Pre- and postprocedure skin care is crucial for patients undergoing energy-based device (EBD) treatments. A serum containing a proprietary blend of peptides to support extracellular matrix remodeling (TriHex Technology®) was developed to aid skin preparation and recovery following aesthetic procedures. This analysis evaluated the skin recovery effects and safety of this serum in Asian subjects following fractional CO2 laser (FCL) and radiofrequency microneedling (RFMN). Two prospective, randomized, evaluator-blind, split-face studies were conducted. In the FCL study (n = 26), subjects applied a reference moisturizer on the entire face and the serum on an assigned hemi-face for 2 weeks preprocedure. Postprocedure, the serum and moisturizer were applied to opposite hemi-faces for 3 days, followed by the preprocedure regimen until day 14. In the RFMN study (n = 25), serum and moisturizer were applied to opposite hemi-faces immediately postprocedure for 3 days, followed by serum on the assigned hemi-face and moisturizer on the entire face until day 14. Blinded clinical evaluations, self-assessments, and skin measurements were performed on days 0, 1, 3, 7, and 14. All 26 subjects (18 female, 8 male) completed the FCL study and 25 (24 female, 1 male) completed the RFMN study. Overall, the serum-treated side showed superior or comparable recovery versus control across multiple parameters. The primary endpoint of investigator-assessed erythema showed significant within-side improvement on both sides in both studies, while between-side differences did not reach statistical significance. Among secondary endpoints, the serum-treated side showed significantly greater recovery that withstood multiplicity correction for transepidermal water loss (TEWL) at day 3, and edema, VISIA redness, and tactile roughness at day 14 in the FCL study, while crusting at day 3 showed numerical improvement. In the RFMN study, the serum-treated side showed significantly greater edema reduction at day 7 that withstood correction; numerical improvements were observed for pain and heat sensation at day 1 and for erythema and crusting at day 7. On day 14, significantly more subjects reported better recovery on the serum-treated side (FCL, 81.8

ABSTRACT Background Microplasma radiofrequency is frequently used for neck rejuvenation. However, the efficacy and safety of different energy protocols for neck treatment remain poorly understood. Objective To explore the optimal energy during plasma radiofrequency for neck laxity treatment. Methods Seventeen patients with mild‐to‐moderate neck wrinkles were enrolled in this split‐neck study. One side of each patient's neck was treated with low‐energy plasma radiofrequency in six sessions at two‐week intervals, while the contralateral side received high‐energy plasma radiofrequency in three sessions at four‐week intervals. Two dermatologists evaluated wrinkle improvement using Antera 3D imaging data collected before treatment and at 1, 3, and 6 months after the final session. Pain severity was assessed with a visual analog scale, and any post‐treatment adverse effects were recorded. Results Both low‐ and high‐energy plasma radiofrequency treatments significantly improved neck wrinkles, with no significant difference in the degree of improvement between the two protocols. One month post‐treatment, the improvement rates from baseline were 18.5% (low‐energy) and 24.23% (high‐energy). At 3 months, the rates were 17.3% and 25.63%, respectively. Six months post‐treatment, the improvement rates were 24.37% for the low‐energy side and 15.45% for the high‐energy side. A significant difference in pain scores was observed between the two protocols ( p < 0.05). Patients experienced mild pain on the low‐energy side and moderate pain on the high‐energy side. Erythema and edema were present on both sides immediately after treatment but subsided within 6 h. No adverse reactions, such as scabbing, post‐inflammatory hyperpigmentation, or scarring, were reported by any patients. Conclusion Both low and high energy plasma radiofrequency can safely and effectively improve mild to moderate neck skin laxity. Low‐energy treatments have the advantage of causing less pain, while high‐energy treatments achieve the desired results with fewer sessions.

BACKGROUND:Ivarmacitinib, an oral JAK1 inhibitor, improved efficacy outcomes versus placebo at Week 16 in a phase 3 trial in patients with moderate-to-severe atopic dermatitis (AD). OBJECTIVES:To describe efficacy and safety outcomes through Week 52. METHODS:In this multicentre, double-blind, phase 3 trial (NCT04875169), patients aged 12-75 years were randomized 1:1:1 to receive once-daily oral ivarmacitinib 4 mg, ivarmacitinib 8 mg, or placebo for 16 weeks, followed by a 36-week double-blind extension. At Week 16, placebo-treated patients who continued in the study were re-randomized to ivarmacitinib 4 mg or 8 mg. Key Week 52 endpoints included Investigator's Global Assessment (IGA) 0/1 with at least a 2-grade improvement, Eczema Area and Severity Index 75 (EASI-75), and Worst Itch Numeric Rating Scale (WI-NRS) response. RESULTS:Of 336 randomized patients, 258 completed 52 weeks of treatment. Among patients initially randomized to ivarmacitinib, Week 52 IGA responses were achieved by 42.3% and 40.2% of patients in the 4 mg and 8 mg groups, respectively. EASI-75 responses were achieved by 60.6% and 55.9%, and WI-NRS responses by 59.6% and 45.1%, respectively. During the active-treatment period, treatment-emergent adverse events (TEAEs) occurred in 87.5% and 85.5% of patients in the 4 mg and 8 mg groups, respectively. The most frequent TEAEs were upper respiratory tract infection, COVID-19, SARS-CoV-2 test positive, and increased blood creatine phosphokinase. Serious TEAEs occurred in 5.6% and 4.4% of patients, respectively. CONCLUSION:Ivarmacitinib was associated with generally maintained improvement through Week 52, with a safety profile generally consistent with that observed during the placebo-controlled period. Because the extension phase had no placebo control after Week 16, long-term efficacy findings should be interpreted as descriptive.

BACKGROUND:Stapokibart is a novel anti-interleukin-4 receptor α (IL-4Rα) monoclonal antibody approved for the treatment of adults with moderate-to-severe atopic dermatitis (AD). OBJECTIVES:To assess the safety, efficacy, pharmacokinetics, pharmacodynamics and immunogenicity of stapokibart in children with moderate-to-severe AD. METHODS:This was a multicentre open-label single-arm phase Ib/IIa trial (NCT06162507) involving 8 weeks of treatment and 8 weeks of follow-up. Children aged 6-11 years received subcutaneous stapokibart based on a bodyweight-tiered regimen (30-60 kg: 300 mg every 3 weeks for a total of three doses, including a 600-mg loading dose; 15-30 kg: 150 mg every 2 weeks for a total of four doses, including a 300-mg loading dose). RESULTS:Twenty-five patients (13 weighing 30-60 kg; 12 weighing 15-30 kg) received stapokibart; 68% reported mild or moderate adverse events. At week 8, 54% (n = 7/13) of those weighing 30-60 kg and 75% (n = 9/12) of those weighing 15-30 kg achieved a ≥ 75% improvement from baseline in Eczema Area and Severity Index. Stapokibart concentrations increased rapidly following the first dose, climbed further with repeated dosing and gradually declined after treatment discontinuation. Stapokibart reduced inflammatory biomarkers in both groups. No treatment-related antidrug antibodies were detected. No new safety signals emerged. CONCLUSIONS:Stapokibart shows potential in improving disease outcomes and appears to be well tolerated in children aged 6-11 years with moderate-to-severe AD. Larger controlled studies are needed to confirm long-term benefits.

Objectives This post-hoc analysis of CM310AD005 conductedaimed to analyze the efficacy and safety of stapokibart in adults with moderate-to-severe atopic dermatitis (AD) with and without prior systemic treatment.Methods In CM310AD005, eligible patients were randomized 1:1 to receive stapokibart 600 (loading dose)-300 mg and placebo Q2W for 16 weeks; all patients subsequently received stapokibart 300 mg Q2W for 36 weeks.Results At week 16, in systemic treatment-naïve patients, stapokibart led to significantly higher response rates than placebo for ≥75% improvement from baseline in the Eczema Area and Severity Index score (EASI-75, 70.3% vs. 29.1%), EASI-90 (38.1% vs. 13.3%), Investigator’s Global Assessment score of 0 or 1 (45.2% vs. 19.4%), and ≥4-point reduction in weekly average of daily Peak Pruritus Numerical Rating Scale score (34.8% vs. 13.9%) (all p < 0.0001). Among patients with prior systemic treatment, these response rates were also significantly higher in the stapokibart group, reaching 61.5% vs. 19.3%, 35.4% vs. 7.2%, 42.7% vs. 9.6%, and 37.5% vs. 7.2% (all p < 0.0001), respectively. All patients showed further improvements through week 52. The most common treatment-emergent adverse events were infections and infestations, occurring in 61.6% and 70.5% of patients with and without prior systemic treatment.Conclusions Stapokibart demonstrated significant clinical efficacy and manageable safety in AD patients irrespective of prior systemic treatment.

Objective To investigate the therapeutic effects and mechanisms of blue light com-bined with gel for skin photoaging in mice.Methods Twenty-five male C57/BL6 mice were ran-domly divided into five groups:blank control,model,blue light,gel,and blue light+gel(com-bination)groups,with five mice per group.Except for the blank control group,a UVA and UVB synergistic irradiation method was used to establish a photoaging model.Mice were irradiated with 1 minimal erythema dose(MED)from week 1 to week 4,followed by 2 MEDs in weeks 5 and 6.Concurrently,starting from the third week,blue light combined with gel therapy was administered on the last day of each week.The control group received no treatment.The gel group received on-ly gel treatment for 6 minutes.The blue light group received only blue light irradiation for 6 mi-nutes.The combined group received gel treatment,followed immediately by blue light therapy.After 6 weeks,dorsal skin samples were collected for hematoxylin and eosin(HE),and Masson＇s trichrome staining.Both cutaneous and serum levels of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and tumor necrosis factor(TNF-α)were measured using ELISA.Results After 6 weeks:The mouse skin exhibited desquamation,dryness,roughness,lesions,leathery texture,and hyperpigmentation.Either the blue light or gel group showed no significant improve-ments in skin desquamation,dryness,roughness,or leathery texture compared with the model group.Moreover,expression levels of SOD,GSH-Px,and collagen were not significantly upregu-lated compared with the model group(P＞0.05).However,the combined group showed signifi-cant improvement in wrinkles,dryness,desquamation,and leathery texture.The expression levels of SOD and GSH-Px in the skin were significantly upregulated to levels comparable to normal(P＜0.05),accompanied by a significant increase in collagen(P＜0.001).TNF-αexpression in the skin,as well as the serum levels of SOD,GSH-Px,and TNF-α,remained no significant change(P＞0.05).Conclusions Blue light combined with gel can alleviate oxidation,reduce inflammation,and increase collagen in photoaged skin,providing experimental evidence for its clinical application in photoaging management.

Abstract Keloids are benign fibroproliferative disorders majorly characterized by excessive extracellular matrix deposition, with recurrence rates exceeding 80% following conventional therapy. Although epigenetic dysregulation has been implicated in keloid pathogenesis, whether genome-wide DNA methylation actively drives pathological cellular reprogramming, and whether this state is therapeutically reversible, remains unclear. We performed genome-wide DNA methylation profiling on keloid tissues, matched primary keloid fibroblasts, and normal controls. Our analysis revealed a shared DNA hypermethylation pattern between keloid tissues and fibroblasts, which was validated by three independent public cohorts. By integrating DNA methylome and transcriptome, we demonstrated that DNA methylation-regulated genes were enriched in osteochondrogenesis-related pathways, such as cartilage and bone development pathways. Furthermore, pharmacologic inhibition of DNA hypermethylation by DNA demethylating agent decitabine reduced the expression of osteochondrogenic markers and inhibited collagen deposition and keloid growth in primary keloid fibroblasts and patient-derived xenograft (PDX) model, offering a potential therapeutic strategy of keloid.

IntroductionKeloid is a fibroproliferative scar with marked ethnic disparities, disproportionately affecting Asian and Black populations. Single-cell RNA sequencing (scRNA-seq) studies have mapped keloid pathology, but cross-study differences complicate generalization. We performed a meta-analysis to identify composition and transcriptional programs associated with keloid across ethnicities.MethodsWe aggregated human skin scRNA-seq datasets containing keloid and healthy samples with documented ethnicity (Asian, Black, White). After quality control and batch integration (scVI/scANVI), we annotated cell types and subtypes. Differential abundance was estimated with scCODA, Milo, and propeller. Pseudobulk differential expression was meta-analyzed using random-effects models. Ligand-receptor signaling was inferred with CellChat/NicheNet.ResultsThe harmonized atlas comprised 112 donors, 147 samples, and 487,293 cells from 8 studies. Keloid demonstrated higher proportions of vascular endothelial cells and fibroblasts across all methods. Ethnicity-stratified analysis revealed endothelial expansion in Asian and Black relative to White populations, while fibroblast expansion was greater in White keloids. Endothelial subtyping showed increased post-capillary venules and arteriolar states. Fibroblast analysis revealed expansion of mesenchymal/ADAM12+ and pro-inflammatory populations. Meta-analysis implicated TGF-β/SMAD, integrin/FAK, and YAP/TAZ mechanotransduction pathways as candidate pathogenic programs warranting functional validation.ConclusionCross-study synthesis identifies shared and ethnicity-stratified endothelial and fibroblast programs in keloid. Expansion of post-capillary venules and ADAM12+ fibroblasts provides candidate therapeutic targets pending functional validation and a framework for understanding ethnic disparities in keloid formation.

Hidradenitis suppurativa (HS), also known as acne inversa (AI), is a chronic, recurrent inflammatory disease of the pilosebaceous unit that primarily affects intertriginous areas and is characterized by recurrent, painful, deep-seated inflammatory lesions. The pathogenesis of HS/AI is multifactorial, involving genetic susceptibility, immune dysregulation, microbial imbalance, and obesity. HS/AI remains difficult to manage, and current treatment aims to reduce the frequency and duration of flares, decrease disease severity, and improve quality of life. Treatment selection should be guided by disease severity and activity. Pharmacologic therapies include antibiotics, biologics, small-molecule agents, retinoids, and immunosuppressants, while adjunctive approaches include surgical interventions and energy-based therapies. This updated consensus aims to standardize the diagnosis and management of HS/AI in China and to improve clinical practice by providing a stepwise, multidisciplinary treatment framework in which interventions are stratified according to disease severity and recommendation strength. Recommendation strength was determined by expert voting: an agreement rate of ≥85% indicated “Should be recommended,” ≥75% to <85% indicated “Could be recommended,” ≥50% to <75% indicated “May be considered,” and <50% indicated “No consensus reached.” Key recommendations reaching the ≥85% agreement threshold included severity-based treatment selection, topical clindamycin for mild localized disease, systemic tetracyclines for mild-to-moderate HS/AI, and biologics, including adalimumab, secukinumab, and bimekizumab, for moderate-to-severe disease. The consensus has been registered on the International Practice Guidelines Registry Platform (No: PREPARE-2025CN1964).

BACKGROUND:Eosinophils are involved in the pathogenesis of atopic dermatitis (AD). OBJECTIVE:This post-hoc analysis evaluated the effect of stapokibart on blood eosinophil counts in moderate-to-severe AD patients. METHODS:The phase II AD002 trial (n = 120) randomly assigned patients to stapokibart 300 mg every 2 weeks (Q2W), 150 mg Q2W, or placebo for 16 weeks. The phase III AD005 trial (n = 500) randomly assigned patients to stapokibart 300 mg Q2W or placebo for 16 weeks, followed by open-label stapokibart 300 mg Q2W for 36 weeks. Efficacy and safety were analyzed in subgroups stratified by baseline blood eosinophil counts (≥500 or <500 cells/µL). RESULTS:Stapokibart treatment resulted in sustained reductions in blood eosinophil counts versus placebo (baseline vs. Week 16: high-dose 420 vs. 235 cells/μL, low-dose 530 vs. 315 cells/μL in AD002; 370 vs. 210 cells/μL in AD005). Furthermore, stapokibart demonstrated superior efficacy over placebo in achieving higher Eczema Area and Severity Index (EASI)-75 response rates at Week 16 in both eosinophil subgroups. The incidence of adverse events was similar across eosinophil subgroups, with most events being mild or moderate. CONCLUSION:Stapokibart reduced blood eosinophil counts in AD patients and demonstrated favorable efficacy and safety regardless of baseline blood eosinophil counts.

Keloid scars represent a complex fibroproliferative disorder characterized by abnormal wound healing and excessive collagen deposition. Central to keloid pathogenesis are dynamic fibroblast populations that undergo extensive phenotypic transitions, including heterogeneous subpopulation differentiation, enhanced migration, myofibroblast transdifferentiation, and sustained activation states. This review examines fibroblast dynamics as the central orchestrator of keloid formation, analyzing how these cells interact with keratinocytes, immune cells, endothelial cells, and melanocytes to drive pathological scarring. We focus on key signaling pathways that directly regulate fibroblast function, including TGF-β/Smad, VEGF, Wnt, and emerging regulators such as miR-3606-3p that integrate multiple fibrotic cascades. Current therapeutic approaches show variable efficacy, with surgical excision alone resulting in 45%-100% recurrence rates, while combination therapies incorporating radiation, intralesional injections, and novel molecular targets achieve improved outcomes. Emerging strategies include COX-2 inhibition for dual antiproliferative and proapoptotic effects on keloid fibroblasts, stem cell therapies, and precision medicine approaches based on molecular profiling. Through deeper understanding of fibroblast dynamics and their regulatory networks, more effective therapeutic strategies can be developed to improve patient outcomes and quality of life.

Teat number is an important economic trait in pigs because it affects sow reproductive performance and piglet nursing ability, yet its genetic basis and molecular regulatory mechanisms remain incompletely understood. In this study, a combined-population genome-wide association study was performed in Canadian and French Large White pigs to identify loci associated with teat number traits. A total of 4217 pigs were genotyped, and 2,244,684 autosomal single-nucleotide polymorphisms were retained after quality control and genotype imputation. Multiple association signals for total teat number were detected, with major peaks located on chromosomes 7 and 10. Among the positional candidate genes, PROX2 was prioritized for further validation, and genotype–phenotype association analysis showed that pigs with the CC genotype at the PROX2 polymorphic locus had significantly lower total teat number than those with the CT and TT genotypes. To investigate its biological role, PROX2 was silenced in porcine mammary epithelial cells. Transcriptome analysis identified 887 differentially expressed genes after PROX2 knockdown, and functional assays showed that PROX2 silencing inhibited cell proliferation, altered cell cycle progression, and affected the expression of proliferation- and development-related genes. These findings indicate that PROX2 is an important candidate gene associated with teat number variation in pigs.

The long-term efficacy of biologics in psoriasis is compromised by primary or secondary resistance, and poor treatment adherence due to frequent dosing. We assessed the efficacy and safety of switching to an interleukin-23 subunit p19 (IL23p19) inhibitor picankibart at 200 mg every 12 weeks, without a washout period, on skin clearance and quality of life (QoL) in patients with plaque psoriasis. A total of 152 patients were enrolled, comprising 83 suboptimal responders (static Physician’s Global Assessment [sPGA] ≥ 2 or body surface area [BSA] ≥ 3

BackgroundKeloids are fibroproliferative disorders conditions of the dermis with dysregulated immune responses contributing to disease progression. However, the causal inflammatory mediators and their pathogenic mechanisms remain undefined.PurposeThis study aims to identify causal inflammatory mediators for keloids and their pathogenic mechanisms.MethodologyTwo–sample Mendelian randomization (MR) analyses were performed using genetic instruments for 91 inflammatory proteins as exposures and genome–wide association study (GWAS) summary statistics for keloid susceptibility as the outcome. Sensitivity analyses were conducted to assess the robustness of MR findings. Single–cell RNA sequencing (scRNA–seq) datasets from keloid tissues were analyzed to identify the cellular distribution of prioritized candidates. Functional validation was performed using immunohistochemistry (IHC), immunofluorescence staining, qRT–PCR, western blotting, siRNA–mediated knockdown, recombinant protein stimulation, and transcriptome sequencing. Pharmacological inhibition and rescue experiments were further performed to investigate the downstream signaling pathway.ResultsMR analysis identified five inflammatory proteins with potential causal associations with keloid susceptibility, among which urokinase–type plasminogen activator (PLAU) was the only one consistently enriched in fibroblasts across two independent scRNA–seq datasets. PLAU expression was significantly elevated at both the mRNA and protein levels in keloid tissues and primary fibroblasts. PLAU knockdown in keloid fibroblasts reduced collagen I/III expression, proliferation, and migration, whereas recombinant PLAU stimulation enhanced these profibrotic phenotypes in normal dermal fibroblasts. Mechanistically, RNA–sequencing implicated activation of the TGF–β signaling pathway. Furthermore, inhibition of TGF–β receptor signaling attenuated PLAU–induced profibrotic responses, while exogenous TGF–β1 rescued the effects of PLAU depletion. Importantly, PLAUR knockdown attenuated PLAU–induced TGF–β/Smad activation and reduced PLAU–mediated enhancement of fibroblast activation.ConclusionsThis integrative study identifies PLAU as a genetically supported and biologically relevant mediator of keloid fibrosis. PLAU promotes fibroblast activation through PLAUR–dependent regulation of the TGF–β/Smad signaling pathway, leading to enhanced collagen production, proliferation, and migration. These findings provide new insights into inflammatory regulation in keloid pathogenesis and highlight PLAU as a potential therapeutic target for keloid intervention.

BACKGROUND:Primary syphilis is frequently undertested in clinical settings due to its protean presentation. China is experiencing a mass syphilis resurgence, but medical community knowledge of syphilis remains low. We assessed clinical performance of Chinese sexually transmitted infection (STI) physicians using data collected by "incognito" or standardized patients (SPs). METHODS:SPs presented cases of postprimary syphilis to physicians who consented to visits in advance but were not told the timing. SPs reported details on diagnostics and examinations performed by the physician. Logistic regression models identified predictors of performance metrics, adjusting for HIV status and sexual orientation of presented cases. RESULTS:One hundred twenty-three visits were conducted with 41 physicians. Physicians recommended syphilis testing in 84.5% of visits and performed at least 2 of 5 recommended clinical indicators in 31.7% of visits. Physicians were less likely to offer syphilis testing to patients with HIV, whether presenting as men who have sex with men (odds ratio [OR], 0.06; 95% confidence interval [CI], 0.01-0.57) or as straight men (OR, 0.13; 95% CI, 0.03-0.61). Those working >40 h a week were less likely to offer testing (OR, 0.3; 95% CI, 0.09-1.01), and those older than the median age were less likely to perform a thorough exam (OR, 0.34; 95% CI, 0.14-0.83). CONCLUSIONS:Chinese STI physicians frequently test patients for syphilis but are less likely to conduct thorough physical examinations. The undertesting of patients with HIV exposes missed opportunities to address the HIV/syphilis syndemic. Future trainings must emphasize the public health importance of dual screening and address physician concerns about occupational HIV exposure.

The biosynthesis of sex pheromones in lepidopteran pheromone glands is tightly regulated by pheromone biosynthesis-activating neuropeptide (PBAN) signaling; yet the contribution of non-coding RNA-mediated post-transcriptional regulation remains largely unclear. This study aimed to characterize temporal transcriptomic changes, candidate non-coding RNA-mediated regulatory associations, and temporal molecular dynamics underlying transcriptional remodeling after PBAN treatment in Ostrinia furnacalis. First, we performed comprehensive whole-transcriptome sequencing (WTS) on 18 biologically independent samples collected at six time points (0, 20, 40, 60, 90, and 120 min) after PBAN injection. Then, we systematically identified and quantified the dynamic expression patterns of differentially expressed (DE) mRNAs, miRNAs, lncRNAs, and circRNAs in response to PBAN stimulation. By integratively analyzing these multidimensional omics datasets and inferring sequence-based interaction relationships, we inferred a dynamic candidate competing endogenous RNA (ceRNA) like regulatory network. The candidate ceRNA network anchored four core node genes: the PBAN receptor (PBANR), the rate-limiting enzyme acetyl-CoA carboxylase (ACC), and the terminal biosynthetic enzymes desaturase (DES) and fatty acyl-CoA reductase (FAR). The qRT-PCR results further support the temporal expression pattern of key genes during the PBAN response, suggesting that this network can provide a valuable resource for further functional studies.

Objective To analyze the clinical characteristics of patients with generalized pus-tular psoriasis,we aimed to provide stronger theoretical support for the health management of GPP patients.Methods A retrospective analysis was conducted on the data of 150 patients with gener-alized pustular psoriasis(GPP)who visited the Dermatology Hospital,Southern Medical Universi-ty from July 2017 to July 2023.The patients were grouped according to age of onset,gender,and whether GPP was accompanied by psoriasis vulgaris(PV).The analysis aimed to explore the differences in clinical characteristics among different groups of GPP patients,including the season of onset and triggers,recurrence frequency,comorbidities,and treatment outcomes.Results A total of 150 patients with generalized pustular psoriasis(GPP),with a mean onset age of 32.83±21.65 years,were included in the analysis.The mean age of onset was significantly lower in pa-tients with GPP alone than in those with both GPP and psoriasis vulgaris(PV)(28.30±19.27 vs.40.87±23.43 years,t=-3.51,P＜0.05).The proportion of patients who were overweight was significantly higher in those with an onset age of ≥18 years(39.4％)compared to those with an onset age of＜18 years(17.4％)(x2=7.04,P＜0.05).The mean waist circumference of all adult male and female patients met the criteria for abdominal obesity.GPP had a predilection for onset in spring and summer.The probability of onset in spring and summer was significantly higher in patients with GPP alone(70.3％)than in those with GPP and PV(50.0％)(x2=5.45,P＜0.05).Improper treatment was identified as the primary triggering factor for GPP.The proportion of patients with improper treatment as a triggering factor was significantly higher in the GPP+PV group than in the GPP alone group(71.7％vs.5.2％,x2=74.22,P＜0.001).Re-garding triggering factors for relapse,improper treatment was the most common in patients with an onset age of＞18 years(39.5％),while upper respiratory tract infections were predominant in patients with an onset age of ≤18 years(40.0％).In female patients,some relapses were associ-ated with special physiological states such as pregnancy and menstruation.The recurrence rate was significantly higher in patients with an onset age of≤18 years than in those＞18 years(91.3％vs.71.7％,x2=7.39,P＜0.05).Females had a significantly higher probability of experiencing 3 to 4 relapses within a year than males(x2=4.20,P＜0.05).Patients with GPP alone were more prone to recurrence,with significantly higher probabilities of experiencing 1 to 2 relapses and 1 to 4 relapses within one year compared to the GPP+PV group(all P＜0.05).Males had a sig-nificantly higher probability of nail involvement and moderate fever than females(both P＜0.05)but a significantly lower probability of high fever(x2=3.90,P＜0.05).The probability of joint involvement was significantly higher in the GPP+PV group than in the GPP alone group(x 2=7.55,P＜0.05).Furthermore,hypertension was more commonly associated with GPP+PV than with GPP alone(x2=5.79,P＜0.05).Acitretin was the most commonly used drug.Patients re-ceiving combination therapy with immunosuppressants had the longest hospital stay(12.57±5.47 days),while those treated with biological agents alone had the shortest hospital stay(5.61±2.33 days)(P＜0.05).Conclusions Factors such as gender,age,and comorbidity with PV signifi-cantly impact the clinical presentation and treatment response of GPP.Early identification of trig-gering factors,precise subgroup-based interventions,and monitoring of biomarkers are crucial strategies to improve the clinical outcomes of GPP patients.

Chronic spontaneous urticaria (CSU), characterized by recurring itchy wheals (hives) and/or angioedema lasting > 6 weeks without identifiable triggers, affects 1.29