A decreased abundance of fecal Akkermansia muciniphila (Akk) has been observed in patients with psoriasis and psoriatic arthritis. The potential beneficial effects of Akk in managing psoriasis have been proposed, yet results remain inconsistent and mechanisms unclear. Using imiquimod (IMQ)-treated C57BL/6 mice, we conducted a metagenomic association study of pasteurized Akk (pAkk) in the IMQ mice through whole-genome shotgun sequencing. We also performed a dextran sodium sulfate (DSS)-induced colitis experiment and an intestinal permeability test. The association among pAkk supplements, skin thickness, inflammatory profiles, fecal microbiota alterations, functional genetic predictions, intestinal epithelium inflammation, and barrier integrity was investigated. The study demonstrated that pAkk supplementation ameliorated IMQ-induced skin thickening, weight loss, spleen weight gain, serum IL-17A, TNF-α levels, and DSS-induced colitis. pAkk supplementation was linked to greater fecal microbial diversity and alterations in fecal microbiota composition, with increased prevalence of Muribaculaceae, Bifidobacterium pseudolongum, Desulfovirionaceae, Erysipelotrichaceae, and Alistipes ihumi, which have been implicated in the Gamma-Aminobutyric Acid (GABA) shunt, cholinergic synapse, cell cycle, and Mitogen-Activated Protein Kinase (MAPK) pathways. In conclusion, pAkk may mitigate IMQ-induced skin thickening and DSS-induced colitis, associated with reduced levels of TNF-α and IL-17A. pAkk supplementation alters fecal microbiota and metabolic pathways in IMQ-treated mice.

OBJECTIVES:Biologic therapies for skin psoriasis (PsO) have been linked to a lower risk of developing psoriatic arthritis (PsA), but their efficacy across different mechanisms of action remains to be fully explored. This study aimed to compare PsA risk in PsO patients prescribed IL-23 inhibitors (IL23i) vs IL-17 inhibitors (IL17i). METHODS:This retrospective cohort study utilized the TriNetX database to categorize adult PsO patients into two cohorts: those newly prescribed IL23i (without IL17i exposure) and those newly prescribed IL17i (without IL23i exposure). Patients with a history of PsA or previous use of anti-TNF-α or anti-IL-12/23 agents were excluded. A total of 5490 patients, matched 1:1 by propensity scores, were analysed for PsA risk using hazard ratios (HR) from Cox regression. RESULTS:The 5-year cumulative incidence of PsA was significantly lower in IL23i users compared with IL17i users (11.68% vs 19.94%; P < 0.001). IL23i treatment was associated with a reduced PsA risk (HR 0.475; 95% CI: 0.382, 0.590). This reduced risk persisted across various subgroups defined by age, sex, race, PsO subtypes, obesity and elevated inflammatory markers. Similar results were observed in individual drug comparisons, with lower risks for guselkumab vs secukinumab (0.480; 0.358, 0.645) and ixekizumab (0.698; 0.509, 0.956), risankizumab vs secukinumab (0.433; 0.306, 0.612) and ixekizumab (0.504; 0.347, 0.732), and tildrakizumab vs secukinumab (0.339, 0.131, 0.875). The comparison of tildrakizumab vs ixekizumab (0.451; 0.171, 1.191) also suggested a lower risk but was not statistically significant. CONCLUSION:PsO patients treated with IL23i had a lower subsequent PsA risk compared with those treated with IL17i.

Pinus morrisonicola Hayata, also known as Taiwan white pine or Taiwan short-leaf pine, is an endemic species to Taiwan. In Asia, particularly Taiwan, China, and Korea, P. morrisonicola needles have been used as a functional beverage for many years. In this study, we investigated the anti-cancer potential of P. morrisonicola leaves and barks against human lung adenocarcinoma (A549) in vitro. Three different extracts, including supercritical CO2 extract, ethanol extract, and steam-distilled essential oils of leaves and barks were obtained. Among them, ethanol extract of P. morrisonicola leaves (PMLE) displayed the strongest cytotoxicity on A549 cells. Next, we found that PMLE treatment arrested lung adenocarcinoma cells induced a pronounced G1/S cell-cycle arrest without triggering apoptosis. Treatment with PMLE resulted in a down regulation of cyclin D1 and phosphorylation of Cdc-2 in A549 cells. In addition, this effect was associated with down regulation of cyclin-dependent kinase 2 (CDK2) and up regulation of CDK inhibitors p21Cip1 and p27Kip1. Moreover, cyclin B1, cyclin D1, and cyclin E expression levels were reduced, which corresponds to a decreased distribution of cells in the S and G2/M phases. Furthermore, PMLE treatment significantly activated p53 in A549 cells, followed by increased nuclear translocation, which may account for the up regulation of p16INK4a, p21Cip1, and p27Kip1 proteins. Taken together, our results indicate that PMLE exerts anti-cancer activity in human lung adenocarcinoma by arresting the cell cycle through activation of the p53-dependent pathway.

Janus kinase inhibitors (JAKis) have emerged as effective treatments for several skin immune-mediated inflammatory diseases (IMIDs). However, safety concerns have been raised due to boxed warnings from rheumatoid arthritis trials, and whether these risks apply to skin IMIDs remains uncertain. This multinational retrospective cohort study used the TriNetX database to compare the real-world safety of JAKis and conventional immunomodulators (cIMs) in patients aged 12 years or older with skin IMIDs (psoriatic disease, atopic dermatitis, or alopecia areata). Patients newly prescribed JAKis (tofacitinib, upadacitinib, deucravacitinib, baricitinib, abrocitinib, or ritlecitinib) were propensity score-matched (1:1) with those prescribed cIMs (methotrexate or cyclosporine) based on demographics, baseline skin IMIDs, and comorbidities, yielding 17,068 matched patients. Over 2 years, the JAKi cohort showed lower incidences of all-cause mortality (0.28% vs. 0.62%; P = 0.015) and major adverse cardiovascular events (MACE; 1.15% vs. 1.95%; P = 0.005) than the cIM cohort, corresponding to reduced risks (mortality: HR, 0.47; 95% CI, 0.25-0.88; MACE: HR, 0.63; 95% CI, 0.46-0.88). Risks of venous thromboembolism (HR, 0.80; 95% CI, 0.43-1.48) and malignancy (HR, 0.85; 95% CI, 0.63-1.16) were not increased. Subgroup analyses, including older adults and those with cardiometabolic risk factors, showed no signal of increased risk, with consistent findings across available agent-level and sensitivity analyses. These results suggest that, over 2 years, JAKis are not associated with increased risks of mortality, MACE, venous thromboembolism, or malignancy compared with conventional systemic agents in patients with skin IMIDs.

BackgroundGeneralized pustular psoriasis (GPP) is a rare, severe inflammatory disease with limited evidence on long-term prognosis and treatment–mortality associations.ObjectiveTo compare mortality and major comorbidities in GPP, psoriasis vulgaris (PV), and non-psoriatic individuals, and treatment–mortality associations in GPP.MethodsAdults with GPP, psoriasis vulgaris (PV) without pustular psoriasis, and non-psoriatic controls were identified. GPP patients were 1:1 propensity score–matched to PV and non-psoriatic controls by age, sex, and race. Among GPP patients, those receiving biologics, conventional anti-psoriatic drugs, or small-molecule inhibitors were separately matched to patients treated with systemic corticosteroids alone. Primary outcome was all-cause mortality; secondary outcomes included major mortality-related comorbidities based on the ten leading causes of death per US CDC. Kaplan–Meier and Cox models estimated cumulative incidence and hazard ratios.ResultsAfter matching, 6,959 GPP–PV and 28,459 GPP–non-psoriatic pairs were analyzed. Over 5 years, GPP patients had higher 5-year mortality than PV (HR, 1.83; 95% CI, 1.28–2.59) and non-psoriatic controls (HR, 2.42; 95% CI, 1.99–2.94). Major comorbidity risks were higher in GPP than in PV, notably ischemic heart disease (HR, 1.34; 95% CI, 1.01–1.78), cerebrovascular disease (HR, 1.62; 95% CI, 1.06–2.47), and neurodegenerative disease (HR, 2.94; 95% CI, 1.47–5.89), and were elevated across all evaluated comorbidities compared with non-psoriatic controls. Mortality risks were particularly pronounced in patients >60 years and males. Among GPP patients, biologic therapy was associated with lower mortality than systemic corticosteroids alone (HR, 0.71; 95% CI, 0.52–0.96), whereas conventional anti-psoriatic drugs and small-molecule inhibitors were not.ConclusionGPP is associated with higher mortality and comorbidity risk than PV and non-psoriatic individuals. Biologic therapy was associated with lower mortality.

Psoriasis and inflammatory bowel disease (IBD) are chronic immune-mediated disorders affecting the skin and gut, respectively, and share underlying mechanisms involving immune dysregulation and microbiota alterations. Imiquimod (IMQ), a compound commonly used to induce psoriasis-like skin inflammation in mice and exacerbate dextran sulfate sodium (DSS)-induced colitis. Accumulated research findings indicate that IMQ-induced reactive oxygen species (ROS) play a crucial role in biological functions and inflammation. In this study, we investigate the role of ROS in the pathogenesis of intestinal colitis and assess its potential as a therapeutic target by exposing mice to IMQ and establishing a novel disease model. Our results demonstrate that IMQ directly induces colitis-like inflammation in the intestines by depleting the mucus layer, reducing mucin 2 production, and increasing intestinal permeability. This induced model exhibits key features of inflammatory bowel disease, including pathological tissue characteristics. IMQ disrupts intestinal tight junctions and weakens barrier function, primarily through the ROS/extracellular signal-regulated kinase pathway. Moreover, antioxidant pretreatment alleviates colitis-like symptoms and restores intestinal barrier integrity. This IMQ-induced colitis model provides new insights into the molecular mechanisms underlying IBD and suggests its utility as a translational platform for assessing the therapeutic potential of redox-modulating interventions.

Psoriasis has been proposed to be associated with non-alcoholic fatty liver disease (NAFLD) through shared inflammatory pathways; however, the NAFLD risk in young psoriasis patients remains unclear. This study aims to investigate the risk of NAFLD in young patients with psoriasis versus non-psoriatic inflammatory skin diseases. We utilized data from the TriNetX global collaborative network, including patients aged 18-30 years with psoriasis or non-psoriatic inflammatory skin diseases. Patients were categorized into the PSO cohort or the NON-PSO skin diseases cohort, with 1:1 propensity score matched. The primary outcome was incident NAFLD with cumulative incidence plotted using Kaplan-Meier estimator and risk assessed via Cox regression. 2,473 patients were included in each cohort. During a 5-year follow-up, the incidence of NAFLD was elevated in the PSO cohort compared to the NON-PSO skin diseases cohort (6.46 vs. 4.11%), and the risk was higher in the PSO cohort (Hazard ratio: 1.607; 95% Confidence interval: 1.252-2.063). The elevated risk persisted across subgroup and sensitivity analyses after adjusting for metabolic factors and washout periods as well as comparing psoriasis with other inflammatory skin diseases. In conclusion, young psoriasis patients were associated with an increased risk of NAFLD compared to non-psoriatic inflammatory skin disease counterparts.

Background/Objectives: Intra-abdominal infections (IAIs) constitute significant clinical challenges that can rapidly progress to life-threatening conditions if not promptly diagnosed and treated. Traditional pathogen identification methodologies, predominantly culture-based, frequently necessitate extended turnaround times (TATs) and exhibit limitations in detecting polymicrobial or anaerobic infections. Methods: We implemented Oxford Nanopore Technology (ONT) sequencing to analyze the microbiota in patients with IAIs at Taichung Veterans General Hospital. The study cohort comprised sixteen patients with IAIs. Following specimen collection, DNA extraction was performed, and then full-length 16S rRNA and ITS region amplification and subsequent ONT sequencing were conducted. Results: Conventional clinical culture-based methodologies detected pathogens in 13 patients. Among the 14 successfully sequenced specimens, ONT sequencing elucidated a diverse spectrum of bacteria and fungi, with read counts ranging from 375 to 19,716. Polymicrobial and anaerobe-enriched communities were predominantly observed in lower gastrointestinal tract infections, specifically colonic or small bowel perforations, whereas upper gastrointestinal perforations, including those of the stomach or duodenum, were frequently dominated by Streptococcus, Granulicatella, or Candida species. The sequencing identified pathogens concordant with culture results, including Escherichia coli, Enterococcus, and Candida albicans. In addition, anaerobic or low-abundance taxa were exclusively identifiable through sequencing methodologies. Conclusions: ONT sequencing facilitated results within up to 24 h and successfully detected pathogens in culture-negative cases. These findings underscore the utility of ONT sequencing as an expeditious and comprehensive diagnostic modality for IAIs.

Importance Patients with atopic dermatitis (AD) have been reported to develop psoriasis during dupilumab treatment. Whether this represents a true association or an incidental event remains unclear. Objective To compare psoriasis risk in patients with AD who are prescribed dupilumab vs other systemic agents. Design, Setting, and Participants This population-based retrospective cohort study with 3-year follow-up, with analyses completed on October 19, 2024, included 214 430 adult patients with AD from the TriNetX Global Collaborative Network. Individuals newly prescribed dupilumab (dupilumab cohort) and those newly prescribed the other systemic agents without dupilumab exposure (control cohort) were included. Propensity score matching at a 1:1 ratio based on age, sex, race, comorbidities, laboratory measurements, and prior medications was conducted. Exposures Dupilumab vs the other systemic agents (corticosteroids, methotrexate, cyclosporine, azathioprine, or mycophenolate mofetil). Main Outcomes and Measures The primary outcome was incident psoriasis. Cumulative incidence was assessed using Kaplan-Meier plots and risks via Cox regression. Results After matching, each cohort comprised 9860 patients, with 10 891 female individuals (55.2%), a mean (SD) age of 44.8 (20.3) years, 3582 African American or Black individuals (18.2%), 2004 Asian individuals (10.2%), and 9901 White individuals (50.2%). The 3-year cumulative psoriasis incidence was higher in the dupilumab cohort than the control cohort (2.86% vs 1.79%; P < .001). The number needed to harm for psoriasis was 94 for dupilumab vs the other systemic agents. The dupilumab cohort showed an increased risk for psoriasis (hazard ratio [HR], 1.58; 95% CI, 1.25-1.99), although the risk for psoriatic arthritis was not significant (HR, 1.97; 95% CI, 0.75-5.18). This increased risk was also observed in various AD subgroups, including those without atopic comorbidities (HR, 1.42; 95% CI, 1.06-1.89) or with pretreatment immunoglobulin E levels less than 0.048 mg/dL (to convert to mg/L, multiply by 10; HR, 1.59; 95% CI, 1.26-2.01). The association between dupilumab and psoriasis was further supported by validation in patients with asthma without AD (HR, 2.13; 95% CI, 1.38-3.31). Conclusions and Relevance The results of this cohort study suggest that patients with AD who were prescribed dupilumab exhibited a higher relative risk of developing psoriasis compared with those receiving other systemic agents. Given an estimated number needed to harm of 94, the absolute risk may have limited clinical relevance and should be weighed against dupilumab’s established efficacy in treating AD.

Background: Pancreatic adenocarcinoma remains a highly lethal malignancy with limited treatment options and poor survival rates. Genetic predisposition, particularly single-nucleotide polymorphisms (SNPs), may play a crucial role in disease susceptibility. This study aimed to investigate the association between specific SNPs and pancreatic adenocarcinoma risk in a Taiwanese population. Materials and Methods: This hospital-based retrospective study analyzed genomic data from 52 individuals diagnosed with pancreatic adenocarcinoma at Taichung Veterans General Hospital. A control group was established using propensity score matching to ensure comparability. We assessed the relationship between SNP carriage and pancreatic cancer risk and survival outcomes. Results: Among the 9 SNPs analyzed, rs10094872 and rs13303010 were significantly associated with pancreatic adenocarcinoma. Carriers of rs10094872 had a 3.79-fold increased risk (P < 0.0001), whereas rs13303010 carriers exhibited a 2.68-fold elevated risk (P = 0.0032). Individuals possessing both SNPs demonstrated an 11.458-fold increased risk (P < 0.0001). Furthermore, rs13303010 carriers exhibited higher mortality within the first 2 years post-diagnosis, whereas rs10094872 carriers showed increased mortality from the third year onward. Conclusions: This study highlights rs10094872 and rs13303010 as potential genetic markers for pancreatic adenocarcinoma risk in Taiwanese individuals. The distinct survival patterns among carriers suggest potential prognostic implications. These findings underscore the importance of genetic screening in early detection and personalized treatment strategies for pancreatic cancer.

Background: The gut-skin-brain axis has been long postulated in acne vulgaris. Few studies focused on bowel habits in patients with acne vulgaris have yielded controversial results. Objectives: To examine the relationship between acne vulgaris and gastrointestinal comorbidities. Methods: We conducted a nationwide case-control study using data from the Taiwan National Health Insurance Research Database spanning the years 1997 to 2013. Acne vulgaris and the control group were stratified by age, and we examined the association of gastrointestinal comorbidities across different age, sex, and antibiotic use through conditional logistic regression analysis. Results: A total of 185,491 patients with acne vulgaris were identified. The primary demographic for acne vulgaris comprised adolescents, followed by adult-onset groups, with a female predominance observed across all age subgroups. Patients with acne vulgaris exhibited a significantly elevated risk of developing gastrointestinal comorbidities, including peptic ulcers, irritable bowel syndrome, gastroenteritis, gastroesophageal reflux disease, and constipation. This increased risk was particularly notable in patients aged $ 12 years, and those with moderate-to-severe acne. Limitations: Miscoding and misclassification might have occurred. Conclusions: Patients with Acne vulgaris have higher risks of gastrointestinal comorbidities. For patients with moderate-to-severe acne, gastroenterology specialty consultation may be warranted. (JAAD Int 2025;18:62-8.)

Lung adenocarcinomas (LUAD) are a pressing global health problem with enduring lethality and rapidly shifting epidemiology. Proteogenomic studies integrating proteomics and post-translational modifications with genomics can identify clinical strata and oncogenic mechanisms, but have been underpowered to examine effects of ethnicity, smoking and environmental exposures, or sex on this heterogeneous disease. This comprehensive proteogenomic analysis of LUAD tumors and matched normal adjacent tissues from 406 patients across diverse geographic and demographic backgrounds explores the impact of understudied driver mutations, prognostic role of chromosomal instability, patterns of immune signaling, differential and sex-specific effects of endogenous mutagens and environmental carcinogens, and pathobiology of early-stage tumors with "late-like" characteristics. Candidate protein biomarkers are proposed for unstable tumors with highly fragmented genomes and for carcinogen exposures, and a LUAD subtype-specific atlas of therapeutic vulnerabilities is presented. These observations and the associated data resource advance the objective of precision management strategies for this devastating disease.

Inflammatory skin diseases often display overlapping visual features, making accurate diagnosis challenging. This study proposes a deep learning framework combining transfer learning, feature fusion, and adaptive ensemble strategies to improve dermatological image classification. Using MobileNetV3-Large as the backbone, expert-defined anatomical metadata and model-derived probabilities were fused to enrich diagnostic features. A fuzzy rank-based ensemble aggregated predictions across multiple regions of interest (ROIs), prioritizing classifier confidence dynamically. The approach achieved consistent performance across ROI settings, with F1-scores reaching 0.8. These findings demonstrate that integrating anatomical context with deep learning enhances the interpretability and diagnostic utility of automated dermatological systems.

The long-term effectiveness of paclitaxel is limited by chemoresistance. In this study, we elucidate the molecular mechanism by which kinesin family member 2C (KIF2C), a well-known microtubule depolymerase, contributes to the development of chemoresistance in triple-negative breast cancer (TNBC). We observed elevated levels of KIF2C, tubulin tyrosination, and polyglutamylation in human and mouse breast cancer cells resistant to paclitaxel. Additionally, these chemoresistant cells possessed cross-resistance to diverse microtubule-targeting agents (MTAs). We demonstrated that KIF2C preferentially depolymerizes polyglutamylated tubulin, even in the presence of paclitaxel. To counter this, we developed 7S9, a chemical inhibitor of KIF2C, that prohibits the dissociation of KIF2C from microtubules. The combination of 7S9 and paclitaxel significantly reduced tumorigenesis in chemoresistant TNBC model in mice. Moreover, 7S9 diminished cancer cell chemoresistance to several clinically available MTAs. Our findings elucidate the molecular mechanism of KIF2C-mediated chemoresistance and highlight KIF2C as a promising target for combating cross-resistance in TNBC.

Background/Objectives: Gastrectomy is among the most effective treatments for gastric adenocarcinoma. Margin status can be categorized into three types: proximal, distal, and radial margins. While the relationship between proximal and distal margin involvement in specimens and prognosis has been extensively studied, the impact of a radial margin has not been thoroughly investigated. This study was conducted to determine whether a positive radial margin could affect the prognosis of patients with gastric adenocarcinoma undergoing gastrectomy. Methods: This is a retrospective cohort study of patients with stage II/III gastric adenocarcinoma who received gastrectomy from January 2009 to December 2019 at Taichung Veterans General Hospital, Taiwan. The clinicopathologic features and outcomes were compared between groups. Results: Among the 431 patients who underwent gastrectomy, 94 patients (21.8%) had a positive margin. Radial margin positivity accounted for 16.2%. Factors associated with a positive margin included perineural invasion and advanced cancer stage. The factors related to poor overall survival (OS) and disease-free survival (DFS) included advanced Borrmann type, positive nodal disease, higher nodal burden (≥5), and margin status. In the subgroup analysis, radial margin positivity could negatively impact OS and DFS in the advanced T stage subgroup and nodal-positive subgroup. Conclusions: Aggressive tumor biology may result in a positive margin following gastrectomy. A positive radial margin was correlated with poorer OS and DFS. Future investigations should focus on developing tailored treatment plans for patients with a positive radial margin.

BACKGROUND:Growing evidence has shown that cholesterol metabolism abnormalities involve carcinogenesis. Proprotein convertase subtilisin/kexin type-9 (PCSK9) inhibitors have been reported to inhibit tumour progression and prevent ultraviolet-related skin damage. OBJECTIVES:To investigate the association of PCSK9 inhibitors with the risk of nonmelanoma skin cancer (NMSC). METHODS:This retrospective cohort study analysed data from the US Collaborative Network in the TriNetX database. Adults aged ≥ 40 years with atherosclerotic cardiovascular disease (ASCVD) under statin therapy between 2016 and 2022 were identified. A target trial design was used to compare the risk of NMSC, including basal cell carcinoma (BCC) and cutaneous squamous cell carcinoma (cSCC), in patients also treated with PCSK9 inhibitors or continuing statin treatment (the control group). Each head-to-head comparison involved propensity score matching. Hazard ratios (HRs) were estimated using Cox proportional hazard models. Stratified analyses based on age, sex, Fitzpatrick skin type and immune status were also performed. RESULTS:A total of 73 636 patients with ASCVD were analysed. Compared with the control group, patients with ASCVD initiating PCSK9 inhibitors had lower risks of developing NMSC [HR 0.78, 95% confidence interval (CI) 0.71-0.87], BCC (HR 0.78, 95% CI 0.69-0.89) and cSCC (HR 0.79, 95% CI 0.67-0.93). Subanalyses revealed a reduced risk of NMSC with each PCSK9 inhibitor, namely evolocumab and alirocumab. Stratified analyses showed similar results in patients aged 65-79 years, those older than 80 years and in men. CONCLUSIONS:Our study indicated that patients with ASCVD taking PCSK9 inhibitors have a lower risk of incident NMSC than those not taking PCSK9 inhibitors.

BACKGROUND:Psoriasis is associated with various cardiovascular diseases (CVDs). The aim of this study was to compare the risk of CVD in patients with psoriasis who were prescribed biologics or oral therapies, and to assess the association between different classes of biologics and CVD risk. METHODS AND FINDINGS:This retrospective cohort study utilized the TriNetX Global Collaborative Network (2014-2025). Patients with psoriasis newly prescribed biologics (BIO-cohort) and those newly initiating oral anti-psoriatic drugs without biologic exposure (Non-BIO-cohort) were enrolled. A propensity score-matched analysis was conducted, accounting for age, sex, race, comorbidities, body mass index, serum lipid profile, and inflammatory marker levels. Cardiovascular risk was compared between the BIO- and Non-BIO-cohorts using Cox regression to calculate hazard ratios (HRs) with 95% confidence intervals (CIs). After matching, each cohort comprised 12,732 patients, with approximately 50% being female, a mean age of 57 years, and 55% identifying as White. The 5-year cumulative incidence of any CVDs was significantly lower in the BIO-cohort (10.68%; 95% CI [10.03%, 11.36%]) than in the Non-BIO-cohort (16.17%; 95% CI: [15.34%, 17.05%]) (p < 0.001). The BIO-cohort had attenuated risks of any CVDs (HR 0.621; 95% CI [0.571, 0.676]), cerebrovascular diseases (HR 0.616; 95% CI [0.519, 0.731]), arrhythmias (HR 0.632; 95% CI [0.565, 0.706]), inflammatory heart diseases (HR 0.566; 95% CI [0.360, 0.891]), ischemic heart diseases (HR 0.579; 95% CI [0.465, 0.721]), heart failure (HR 0.637; 95% CI [0.521, 0.780]), non-ischemic cardiomyopathy (HR 0.654; 95% CI [0.466, 0.918]), thrombotic disorders (HR 0.570; 95% CI [0.444, 0.733]), peripheral arterial occlusive diseases (HR 0.501; 95% CI [0.383, 0.656]), and major adverse cardiac events (HR 0.697; 95% CI [0.614, 0.792]). Receiving only anti-tumor necrosis factor (TNF)-α (HR 0.886; 95% CI [0.807, 0.973]), anti-interleukin (IL)-17 (HR 0.724; 95% CI [0.599, 0.875]), or anti-IL-23 (HR 0.739; 95% CI [0.598, 0.914]) was associated with reduced risks of any CVDs, whereas no significant association was observed for only anti-IL-12/23 (HR 0.915; 95% CI [0.742, 1.128]). This risk reduction remained consistent across various subgroups, including age (≤45 or >45 years), sex (male or female), regions of research data (the United States, Europe, Middle East and Africa, and Asia-Pacific), and comorbidities (psoriatic arthritis, hypertension, diabetes, hyperlipidemia, overweight or obesity). Eight sensitivity analyses, such as extending the washout period or tightening medication definitions, validated our findings. The main limitation of our study is the observational design, which can only establish associations, not causation. CONCLUSIONS:Patients with psoriasis prescribed biologics exhibited a lower risk of CVDs versus those on oral therapy. Anti-TNF-α, anti-IL-17, and anti-IL-23 were associated with decreased cardiovascular hazards, while anti-IL-12/23 was not.