach led to the identification of 32 genes consistently dysregulated across all four datasets. Pathway enrichment highlighted significant involvement in biological processes such as keratinization (p = 1.53 × 10-6) and cornified envelope formation (p = 1.93 × 10-5), which are central to the epidermal alterations observed in psoriasis. Several gene families implicated in skin homeostasis and inflammatory regulation were found to contribute to psoriasis pathogenesis. Conclusion:These findings underscore the relevance of these core genes and pathways in the molecular landscape of psoriasis and offer potential targets for future functional validation and therapeutic intervention.
Purpose:Psoriasis is a chronic immune-mediated skin disease increasingly linked to skin and gut dysbiosis. Microbiota-derived tryptophan catabolites act as endogenous ligands of the aryl hydrocarbon receptor (AhR) and modulate inflammation, but their role in psoriasis remains incompletely defined. Here, we aimed to determine whether the microbiota-derived tryptophan metabolite indole-3-lactic acid (ILA) modulates psoriasiform inflammation and to define its underlying mechanisms and therapeutic potential. Methods:Using the imiquimod (IMQ)-induced mouse model of psoriasiform dermatitis (PsD), we profiled tryptophan metabolites by targeted LC-MS/MS in feces and serum. Mice received oral or topical ILA, with or without the AhR antagonist CH-223191. Ex vivo cervical lymph node (cLN) cells were stimulated with IL-23 + IL-1β to assess IL-17A production by γδ T cells. Separate cohorts received oral Lactobacillus reuteri supplementation. Public transcriptomic datasets were interrogated for cell type-specific AhR expression. Results:Targeted metabolomics revealed reduced ILA levels in both feces and serum of IMQ-treated mice. Oral or topical ILA attenuated disease severity, reduced epidermal proliferation and neutrophil infiltration, and suppressed the expression of inflammatory transcripts, including Il17a. Notably, topical ILA was superior to benvitimod, a synthetic AhR agonist approved for the treatment of psoriasis, in suppressing IMQ-induced PsD. The AhR antagonist CH-223191 partially abrogated the protective effects of oral ILA. Ex vivo, ILA selectively suppressed IL-17A production by γδ T cells, and this effect was reversed by AhR antagonism. Lactobacillus reuteri supplementation ameliorated PsD in an AhR-dependent manner, with fecal ILA levels inversely correlating with ear thickness and cutaneous neutrophil infiltration. Analysis of public datasets showed increased AhR expression in psoriatic T cells and a positive correlation of AhR and CYP1B1 with IL17A/IL17F. Conclusion:These findings identify a microbiota-derived ILA-AhR axis that limits γδT17/IL-17-driven skin inflammation, and support metabolite supplementation or probiotic augmentation as potential therapeutic strategies for psoriasis.
