Clinical, Cosmetic and Investigational Dermatology最新文献

Targeted biologics have proven to be highly effective treatments for both psoriasis and atopic dermatitis; however, they may occasionally induce the onset of the opposite disease phenomenon known as paradoxical reaction. The underlying mechanisms of these reactions remain largely unclear. This review summarizes all currently reported cases of paradoxical reactions and integrates findings from recent sequencing studies to elucidate the latest progress in this field, raising new concerns for dermatologists regarding the long-term use of biological therapies.

Background: This study aimed to elucidate IL-17 inhibitors' mechanisms in psoriasis, offering a theoretical basis for tackling clinical issues like treatment resistance and relapse.

Methods: Datasets GSE226244 and GSE31652 served as the training set, and GSE201827 served as the testing set. Differential hub genes post-IL-17 inhibitor treatment identified via Limma and WGCNA. DEGs were defined by a |log2 fold-change (FC)| greater than 0.585 and a stringent FDR threshold of less than 0.05. CIBERSORT evaluated immune cell infiltration. Comprehensive analysis of 113 machine learning methods identified optimal predictive model. qPCR validated CLCNKB and GFRA3 expression in psoriasis cell models post-IL-17 inhibitor treatment. Mendelian randomization analysis explored causal links between CLCNKB, GFRA3 and cytokines.

Results: Analysis of gene expression in psoriasis patients treated with IL-17 inhibitors identified 95 differential genes enriched in FoxO signaling, Lysine degradation, and cGMP-PKG pathways. The LASSO-glmBoost (a hybrid machine learning method combining Lasso regularization with gradient boosting) model exhibited superior diagnostic performance (AUC: 0.920 in training, 0.858 in test), highlighting CLCNKB and GFRA3 as key genes in the optimal predictive framework. qPCR confirmed their upregulation in IL-17-inhibitor-treated psoriasis cells, and Mendelian randomization linked both genes causally to cytokine dysregulation.

Conclusion: The study reveals new insights into IL-17 inhibitors' mechanisms in psoriasis, suggesting that upregulation of CLCNKB and GFRA3, along with cytokine dysregulation (eg, IL-13, IL-10, IL-12, TGF-β, TNF-α), may underlie potential resistance and relapse in patients. This work demonstrates a novel approach to clinical outcome prediction with potential utility for specific clinical application, warranting further validation in clinical settings.

Objective: The aim of this study was to compare the clinical efficacy of liquid and hydrocolloid dressings in the management of incontinence-associated dermatitis (IAD) among critically ill patients and to evaluate their effects on skin lesion healing, symptom improvement, and complication prevention.

Methods: A total of 136 critically ill patients diagnosed with IAD and admitted to the hospital between January 2023 and January 2024 were included. Patients were randomly assigned using the random number table method to the hydrocolloid dressing group (n = 68) or the liquid dressing group (n = 68). The hydrocolloid dressing group received DuoDERM^® hydrocolloid dressing, while the liquid dressing group received 3M™ Cavilon™ liquid dressing. Outcomes assessed included the Scoring Atopic Dermatitis (SCORAD), Dermatology Life Quality Index (DLQI), Perineal Assessment Tool (PAT) score, Visual Analogue Scale (VAS), skin lesion healing time, recurrence rate, and complications. Measurements were recorded before and after treatment, and clinical efficacy was evaluated.

Results: Following treatment, SCORAD, DLQI, PAT, and VAS scores decreased significantly in both groups compared with baseline (all p < 0.05). SCORAD, PAT, and VAS scores in the hydrocolloid dressing group were significantly lower than those in the liquid dressing group, while the DLQI scores were higher (all p < 0.05). In addition, the hydrocolloid dressing group demonstrated a shorter skin lesion healing time, lower recurrence rate, and reduced overall complication rate (all p < 0.05). The difference in clinical efficacy between the two groups was statistically significant, favoring the hydrocolloid dressing group (p < 0.05).

Conclusion: For critically ill patients with IAD, hydrocolloid dressings demonstrated superior efficacy compared with liquid dressings. Hydrocolloid dressings promoted faster healing of skin lesions, decreased recurrence and complication rates, and improved overall clinical outcomes.

Background: Ichthyosis follicularis, alopecia, and photophobia (IFAP) syndrome is a rare X-linked genodermatosis with follicular hyperkeratosis, non-scarring alopecia, and ocular abnormalities. Female cases are very uncommon and typically manifest with a milder phenotype, though severe presentations can occur. Orthopedic complications are not commonly described in IFAP.

Case presentation: We present a 10-year-old girl with congenital alopecia and diffuse follicular hyperkeratosis who, despite lacking photophobia, progressed to develop flexion contractures of the knees and equinus deformities of the ankles, resulting in marked restriction of mobility. Ophthalmological examination demonstrated mild astigmatism and decreased visual acuity without corneal disease. Skin biopsy histopathology demonstrated orthokeratotic hyperkeratosis, acanthosis, and follicular plugging, which was in line with IFAP syndrome. The patient underwent posterior soft tissue release of the knees and Achilles tendon lengthening, which led to marked postoperative functional improvement in ambulation.

Conclusion: This case expands the phenotypic range of IFAP syndrome by describing a non-classical female presentation with no photophobia but with extreme musculoskeletal contractures requiring surgery. It emphasizes the need for early identification and multidisciplinary treatment, such as orthopedic intervention, to avert long-term disability and enhance the quality of life.

Hypereosinophilic syndrome (HES) is a rare disorder characterized by persistent eosinophilia and end-organ damage. Cutaneous manifestations are frequently refractory to conventional therapies, including corticosteroids and immunosuppressants, creating a significant clinical challenge. The Janus kinase (JAK)-STAT pathway has been implicated in eosinophil activation and survival, suggesting a potential role for JAK inhibitors in management. In this context, we present the case of a 58-year-old female with a 10-year history of refractory generalized erythema, papules, and severe pruritus progressing to erythroderma with scaling. Previous treatments including antihistamines, tripterygium glycosides, glycyrrhizin, sodium thiosulfate, and topical glucocorticoids had failed. Laboratory investigations revealed leukocytosis with severe hypereosinophilia (peak 8.65×10⁹/L, 52.6% of total WBC), hypoalbuminemia, elevated lactate dehydrogenase, and transaminitis. Skin biopsy demonstrated spongiotic edema and eosinophil-rich perivasculitis. Bone marrow examination confirmed eosinophilic hyperplasia (32.5% eosinophils) without evidence of clonality. Comprehensive parasitic and secondary causes were excluded. Following diagnosis of HES, the patient was initiated on methylprednisolone (40 mg/day) combined with abrocitinib (100 mg/day). Within one week, eosinophil count reduced significantly (1.24×10⁹/L, 7%) with concurrent improvement in liver enzymes. Complete cutaneous remission was achieved at 2-month follow-up, enabling substantial steroid reduction. This case underscores that the combination therapy of abrocitinib and methylprednisolone can offer a promising approach for the HES.

Granular parakeratosis (GP) is a rare dermatosis characterized by intertriginous erythematosquamous lesions and parchment-like desquamation, often linked to benzalkonium chloride exposure. We report a 32-year-old male with well-controlled HIV who developed pruritic plaques in the groin and thighs, progressing to pustules and erosions. Diagnosis was confirmed histologically as GP with concurrent Candida albicans infection. The cutaneous lesions resolved completely following an 8-day course of intravenous compound glycyrrhizin (60 mL once daily) combined with cessation of benzalkonium chloride exposure. This article describes the first documented case of HIV-associated GP and details its distinctive clinical features and therapeutic approach.

Hidradenitis suppurativa (HS) is a chronic, debilitating inflammatory disorder of the hair follicles affecting areas rich in apocrine glands. Moderate-to-severe forms often require biologic therapies, including bimekizumab, a humanized monoclonal antibody that selectively inhibits IL-17A and IL-17F. Secukinumab, a fully human monoclonal antibody targeting IL-17A, and adalimumab, an anti-TNFα monoclonal antibody and the first biologic approved for HS, also represent established therapeutic options, reducing inflammatory lesions and pain with variable long-term response among patients. Approved in Europe and the USA in 2024 for HS, bimekizumab has shown promising efficacy in the BE HEARD I and II clinical trials, with significantly higher HiSCR response rates compared to placebo and improvements sustained through 48 weeks; the BE HEARD EXT extension study confirmed durable benefits at two years, with reduced disease severity and improved quality of life. This review included six studies (two trials, three case series, and one case report), highlighting consistent results in real-world settings, though limited by the drug's recent introduction. Observational studies reported significant reductions in IHS4, pain, and DLQI scores, with complete remission in some cases. The most frequent adverse events were mucocutaneous candidiasis, generally mild and manageable. Dual inhibition of IL-17A and IL-17F represents an innovative therapeutic approach for HS, with potentially greater efficacy than selective inhibitors. However, further large-scale, long-term real-world data are needed to confirm the drug's safety and effectiveness and to define the optimal role of bimekizumab in HS management.

Purpose: There are few reports on the comprehensive surgical management of extensive nevus comedonicus, and the genetic mechanism of this rare disease is not yet fully understood.

Patients and methods: We report a case of a 38-year-old woman with extensive nevus comedonicus, refractory to multiple medical treatments. She underwent comb flap reconstruction combined with super tension-relieving sutures and vacuum sealing drainage. In addition, whole-exome sequencing was performed on the lesional tissue samples.

Results: Nevus comedonicus was confirmed by physical and histopathological examination. Postoperative recovery was uneventful, and the patient was satisfied with the efficacy. Furthermore, no rare or deleterious mutations were detected in NEK9, FGFR2, ABCA12, or KRT10.

Conclusion: Comprehensive surgical intervention is a viable therapeutic option for extensive nevus comedonicus refractory to medical management. Further investigation into the underlying genetic mechanisms of this disease is warranted.

Vitiligo is a complex, multifactorial disorder characterized by acquired skin pigment loss that strongly influences the physical and mental well-being of patients with vitiligo. The precise pathogenesis remains incompletely elucidated, but recent studies emphasize the significant roles of both innate and adaptive immunity. Pattern recognition receptors (PRRs), essential for innate immune sensing, significantly contribute to melanocyte destruction in vitiligo. In vitiligo patients, melanocytes and keratinocytes secrete substances like heat shock protein 70 (HSP70), high-mobility group box 1 protein (HMGB1), calreticulin (CRT), and S100 calcium-binding protein B (S100B) due to various internal and external influences. PRRs are capable of recognizing these "danger signals". This recognition activates the immune response by stimulating innate immune cells, like plasmacytoid dendritic cells (pDCs) and natural killer cells (NK cells). The activation of innate immune cells leads to the release of cytokines and the presentation of melanocyte antigens to T cells, triggering the adaptive immune response. Activated CD8⁺ T cells release cytotoxic substances such as perforin and granzyme, which directly target and kill melanocytes. Cytokines like IFN-γ can concurrently stimulate keratinocytes to produce chemokines such as CXCL9 and CXCL10, which further recruit additional T cells, establishing an inflammatory amplification loop. This loop leads to continuous damage of melanocytes and ultimately results in the development of vitiligo. PRR inhibitors target the initial phase of the immune response cascade in vitiligo, offering a more fundamental and precise therapeutic approach with potential advantages in controlling disease activity and preventing recurrence. This review provides an overview of current research regarding PRRs and their ligands in vitiligo pathogenesis, with a focus on potential therapeutic strategies.

This study provide a comprehensive analysis of using oral isotretinoin as a promising therapy for severe to moderate seborrheic dermatitis, which is a chronic inflammatory skin condition that results in scaling as well as erythema that affects specific sites of the skin such as the scalp, face, upper trunk, or flexures. However, the exact cause of this condition is unclear.Various internal and external factors are associated with its pathogenesis. It is believed that the main factor is the overgrowth of Malassezia yeast, which is a part of the normal skin flora,proliferates in the sebum-rich areas.Other causes include host related factors like genetic predisposition, altered inflammatory responses as well as immune dysregulation, caused by conditions such as HIV or malignancies. In addition, neurophysiological and environmental factors can influence the disease onset. Cold climate, stress, and neurological disorders such as Parkinson's disease all are key factors influencing the onset and relapse of the disease.Pathogenesis involves a complicated interaction between microbial, immunological, and epidermal factors. Malassezia antigens and metabolites in predisposed individuals can trigger both innate and adaptive immunity leading to inflammatory reactions. In addition, Malassezia's lipase activity damages the skin barrier by.producing unsaturated fatty acids, leading to raised epidermal turnover and scaling.