Clinical, Cosmetic and Investigational Dermatology最新文献

Purpose: Psoriasis is a chronic, immune-mediated skin disease that significantly affects patients' quality of life. Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, has emerged as a promising treatment for moderate to severe psoriasis, offering an alternative to biologics with a favorable safety profile. This study analyzes global research trends, key contributors, and emerging focus areas concerning apremilast in the treatment of psoriasis.

Patients and methods: Publications related to apremilast and psoriasis from 2008 to 2024 were retrieved from the Web of Science Core Collection (WoSCC). Bibliometric and visual analyses were performed using tools such as VOSviewer, CiteSpace, and R 4.3.3.

Results: A total of 437 publications on apremilast and psoriasis were identified. The United States led with 158 publications, followed by Japan with 39 and Italy with 33. Celgene Corporation was the most productive institution, contributing 96 articles. The top journals include Journal of Dermatology, Journal of the European Academy of Dermatology and Venereology, and Journal of the American Academy of Dermatology. Key researchers, such as Shinichi Imafuku and Bruce Strober, were identified as leading contributors. Burst analysis revealed that since 2020, keywords like "monotherapy", "nail psoriasis", and "pathogenesis" have gained prominence, indicating emerging research areas.

Conclusion: This bibliometric analysis demonstrates that research on Apremilast for psoriasis has evolved from clinical trials focused on efficacy and safety to broader applications in real-world settings, including nail psoriasis and pathogenesis. Future research is likely to concentrate on long-term outcomes, optimizing treatment regimens, and addressing unmet needs in psoriasis management, particularly among specific patient subgroups.

Introduction and purpose: Marine collagens are environmentally friendly and biologically compatible collagens derived from aquatic organisms, including invertebrates like sponges and jellyfish. Starting from marine collagens as raw materials, sophisticated purification procedures lead to low-molecular-weight, bioactive fragments that are valuable functional ingredients for nutritional supplements, cosmeceuticals, and medical devices in regenerative medicine. From the mid-2010s to the late 2010s, several high-quality studies highlighted the skin bioregenerative properties of marine collagen-derived oligopeptides. The purpose of this review is to discuss these properties and their rationale.

Methods: This review only analyzes studies focused on skin regeneration published in indexed journals with significant impact factors (the rule was rigid for human studies), supplemented by a few contributions from Google Scholar for methodologically sound in vitro and animal studies.

Results: Activation of skin fibroblasts with high systemic bioavailability after oral intake supports the bioregenerative properties of hydrolyzed marine collagen. Marine collagen hydrolysates do not cause irritation or inflammation and have a negligible impact on pro-inflammatory mediators in animal studies. Preclinical research indicates that 50 µg/mL of hydrolyzed marine collagen peptides accelerates cell migration almost as effectively as 10 µg/mL of recombinant human epidermal growth factor, although the predictive value of in vitro studies for humans remains uncertain. Accelerated wound healing with collagen neosynthesis is associated with increased expression in immunohistochemistry of platelet-endothelial cell adhesion molecule-1, basic fibroblast growth factor, and transforming growth factor ß-1. Furthermore, enzyme-treated hydrolysates produced under acidic conditions exhibit antioxidant effects without affecting pro-inflammatory cytokines, while enzyme-treated hydrolysates under alkaline conditions have the opposite effect.

Conclusion: An increasing number of preclinical and human studies highlight the skin and overall bioregenerative properties of hydrolyzed marine collagens. Their high systemic intestinal absorption after oral intake distinguishes them from hydrolysates from other sources. Long-term safety should be a primary concern of future research.

Objective: Observational studies have consistently highlighted a robust clinical association between celiac disease (CD) and dermatitis herpetiformis (DH). Building on this foundation, the present study aims to investigate whether this observed relationship is underpinned by a causal genetic mechanism, providing insights into the potential hereditary basis of their connection.

Methods: This study employed bidirectional two-sample Mendelian randomization (MR) analysis to investigate the potential genetic causality between CD and DH, utilizing genome-wide association study (GWAS) summary data. To comprehensively examine the genetic relationship between CD and DH, we applied multiple MR methodologies. Furthermore, to enhance the robustness and credibility of our results, we conducted extensive sensitivity analyses.

Results: The fixed-effects inverse variance weighted (IVW) analysis revealed a significant positive genetic causal relationship between CD and DH (P = 0.001, odds ratio [OR] 95% confidence interval [CI]: 1.546 [1.195-1.999]). In contrast, no significant genetic causality was found in the reverse direction, from DH to CD (P = 0.113, OR 95% CI: 1.039 [0.991-1.090]). Notably, the MR analysis revealed no evidence of heterogeneity, further reinforcing the reliability of the fixed-effects IVW model. Additionally, sensitivity analyses confirmed the stability and robustness of the results, further validating the integrity of the conclusions drawn from the MR analysis.

Conclusion: The results of our study indicate that CD acts as a genetic susceptibility factor for the development of DH. Furthermore, the occurrence of DH in individuals with a history of CD appears to be attributed to a causal genetic relationship, suggesting that the genetic predisposition linked to CD may drive the manifestation of DH.

Background and objectives: Acne vulgaris is a common inflammatory skin disease with a strong hormonal component, especially in women. Hormonal therapies are increasingly used in moderate-to-severe or treatment-resistant cases. This review aims to summarize current evidence on the efficacy and safety of hormonal treatments for acne.

Materials and methods: A narrative review was conducted using PubMed, Scopus, and Web of Science, including studies published from 2010 to 2025. Eligible articles included randomized controlled trials, cohort studies, systematic reviews, and meta-analyses evaluating hormonal therapies such as combined oral contraceptives (COCs), spironolactone, cyproterone acetate, and topical antiandrogens (eg, clascoterone). Data were extracted on mechanisms of action, clinical efficacy, safety, and treatment indications to ensure consistent synthesis across therapies.

Results: Spironolactone consistently reduced lesion counts and improved quality of life in adult women, with good tolerability and a low risk of hyperkalemia. COCs effectively decreased both inflammatory and non-inflammatory lesions, with similar efficacy across different progestins. Clascoterone, a topical antiandrogen, showed significant improvement in lesion counts with minimal systemic absorption. Preliminary evidence also supports the use of topical spironolactone. Compared with antibiotics, hormonal therapies provide durable disease control and avoid antimicrobial resistance.

Conclusion: Hormonal therapies are effective and well-tolerated options for acne, particularly in women with hormonal patterns or refractory disease. By specifically targeting androgen-driven pathways, hormonal agents offer sustained improvement and should be incorporated into personalized acne management.

Perianal herpes simplex virus (HSV) infection represents a rarely reported clinical variant that is frequently misdiagnosed. We present a case of perianal HSV in a patient with a history of renal transplantation and type 2 diabetes mellitus. Following a previous diagnosis of perianal eczema, the patient's cutaneous lesions slowly worsened despite treatment with topical corticosteroids. Notably, the presence of well-demarcated superficial erosions, combined with immunosuppressive conditions including diabetes mellitus and renal transplantation, prompted targeted HSV screening which confirmed the diagnosis. This case underscores the importance of considering HSV testing in patients presenting with atypical perianal eruptions.

Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) production and antioxidant defense mechanisms, has a profound effect on skin health. This imbalance contributes to skin damage, premature aging, and the development of various dermatological conditions by modulating key signaling pathways with pro-inflammatory or antioxidant effects, such as NF-κB, JAK/STAT, Nrf2, MAPK/AP1, and SIRT1/FOXO. So, the application of antioxidant compounds, particularly those derived from natural sources, is essential for protecting the skin against ROS-induced damage. Sea cucumber, a marine invertebrate known for its remarkable regenerative capacity, contains bioactive compounds, including phenolics, proteins, and polysaccharides, which exhibit antioxidative and anti-inflammatory properties. These bioactive components may offer protective effects against oxidative stress within the skin. Therefore, this study will first evaluate the potential of sea cucumber-derived bioactive compounds in mitigating oxidative stress by examining their ability to counteract ROS-induced cellular damage caused by ROS and their potential role in promoting skin repair and regeneration. The review will also discuss the underlying mechanisms, including key signaling pathways, and explore the therapeutic potential of sea cucumber-derived exosomes as a novel strategy to treating oxidative stress-related skin disorders. Finally, a comparison is made between the efficacy of the sea cucumber crud extract with its derived exosome in treating oxidative stress-induced skin damage.

Purpose: Ferroptosis, a form of iron-dependent lipid peroxidation cell death. However, the mechanism of ferroptosis in psoriasis remains to be further investigated. Therefore, our research focuses on uncovering the role of ferroptosis in the pathogenesis of psoriasis and providing accurate biomarkers as therapeutic targets.

Patients and methods: We merged differentially expressed genes (DEGs) from the gene expression omnibus (GEO) with ferroptosis-related genes from FerrDb database. Key genes were further identified using weighted gene co-expression network analysis (WGCNA) and machine learning. Additionally, we used non-negative matrix factorization (NMF) clustering to identify two ferroptosis molecular subgroups.

Results: CHAC1, PARP9 and LCN2 are identified as key ferroptosis-related genes in psoriasis. The psoriatic skin samples were divided into cluster 1 and cluster 2, with cluster 1 being the more severe subtype of psoriatic lesions. The expression of CHAC1 had the highest correlation with activated CD4 T cells, neutrophil, regulatory T cell (Tregs) and type 2 T helper cell (Th2), which were significantly enriched in cluster1.

Conclusion: In conclusion, the ferroptosis associated diagnostic gene CHAC1 exacerbates psoriasis by regulating activated CD4 T cells, neutrophil, Tregs and Th2, serving as a reliable biomarker to predict patient survival.

Clonal seborrheic keratosis (SK) represents a rare histological subtype of seborrheic keratosis that is challenging to distinguish from conventional SK and other skin neoplasms based solely on clinical presentation and dermoscopic features. Current clinical observations indicate that vascular-related manifestations in this subtype are exceedingly rare. Our report herein reports the uncommon globular vascular findings identified on dermoscopic examination of clonal SK, which not only holds great significance for the diagnosis and differential diagnosis between clonal SK, ordinary SK and other cutaneous tumors, but also provides strong support for the development of standardized dermoscopic diagnostic criteria and treatment advice for clonal SK.

Objective: Psoriasis (PsO) is a chronic inflammatory dermatosis that affects a significant portion of the global population and is associated with various comorbidities, including psoriatic arthritis (PsA). PsA develops in 20-30% of psoriasis patients and significantly impacts patient quality of life. Currently, early detection of PsA remains challenging, with no reliable, non-invasive biomarker for risk assessment. This study aims to evaluate the utility of pan-immune-inflammation value (PIV), along with other inflammatory indices, in predicting the development of PsA in patients with PsO.

Methods: A retrospective analysis was conducted on 101 psoriasis patients (51 PsO, 50 PsA). Hematological parameters, including neutrophil, lymphocyte, monocyte, and platelet counts, were collected, and various inflammatory indices (PIV, SIRI, SII, NLR) were calculated. The diagnostic performance of these indices was assessed using Receiver Operating Characteristic (ROC) curve analysis. As a retrospective, double-center study with a limited sample size, the findings should be interpreted with caution and validated in larger, prospective cohorts.

Results: The study found significant differences between PsA and PsO patients in terms of inflammatory indices, with higher PIV, SII, SIRI, and NLR levels observed in PsA patients. The diagnostic performance of PIV (AUC 0.63), SII (AUC 0.70), SIRI (AUC 0.64), and NLR (AUC 0.71) indicated that elevated levels of these indices could serve as potential markers for PsA risk. Additionally, PIV was significantly correlated with SII, SIRI, and NLR levels.

Conclusion: PIV and other inflammatory indices, particularly NLR and SII, show promise as biomarkers for predicting the onset of PsA in patients with PsO. These findings may aid in early identification and timely intervention for PsA, improving patient outcomes and informing treatment strategies.

Introduction: Sitosterolemia is a rare autosomal recessive disorder characterized by disrupted lipid metabolism and elevated plasma plant sterol levels. Clinical manifestations often include cutaneous and tendon xanthomas and hypercholesterolemia; delayed diagnosis can lead to cardiovascular disease and hematological abnormalities. This case report describes an 11-month-old female infant with sitosterolemia who presented with xanthomas appearing around 6 months of age. Genetic sequencing identified a homozygous ABCG5 c.1166G>A (p.Arg389His) mutation. This report aims to discuss the clinical features and genetic diagnosis of sitosterolemia caused by ABCG5 mutations, highlighting the challenges and key characteristics for early diagnosis to improve clinical awareness.

Case and methods: Clinical data of a pediatric patient with sitosterolemia caused by a homozygous ABCG5 gene mutation were retrospectively analyzed.

Results: An 11-month-old female infant developed linear xanthomas in the skin folds of her ankles at approximately 6 months of age, which progressively worsened. Blood tests revealed significantly elevated total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels. Sequencing of coding regions for genes associated with familial hypercholesterolemia and sitosterolemia identified a homozygous ABCG5 mutation: c.1166G>A (p.Arg389His). Sanger sequencing confirmed that this variant was inherited from each parent in a heterozygous state. The diagnosis of sitosterolemia was confirmed based on genetic testing (ABCG5/ABCG8), lipid profile results, and clinical presentation.

Conclusion: Sitosterolemia should be suspected in patients presenting with cutaneous xanthomas, prompting thorough investigation including lipid profiling, genetic testing, and plasma plant sterol quantification to avoid misdiagnosis as familial hypercholesterolemia (FH).