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[This corrects the article DOI: 10.1016/j.jdin.2026.02.011.].
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[This corrects the article DOI: 10.1016/j.jdin.2025.12.009.].
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Some patients are referred unnecessarily from urgent care (UC) to dermatology, while others who need additional care are not referred or do not complete the referral, highlighting the need for improved triage of skin concerns at UC centers. To identify factors that predict UC referral to dermatology and to better understand UC perspectives on improving urgent access for skin concerns. This study includes a retrospective nominal logistic regression cohort analysis of 6988 skin-related UC encounters to identify predictors of referral to dermatology and a survey of UC perspectives on managing dermatologic conditions and improving dermatology access. Non-White patients and those evaluated at UC sites closer to dermatology had higher odds of referral. Uninsured patients and those requiring procedures or ongoing follow-up were also more likely to be referred. Dermatology education for UC providers, teledermatology, and urgent-access clinics were favored to improve dermatologic care access. Limitations include single-system design, unmeasured provider factors, limited disease severity assessment, and potential survey response bias. Several patient-related factors and UC proximity to dermatology influence UC referral to dermatology. Dermatology training for nondermatologists, teledermatology services to support UC, and dermatology-specific urgent-access clinics may improve patient triage and reduce unnecessary referrals.
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The IL-23/Th17 axis is the cornerstone of psoriasis pathogenesis, but molecular heterogeneity across different ethnicities remains poorly defined. To comprehensively define the immunological and pathogenic transcriptomic profiles of a Taiwanese psoriasis cohort. Lesional skin (LS) and non-lesional skin (NL) biopsies from 11 patients with chronic plaque psoriasis and normal skin (N) from 9 healthy controls were analyzed via bulk RNA-sequencing. Differential gene expression (DEG), pathway enrichment (GSEA), and clinical correlations (PASI score) were performed. Serum levels of cytokines were validated via ELISA from all 50 psoriasis patients and 9 healthy controls. Analysis identified 4,694 DEGs in LS vs. N. We confirmed robust Th17 upregulation (IL-17A/C, IL-23A). Unanticipatedly, a profound dual immune dysregulation was identified, involving significant upregulation of Type 2 (Th2) signatures (IL-4R, CCL17, TSLP). The IL-36 family was the most highly activated cytokine axis (IL-36G log2FCH=5.5). Barrier function genes (KRT77, GJB4) were significantly downregulated. Correlation analysis identified IL-36RN and the combination of AREG/CDSN (r ≈ -0.9, p=0.002) as potential severity biomarkers. The small sample size and focus on a single ethnic group. Transcriptomic findings represent associations rather than mechanistic evidence of pathogenesis. Taiwanese psoriasis is characterized by a dual Th17/Type 2 endotype and extreme IL-36 activation. This molecular landscape underscores the need for stratified therapeutic strategies in Taiwanese populations.
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