Archives of Dermatological Research最新文献

Kyrle disease (KD) is a rare dermatologic condition characterized by hyperkeratotic papules with central keratotic plugs, often associated with systemic conditions such as diabetes and chronic kidney disease. Due to its clinical overlap with other dermatologic disorders, KD is frequently misdiagnosed. Diagnosis primarily relies on characteristic histopathological findings, with dermoscopy serving as a valuable adjunct for clinical assessment. This systematic review highlights KD’s clinical features, systemic associations, dermoscopy findings, differential diagnosis, and current treatment approaches. While some therapies have shown promise, the lack of standardized management underscores the need for further research. By consolidating the existing literature, this systematic review emphasizes the importance of a multidisciplinary approach in managing KD and calls for future studies to establish standardized diagnostic and therapeutic protocols to improve patient outcomes.

The objective of this study was to evaluate the real-world use of ixekizumab, switching to other biologics, and associated efficacy. This two-year, single-center, retrospective, real-world study collected patient histories and medication records and assessed overall and difficult-to-treat efficacy. Of 258 patients, 31 patients (12%) extended the dosing interval to a mean of 2.6 ± 1.3 months after a mean of 6.6 ± 3.6 months of treatment, with similar efficacy to patients using the labeled dosing interval. In 98 patients who crossed over from secukinumab to ixekizumab, the Psoriasis Area and Severity Index (PASI) 75/90/100 response at 3 months was 78.8%, 61.2% and 41.2%, respectively. The PASI 75/90/100 response at 3 months in patients who switched from ixekizumab to secukinumab (27 patients) was 62.5%, 41.7%, and 33.3%, respectively, while the PASI 75/90/100 response in patients who switched from ixekizumab to adalimumab (12 patients) was 54.5%, 36.4%, and 0%, respectively. Switching from secukinumab to ixekizumab, from ixekizumab to secukinumab, and from ixekizumab to adalimumab in difficult-to-treat areas such as the scalp, genitals, and nails resulted in good responses. Ixekizumab can extend the dosing interval in patients who respond well. Switching biologic therapy between ixekizumab and secukinumab and adalimumab may be considered, as this switching strategy is also used in difficult-to-treat areas.

Angiostatin, a 38–45 KDa proteolytic fragment derived from plasminogen, has garnered significant attention for its dual roles in inhibiting angiogenesis and modulating inflammation. We employed bidirectional Mendelian randomization (MR), meta-analysis, and colocalization to investigate the causal relationship between angiostatin and atopic dermatitis (AD) using three angiostatin and two AD datasets. Additionally, we analyzed global epidemiological trends (1990–2021) and performed transcriptomic profiling of AD. MR analyses revealed a protective effect of angiostatin on AD risk (combined odds ratio: 0.9437, 95% confidence interval [CI]: 0.9198–0.9683, p < 0.0001), while reverse analyses showed no association (standardized mean difference: -0.0029, 95% CI: -0.0516-0.0459, p = 0.9084). Colocalization indicated no shared causal variants (H4 probabilities < 80%). Epidemiological trends highlighted declining age-standardized AD rates despite rising case numbers. Transcriptomic analyses implicated NF-κB, PI3K-Akt, and JAK-STAT pathways in AD pathogenesis. These findings position angiostatin as a dual-action therapeutic candidate, offering novel opportunities to simultaneously target vascular remodeling and immune dysregulation in AD. Translational research is warranted to harness its clinical potential.

Alopecia areata (AA) is an autoimmune disorder characterized by non-scarring hair loss. Despite the growing understanding of its immune-related pathogenesis, biomarkers for early diagnosis and disease severity assessment remain limited. Recent studies have suggested that microRNAs (miRNAs) play a crucial role in regulating immune responses and inflammation in autoimmune diseases. This study aimed to investigate the expression levels of three miRNAs, miR-19b-3p, miR-182-5p, and miR-155-5p, in AA patients and their potential as diagnostic markers and indicators of disease severity. A total of 67 AA patients and 62 healthy controls were included in this case-control study. The severity of AA was evaluated using the Severity of Alopecia Tool (SALT) score, categorizing patients into mild, moderate, and severe groups. Plasma miRNA extraction was performed using the Direct-zol™ RNA MiniPrep kit, and qRT-PCR analysis was conducted to quantify the expression levels of miR-19b-3p, miR-182-5p, and miR-155-5p. Diagnostic accuracy was assessed using Receiver Operating Characteristic (ROC) curve analysis, and correlation analysis was performed to examine the relationship between miRNA expression and disease severity. The results revealed that the expression of miR-19b-3p, miR-182-5p, and miR-155-5p was significantly higher in AA patients compared to healthy controls (p = 0.001 for all three miRNAs). ROC curve analysis demonstrated high diagnostic accuracy, with AUC values of 0.99 for miR-19b-3p, 0.95 for miR-182-5p, and 0.97 for miR-155-5p. These miRNAs showed high sensitivity and specificity, indicating their strong potential as diagnostic biomarkers. Moreover, correlation analysis revealed a significant association between miR-155-5p expression and the severity of AA (p < 0.001), suggesting its potential as a marker of disease progression. This study highlights the significant upregulation of miR-19b-3p, miR-182-5p, and miR-155-5p in AA patients, indicating their potential as minimally invasive diagnostic markers. Furthermore, the correlation between miRNA expression and disease severity provides valuable insights into the molecular mechanisms underlying AA. These findings suggest that miRNAs, particularly miR-155-5p, may serve as promising biomarkers for diagnosing and monitoring the progression of AA, potentially aiding in the development of targeted therapeutic strategies.

Background: Methyl-CpG binding protein 2 (MeCP2) has been reported to participate in the progression of human diseases. In this study, we aimed to explore the functions and related mechanisms of MeCP2 in keloid progression. Methods: Expression of MeCP2 and A Disintegrin and Metalloprotease 12 (ADAM12) was measured by qRT-PCR and western blot assay. Cell proliferation was explored by CCK-8 assay. Cell migration and invasion were investigated by transwell assay. Cell apoptosis was analyzed by flow cytometry analysis. The relation between ADAM12 and MeCP2 was analyzed by CHIP RT-PCR assay and dual-luciferase reporter assay. Results: ADAM12 was highly expressed in keloid tissues and keloid fibroblasts. Silencing of ADAM12 suppressed the proliferation, migration, invasion, ECM accumulation, facilitated the apoptosis and blocked Wnt/β-catenin pathway in keloid fibroblasts. Furthermore, we verified that MeCP2 could modulate ADAM12 expression by binding to its promoter. MeCP2 knockdown inhibited keloid fibroblasts proliferation, migration, invasion and ECM accumulation, with ADAM12 overexpression ameliorated the effects. Besides, MeCP2 silencing inhibited Wnt/β-catenin pathway by altering ADAM12 expression. Conclusion: MeCP2 regulated ADAM12 expression and Wnt/β-catenin pathway to promote cell proliferation, migration, invasion and ECM accumulation in keloid fibroblasts.