European Journal of Dermatology最新文献

Immune dysregulation is implicated in fibrotic skin pathogenesis. However, causal inflammatory cytokines remain inadequately characterized. To identify inflammatory cytokines with potential causal roles in fibrotic skin disorders using integrative genetic and experimental approaches. Two-sample Mendelian randomization (MR) analysis was conducted utilizing summary statistics from genome-wide association studies (GWAS) for 41 inflammatory cytokines and four fibrotic skin diseases. Differences in selected inflammatory cytokine levels in tissues, sera and cells between hypertrophic scar (HS) patients and healthy volunteers were investigated. In addition, primary human HS fibroblasts were stimulated using recombinant proteins of selected inflammatory cytokines. The effects of recombinant proteins on proliferation, apoptosis, migration and collagen deposition of fibroblasts were examined by EdU (5-ethynyl-2'-deoxyuridine), annexin V-FITC/PI double staining, Transwell migration and western blot assay, respectively. The levels of stem cell growth factor beta (SCGF-β) were significantly associated with all four fibrotic skin diseases, with OR=1.24 (p=0.016) for HS, OR=0.77 (p=0.048) for keloid, OR=1.20 (p=0.022) for lichen sclerosus, and OR=1.40 (p=0.021) for systemic sclerosis. Moreover, SCGF-β levels in HS tissues and sera were elevated. Fibroblasts cultured with recombinant proteins of SCGF-β showed enhanced proliferation and collagen production, reduced apoptosis (p<0.05), and no significant effect on migration (p>0.05). This study establishes SCGF-β as a putative causal mediator of fibrotic skin diseases, with experimental validation for HS, demonstrating its pro-fibrotic activity.

Dermatophytomas are hyperkeratotic fungal masses located in subungual areas or on hairless skin, characterized by dense whitish or yellowish areas forming longitudinal streaks or patches, while in hairless skin an exacerbation of the erythematousquamous area is observed. "Dermatophytoma" has been applied to fungal masses caused by dermatophytes, yeasts, and other moulds. In this study, we differentiate between fungal masses caused by dermatophytes (referred to as dermatophytomas) and those caused by non-dermatophyte fungi, which we term "fungal conglomerates". To analyse clinical and mycological data from patients diagnosed with dermatophytomas or fungal conglomerates. Conducted at the Mycology Section of a tertiary hospital, this study included patients diagnosed with dermatophytomas and fungal conglomerates based on clinical history. In total, 606 cases were analysed, with Trichophyton rubrum (35.97%) as the principal agent. Females comprised 64.7%, toenails and fingernails were affected in 86.1%, and total dystrophic onychomycosis was the predominant form, identified in 61.4%. Hypertension (14.3%), type 2 diabetes, dyslipidaemia, and metabolic syndrome (11.39%) were the principal comorbidities. The multiple ordinal regression model for type of fungal pathology (dermatophytomas and fungal conglomerates) adjusted for age revealed that the groups ≤18 and 19-65 years had a higher risk (OR=3.616 and OR=2.143) of dermatophytomas than those ≥66 years. Hypertension was associated with a higher proportion of dermatophytomas compared to fungal conglomerates (OR=5.470). This study underscores the clinical relevance of dermatophytomas and fungal conglomerates, predominantly affecting toenails. T. rubrum and total dystrophic onychomycosis were frequently observed. The high prevalence of associated comorbidities (hypertension and diabetes mellitus) highlights the need for comprehensive management strategies to prevent recurrence.