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.
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.
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.
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.
Background: To the best of our knowledge, no validated scoring instrument currently exists that comprehensively evaluates both cutaneous manifestations and systemic comorbidities of psoriasis. This multicenter study aimed to develop and validate a novel multidimensional scoring system addressing this clinical gap. Methods: Under the guidance of the Shenzhen Psoriasis Academy, we conducted seven expert meetings to analyze existing evidence from PubMed, Wanfang, and CNKI databases. Through iterative Delphi consensus processes involving 26 specialists across 10 disciplines, we established the Psoriasis Disease Assessment Index (PSODAI). This 60-point composite instrument evaluates cutaneous involvement and nine key organ/system comorbidities. An accompanying online calculator (http://www.psodai.com.cn/) was developed for clinical implementation. Validation involved 254 psoriasis patients from six tertiary centers, with comparative analyses against PASI and DLQI metrics. Results: The PSODAI framework stratifies disease severity as mild (0- 20), moderate (21- 40), and severe (41- 60). Comparative analysis revealed comparable proportions of moderate-to-severe cases between PSODAI and conventional tools (PASI/DLQI) (p> 0.05). Notably, 11 patients (4.3%) classified as severe by PASI were re-categorized as mild through PSODAI's systemic evaluation, primarily due to limited extracutaneous manifestations. Conclusion: As the first comorbidity-integrated assessment tool, PSODAI enables cross-specialty collaboration for holistic patient management. Its clinical adoption may facilitate timely comorbidity detection and preventive interventions. Further multicenter validation is warranted to confirm these preliminary findings.
Introduction:Interleukin-17 inhibitors (IL-17i) and interleukin-23 inhibitors (IL-23i) are advanced therapeutic options for moderate-to-severe psoriasis. In real-world settings, biologic persistence is commonly used as a proxy for effectiveness and safety, and a treatment-free status following biologic discontinuation may provide insights into disease remission. This study aimed to assess persistence and treatment-free status for IL-17i versus IL-23i among biologic-naïve patients with psoriasis in Japan. Patients and Methods:This retrospective cohort study analyzed data from the Japanese Medical Data Vision database from 01 January 2015 to 31 December 2022. Patients diagnosed with psoriasis who initiated IL-17i or IL-23i during this study period were included. Persistence of the index biologic and post-discontinuation treatment-free status were assessed using Kaplan-Meier methodology. Propensity score methods with inverse probability of treatment weighting and matching were employed to control potential confounding between treatment cohorts. Results:There were 1,751 and 1,721 patients included in the IL-17i cohort and IL-23i cohort, respectively. Persistence rates for IL-17i were 55.7% [95% CI 53.2-58.1%] at the first year and 21.5% [95% CI 18.9-24.2%] at the fourth year, versus 77.7% [95% CI 75.4-79.8%] and 47.8% [95% CI 42.2-53.2%], respectively, for IL-23i. The risk of discontinuation of IL-23i was half that of IL-17i (adjusted hazard ratio [aHR]=0.49 [95% CI 0.44-0.54]). After discontinuation, 19.2% [95% CI 16.1-22.4%] and 31.5% [95% CI 27.8-41.2%] of patients in the IL-17i and IL-23i cohorts, respectively, remained treatment-free for at least 1 year. Patients treated with IL-23i had a lower risk for resuming systemic therapy after biologic discontinuation (aHR=0.57 [95% CI 0.49-0.67]). Conclusion:IL-23i was associated with longer persistence and a longer post-discontinuation treatment-free period than IL-17i in patients with psoriasis. These findings may provide actionable insights for healthcare providers and patients as they develop treatment strategies. Future research integrating comprehensive clinical data is warranted to evaluate different treatment strategies, thereby informing clinical decision-making.
Purpose: Psoriatic disease (PsO) involving the genital region (GenPsO) or areas of sexual interest (ASI; anal region, gluteal area, groin, lower back, and chest/breast) is associated with impaired quality of life (QoL), sexual burden, and avoidance of sexual life. This nested cohort study investigated the prevalence and effect of GenPsO and PsO at any ASI in routine German care. Methods: Adult patients enrolled in the PsoBest registry were surveyed by mail. Main endpoints were prevalences of GenPsO and PsO at any ASI in the past 12 and 24 months. The reasons for sexual impairment (RSI) questionnaire, the Genital Psoriasis Symptoms Scale (GPSS), the Genital Psoriasis Sexual Impact Scale, demographics, and disease characteristics were assessed. Results: Questionnaires were returned by 811/2010 (40.3%) patients; 795 (39.6%) complete sets were analyzed. Mean (SD) age at onset was 35.0 (14.0) years for GenPsO, and 34.1 (14.9) years for PsO at any ASI. Period prevalence was 21.6% (n=172) for GenPsO and 49.2% (n=391), for PsO at any ASI in the last 24 months, and 10.8% (n=86) and 26.7% (n=212), respectively, at day of survey. Systemic therapy was used by 84.9% (n=73) of patients with GenPsO and 83.0% (n=176) with PsO at any ASI. Mean (SD) GPSS sum score was 27.6 (18.6). In the past 30 days, 60.5% (n=52) of patients with GenPsO and 35.4% (n=75) with PsO at any ASI experienced sexual impairment. Among patients with GenPsO, 40.7% (n=35) reported always avoiding sexual activities during the past week. RSI included stress, lack of self-confidence, and PsO-related pain/movement restrictions. Conclusion: Given the high prevalence of GenPsO and its extensive effect on patient QoL and sexual well-being, it is essential that genital and ASI regions are examined at each routine clinical appointment and that appropriate treatment is offered to minimize negative consequences and cumulative life course impairment.
Background:Psoriasis and substance abuse remains a serious healthcare burden. However, associations between substance abuse and psoriasis have not been elucidated. Objective:To evaluate the bidirectional associations between substance abuse and psoriasis. Methods and Subjects:Based on the UK Biobank data, we conducted two prospective cohort studies to compare the risk of incident psoriasis in participants with versus without substance abuse (Cohort 1) and the risk of incident substance abuse in participants with versus without psoriasis (Cohort 2). Incident substance abuse (ICD: F10-F19) and psoriasis (ICD: L40) were primarily determined from hospital and primary care data, death registries and self-assessments. Results:In Cohort 1, 4,097 of 454,245 developed psoriasis during follow-up. Baseline substance abuse was linked to an increased psoriasis risk (hazard ratio [HR]: 2.31, P<0.001), notably in alcohol and tobacco users (HRs: 2.29 and 2.33, P<0.001). Those with high genetic risk and substance abuse had the greatest psoriasis risk (HR: 5.19, P<0.001). In Cohort 2, 25,176 out of 451,547 were diagnosed with substance abuse during follow-up. A notable association between baseline psoriasis and subsequent substance abuse (HR: 1.28, P<0.001) was observed, slightly mediated by depression, anxiety, and sleep quality (1.7% to 3.4%; all P<0.001). Sensitivity analyses showed consistent results. Conclusion:Our findings identify bidirectional positive associations of substance abuse with psoriasis. This association is especially pronounced in those with both high genetic risk and alcohol or tobacco abuse. It is suggested that clinicians should consider alcohol or tobacco abuse among psoriasis patients to improve their life quality.
Pediatric erythroderma can arise from either inherited keratin defects or cytokine-driven inflammation, yet evidence for biologic therapies in these settings is limited. We report two rare pediatric cases successfully treated with secukinumab, an IL17A-targeted monoclonal antibody: (i) a 2-year-old boy with genetically confirmed epidermolytic ichthyosis (EI, KRT10 mutation:c.467G>A, p.Arg156His) refractory to conventional care, who achieved >60% improvement in erythema and scaling one week after a single off-label 150 mg subcutaneous secukinumab dose, with remission maintained for 12 months on monthly dosing; and (ii) an 11-year-old girl with coexistent Type III (juvenile) pityriasis rubra pilaris and acute generalized pustular psoriasis (PRP-GPP overlap) unresponsive to acitretin and methotrexate, who attained complete remission for 12 months following standard secukinumab induction (300mg weekly ×5) and maintenance every four weeks. These cases extend the potential utility of IL17A blockade beyond psoriasis vulgaris to both structural keratinopathies and inflammatory pustular dermatoses in children. While limited by the nature of a two-patient case series, these findings warrant prospective studies to clarify optimal dosing and long-term safety of IL-17A blockade in pediatric dermatology.
Introduction:Psoriasis is a chronic inflammatory disease whose burden peaks in older age groups. Despite the increasing prevalence of elderly patients with moderate-to-severe psoriasis, real-world data on biologics in this population remain limited, particularly for anti-IL-23 agents like guselkumab. This study evaluates the long-term effectiveness and safety of guselkumab in patients aged ≥65 years. Methods:This retrospective study included 66 patients aged ≥65 years with plaque psoriasis treated with guselkumab 100 mg between June 2019 and June 2024. PASI scores were recorded at baseline and during follow-up visits at weeks 4, 16, 24, 36, 52, 76, and 104. Effectiveness was assessed using PASI75/90/100 and PASI ≤ 2 responses. Multivariable logistic regression with Firth correction identified baseline predictors of PASI90 and PASI100 at weeks 16 and 52. Safety outcomes included treatment-emergent adverse events (TEAEs). Results:Mean PASI improved from 13.3 at baseline to 1.0 at week 24 and remained stable through week 104. PASI90 and PASI100 were achieved by 83.9% and 71.0% at week 36 and maintained in 69.2% and 61.5% at week 104. Higher baseline PASI independently predicted PASI90 and PASI100 at week 16, while lower eosinophil-to-lymphocyte ratio (ELR) independently predicted PASI100. At week 52, chronic beta-blocker intake and PASI90 at week 16 predicted PASI90 response, while PASI100 was independently associated with low-dose aspirin use and positive family history of psoriasis. TEAEs occurred in 16.7% of patients, with treatment discontinued in 9.1%. Eczematous or urticarial AEs were associated with elevated baseline eosinophils and ELR. Conclusion:Guselkumab is effective and well tolerated in older adults with psoriasis. Baseline ELR, early PASI response, and chronic use of beta-blockers or aspirin may influence long-term treatment outcomes. While limited by the small sample size (66 patients), our findings represent the longest real-world follow-up to date among older psoriatic patients treated with guselkumab and support its use as a valuable therapeutic option in this population.
Background:Psoriasis is a common chronic inflammatory skin disorder, and the global burden of psoriasis has not been fully disclosed. Methods:We extracted prevalence, incidence and disability-adjusted life years (DALYs) for psoriasis from 1990 to 2021 in Global Burden of Disease (GBD) and predicted trends in the next 15 years though ARIMA model. Results:Globally, age-standardized incidence rate (ASIR) of psoriasis increased from 57 cases/100,000 people (95% CI: 55.3~58.8) in 1990 to 62 cases/100,000 people (95% CI: 60.1~63.9) in 2021. Age-standardized prevalence rate (ASPR) and age-standardized disability-adjusted life year rate (ASDR) exhibited similar trends of increases. The global ASIR, ASPR, and ASDR for males were significantly higher than females. In 2021, ASIR peaked in the 55-69 ages, while ASPR and ASDR reached peaks between the ages of 65-74. Regionally, ASPR, ASIR, and ASDR in 2021 were highest in high Socio-demographic index (SDI) regions. The highest global regions and countries of ASPR, ASIR and ASDR were Western Europe and Germany, respectively. The East Asia region and Republic of Equatorial Guinea showed most significant growth in these psoriasis indicators since 1990. Furthermore, there was a significant increase in ASIR (8.06%), ASPR (8.14%), and ASDR (13.64%) of global psoriasis over the next 15 years. Conclusions:Global burden of psoriasis is expected to continuously increase, and strengthening risk-factor management and prioritizing high-risk subgroups (males, elderly, high SDI regions and Western Europe, etc) will be essential for region-specific strategies and future healthcare planning.
