Onset Of Atopic Dermatitis Research Articles

Transcriptomic evidence for atopic dermatitis as a systemic disease in NC/Nga mice

BackgroundIn the current study, we evaluated whether atopic dermatitis (AD) affects the entire body rather than being limited to skin barrier damage and inflammation. We hypothesized that medium-term exposure of distant organs to systemic inflammatory cytokines in sub-chronic inflammatory skin diseases has detrimental effects on distant tissues.ResultsOur findings demonstrated the dysregulation of genes and pathways associated with inflammation and the skin barrier, as well as genes and pathways involved in muscle development that respond to chemicals or stress in muscle tissues, all of which were reversed by hydrocortisone (Hc) administration. The expression of Ces1d showed significant differences during disease onset and after treatment in both skin and skeletal muscle, suggesting that Ces1d is likely responsible for the alleviation of subchronic AD.ConclusionsUsing NC/Nga mice with AD-like symptoms, we compared the transcriptomes of the skeletal muscle (a tissue that is relatively distant from the skin) with those of the skin (the lesion induction site) before and after disease induction, after which Hc was administered. Although further study is needed to better understand the effects of Ces1d on AD, skeletal muscle was associated with AD pathogenesis, and AD-like symptoms appeared to affect the body in a systemic manner. Given the importance of evidence-based medicine and the development of precision medicine, our findings provide insights into the mechanisms of AD onset and progression.

Clinical-epidemiological profile, and treatment response in relation to associated atopic comorbidity in atopic dermatitis. Experience from the BIOBADATOP Registry.

Despite advances made in treatments for atopic dermatitis (AD), information on its impact and interaction with atopic comorbidities, such as asthma, rhinoconjunctivitis, and ocular disease is limited. This study aims to assess the clinical-epidemiological characteristics of patients with AD-treatment response included-while taking into consideration atopic comorbidities like these. Data were analyzed from the multicenter BIOBADATOP registry (a prospective cohort of AD patients initiating systemic treatment). We conducted a descriptive analysis of the main characteristics collected in the registry in relation to atopic comorbidity. We included a total of 509 patients, mostly adults (81.9%) with severe AD (73.7%). Patients with personal atopic comorbidity (64%) more frequently exhibited flexural dermatitis (89.7% vs 81.5%), a higher mean of previous systemic treatments (1.6 vs 1.3), and higher baseline values on the POEM scale (19.6 vs 17.9). Patients with familial atopic comorbidity (40.7%) had a higher incidence of pediatric/adolescent patients (24.2% vs 13.9%) and a history of allergic rhinoconjunctivitis (61.1% vs 47.1%). No differences regarding treatment response were observed at the 6- and 12-month follow-ups based on the presence or absence of atopic comorbidities. Results suggest that a history of atopic comorbidity is associated with an early onset and persistent course of AD. Although no differences were reported in the short-term treatment response, further follow-up is required to better understand the impact of comorbidities on AD.

The levels of amino acid metabolites in serum induce the pathogenesis of atopic dermatitis by mediating the inflammatory protein S100A12

Atopic dermatitis (AD) is a chronic inflammatory skin disease affecting tens of millions of people globally. The causal relationship between metabolites and AD pathology has not yet been formally indicated, and the mediating mechanism by which metabolites affect AD has not yet been explored. This study aimed to determine the genetic relationship between metabolites and AD and to determine the pathways through which amino acid metabolites affect AD. Meta-analysis integrates the results of multiple GWAS analyses using METAL software. Using bidirectional two-sample Mendelian randomization (MR), we analyzed the causal relationships between metabolites and AD. The principal MR test of causal effects was conducted using inverse-variance weighted regression, and we used reverse MR analysis to exclude reverse causality. We also performed the MR-PRESSO test to detect and correct for possible pleiotropic effects, and used the Cochran Q test to assess heterogeneity. Two-step MR was utilized to analyze the mediating factors between amino acid metabolites and the onset of AD. The correlation between mediating factors (inflammatory protein S100A12) and immune cell infiltration was analyzed using the edgeR and GSVA software packages. Using single-cell sequencing data from skin tissues of patients with AD, we studied the regulatory role of the S100A12 gene in immune cells. Multiple drug databases and macromolecular docking were used to search for S100A12-targeting drugs. Bidirectional two-sample MR analyses indicated that twenty-two metabolites and one inflammatory protein (S100A12) were significantly associated with AD pathogenesis. S100A12 is a mediator of amino acid metabolites (N6-methyllysine; N2-acetyl,N6,N6-dimethyllysine and N6,N6-dimethyllysine) that are genetically associated with AD. S100A12 was positively correlated with the infiltration of multiple immune cell types in lesional AD skin. The amino acid metabolites N6-methyllysine; N2-acetyl,N6,N6-dimethyllysine and N6,N6-dimethyllysine influence AD pathogenesis by mediating S100A12 expression.

The association between atopic dermatitis and linear growth in children- a systematic review.

To evaluate the association between atopic dermatitis (AD) and linear growth in children, and determine factors associated with compromised linear growth in children with AD. A PRISMA-compliant systematic review was conducted. Databases (PubMed, Embase, Scopus and Cochrane) were searched from inception to June 2024 for articles that reported a quantitative relationship between AD and linear growth in children (< 18years old). Quality of included articles was assessed using the Joanna Briggs Institute Critical Appraisal Tools while quality of evidence in these studies was evaluated using Grading of Recommendations Assessment, Development and Evaluation (GRADE) criteria. Fourteen studies (comprising 50,146 patients with AD) were included. Seven studies reported a strong positive or positive association between AD and reduced height standard deviation score (SDS) in children; the others reported no association. Only 3 studies had moderate quality of evidence, all of which reported an association between AD and poorer height SDS; the remaining 11 studies scored low in quality of evidence. Three studies reported the impact of AD on height to be transient. Secondary analysis showed AD severity, earlier AD onset, sleep disruption and, food restriction, to be risk factors for linear growth impairment in patients with AD. Topical steroid use was not associated with shorter stature in patients with AD. Conclusion: Current evidence on the association between childhood AD and poor linear growth is weak and inconsistent. However, patients with more severe AD, earlier disease onset, poorer sleep quality and higher nutritional restrictions appear more susceptible to linear growth impairment. What is known? • There is inconsistent evidence of the association between atopic dermatitis (AD) and linear growth in children in current literature, with some studies suggesting that AD may negatively impact linear height while other studies do not report similar associations. What is new? • There is no strong association between AD in childhood and poorer linear growth. • There may be a transient slowing of linear growth in children with AD, mimicking constitutional growth delay. • Children with severe AD, earlier disease onset, poorer sleep quality and nutritional restrictions may be at risk of more significant linear growth impairment. • Topical steroid use does not appear to contribute to shorter height in children with AD.

The causal relationship between immune cells and atopic dermatitis: A bidirectional Mendelian randomization study.

Atopic dermatitis (AD) is a chronic inflammatory skin condition whose origins remain unclear. Existing epidemiological evidence suggests that inflammation and immune factors play pivotal roles in the onset and progression of AD. However, previous research on the connection between immune inflammation and AD has yielded inconclusive results. To evaluate the causal relationship between immunological characteristics and AD, this study employed a bidirectional, two-sample Mendelian randomization (MR) approach. We utilized large-scale, publicly available genome-wide association studies to investigate the causal associations between 731 immunological feature cells and the risk of AD. Significant associations were identified between six immune phenotypes and AD risk: increased Basophil %CD33dim HLA DR-CD66b-, CD25 on IgD+ CD24+, CD40 on monocytes, HLA DR on CD14+ CD16-monocytes, HLA DR on CD14+monocytes correlated with higher AD risk, while elevated CD3 on CD4 Treg was linked to lower risk. Reverse MR analysis revealed AD as a risk factor for IgD+ CD38br AC and IgD+ CD38br %B cell, but a protective factor against CD20 on IgD+ CD38- naive and CD8 on NKT. Our findings elucidate the intricate interplay between immune cells and AD, informing future research into AD pathophysiology and therapeutics.

Association between Vitamin D Receptor Polymorphisms, Tight Junction Proteins and Clinical Features of Adult Patients with Atopic Dermatitis.

Few studies have explored the intricate connections between vitamin D receptor (VDR) gene polymorphisms, VDR, tight junction (TJ) protein expression and clinical features of atopic dermatitis (AD). From 43 adult AD patients, VDR polymorphisms were genotyped from peripheral blood samples using polymerase chain reaction-restriction fragment length polymorphism. VDR, occludin, claudin-1 and ZO-1 protein expression from skin lesion biopsies were assessed by immunohistochemistry. The A1012G heterozygous VDR polymorphism exhibited a lower odds ratio (OR) for juvenile AD onset (OR: 0.046, 95% CI 0.004-0.51, p=0.012). In contrast, the presence of ≥2 homozygous VDR polymorphisms were significantly associated with positive skin prick test (SPT) (10/20, 50%) vs. negative SPT (1/23, 4.3%; p=0.0003). The most highly expressed TJ proteins in lesions of AD patients were claudin-1 and zonulin-1 (ZO-1), while VDR and occludin were less prevalent. A significant correlation was observed between ZO-1 expression and a body mass index ≥30 kg/m2 (OR: 12.1, 95% CI 1.06-137.9, p=0.045). Claudin-1 expression was associated with a positive SPT (OR: 8.23, 95% CI 1.04-65.5, p=0.046) and serum 25(OH)D levels were negatively correlated with ZO-1 expression (rho= -0.43, p=0.0058). This study provides novel insights into the relationship between VDR gene polymorphisms, VDR, TJ protein expression, and clinical features in adult AD patients, highlighting a significant role of vitamin D in the pathophysiology of this disease.

Association of breast milk-derived arachidonic acid-induced infant gut dysbiosis with the onset of atopic dermatitis

ObjectiveThe specific breast milk-derived metabolites that mediate host–microbiota interactions and contribute to the onset of atopic dermatitis (AD) remain unknown and require further investigation.DesignWe enrolled 250 mother–infant pairs and collected...

The Roles of Innate Immune Cells in Atopic Dermatitis.

Atopic dermatitis (AD) is a chronic inflammatory skin condition characterized by recurrent eczematous lesions and severe pruritus. The economic burden and time penalty caused by the relapse of AD reduce patients' life quality. AD has complex pathogenesis, including genetic disorders, epidermal barrier dysfunction, abnormal immune responses, microbial dysbiosis of the skin, and environmental factors. Recently, the role of innate immune cells in AD has attracted considerable attention. This review highlighted recent findings on innate immune cells in the onset and progression of AD. Innate immune cells play essential roles in the pathogenesis of AD and enough attention should be given for treating AD from the perspective of innate immunity in clinics.

Clinical Spectrum of Atopic Dermatitis in Pediatric Age Group from a Tertiary Care Center in India: A Cross-sectional Study

Introduction: Atopic dermatitis (AD) is a chronic, inflammatory, relapsing skin disorder with early age of onset in infancy and early childhood. A gradual increase in the prevalence of AD has been observed recently, especially in low-income countries like ours. Objective: We aimed to study the epidemiology and clinical profile of AD among pediatric age group in a tertiary care hospital in North India. Materials and Methods: A hospital-based cross-sectional study was conducted over 1 year in the department of dermatology and sexually transmitted diseases in a tertiary care center in India. All children diagnosed with AD, aged 0–18 years, were recruited, and their clinical and demographic data were recorded. Results: In the 62 children having AD, the mean age was 7.7 ± 6.3 years. Majority of children belonged to the age group of 1–5 years. The mean age of onset of AD was 2.3 ± 2.2 years. A personal history of atopy was present in 53.2% of children, whereas 48.3% of children had a family history of atopy. Acute AD was the most common clinical type that was noted in 43.5%. Hyperlinearity of palms, keratosis pilaris, pityriasis alba, and periorbital darkening were found in 59.6%, 33.8%, 24.1%, and 29% of children, respectively. Conclusion: The prevalence of AD is low in developing countries like India, but it is slowly rising due to rapidly evolving urbanization and environmental changes. Disease manifestation is usually mild to moderate in Indian patients; hence, vigilant eyes and high clinical suspicion are required for accurate diagnosis and efficient management of AD in Indian settings.

Lignin-Based Antioxidant Hydrogel Patch for the Management of Atopic Dermatitis by Mitigating Oxidative Stress in the Skin.

Atopic dermatitis (AD), a chronic skin condition characterized by itching, redness, and inflammation, is closely associated with heightened levels of endogenous reactive oxygen species (ROS) in the skin. ROS can contribute to the onset and progression of AD through oxidative stress, which leads to the release of proinflammatory cytokines, T-cell differentiation, and the exacerbation of skin symptoms. In this study, we aim to develop a therapeutic antioxidant hydrogel patch for the potential treatment of AD using lignin, a biomass waste material. Lignin contains polyphenol groups that enable it to scavenge ROS and exhibit antioxidant properties. The lignin hydrogel patches, possessing optimized mechanical properties through the control of the lignin and cross-linker ratio, demonstrated high ROS-scavenging capabilities. Furthermore, the lignin hydrogel demonstrated excellent biocompatibility with the skin, exhibiting beneficial properties in protecting human keratinocytes under high oxidative conditions. When applied to an AD mouse model, the hydrogel patch effectively reduced epidermal thickness in inflamed regions, decreased mast cell infiltration, and regulated inflammatory cytokine levels. These findings collectively suggest that lignin serves as a therapeutic hydrogel patch for managing AD by modulating oxidative stress through its ROS-scavenging ability.

IL-24 promotes atopic dermatitis-like inflammation through driving MRSA-induced allergic responses.

Atopic dermatitis (AD) is a prevalent inflammatory skin disorder in which patients experience recurrent eczematous lesions and intense itching. The colonization of Staphylococcus aureus (S. aureus) is correlated with the severity of the disease, but its role in AD development remains elusive. Using single-cell RNA sequencing, we uncovered that keratinocytes activate a distinct immune response characterized by induction of Il24 when exposed to methicillin-resistant S. aureus (MRSA). Further experiments using animal models showed that the administration of recombinant IL-24 protein worsened AD-like pathology. Genetic ablation of Il24 or the receptor Il20rb in keratinocytes alleviated allergic inflammation and atopic march. Mechanistically, IL-24 acted through its heterodimeric receptors on keratinocytes and augmented the production of IL-33, which in turn aggravated type 2 immunity and AD-like skin conditions. Overall, these findings establish IL-24 as a critical factor for onset and progression of AD and a compelling therapeutic target.

Atopic Dermatitis Onset in a Melanoma Patient Under Pembrolizumab Therapy: A Case of Successful Treatment with Dupilumab.

Atopic Dermatitis Onset in a Melanoma Patient Under Pembrolizumab Therapy: A Case of Successful Treatment with Dupilumab.

Early Detection of Allergy Symptoms in Children and Adolescents, Characteristics of Possible Pathogens, Pre-Treatment Prevention Measures (in Poland)

Background: The purpose of this study was to investigate the main allergens and signs of the onset of allergic diseases and explore methods of prevention that do not include medicines. Methods: Non-parametric statistical methods were used. A retrospective study was conducted, which included 270 case histories. The average age of the patients was 19 (12.5; 40.1) years, 127 (47%) were men and 143 (53%) were women. Clinical diagnoses, early symptoms, allergen spectrum, and treatment recommendations provided by doctors were analyzed. It was established that the early signs of allergic rhinitis and rhinoconjunctivitis are nasal congestion, runny nose, and lacrimation, and the onset of atopic dermatitis is -characterized by dry and itchy skin. Results: Allergy to triggers from one group was present in 136 (50.4%) patients, irritants from two groups – in 95 (35.2%) patients, and irritants from three groups – in 39 (14.4%) patients. Polish doctors advised patients to limit their exposure to allergens but did not give recommendations for concrete actions. Conclusion: The results of the study can be used to help in the identification of the most common symptoms of allergic diseases and allergens, which is vital for the early diagnosis of this pathology by clinicians.

Associations of demographics, aggravating factors, comorbidities, and treatments with atopic dermatitis severity in China: A national cross-sectional study.

Atopic dermatitis (AD) is a chronic inflammatory skin disorder impacting populations worldwide, although its clinical characteristics and patient demographics remain uncharacterized in China. The aim of this study was to investigate the demographics, comorbidities, aggravating factors, and treatments in AD patients across different age groups in China. This cross-sectional study included Chinese AD patients from 205 hospitals spanning 30 provinces. Patients completed dermatologist-led surveys of general medical history, comorbidities, AD-related aggravating factors, and medications. Two-level mixed-ordered logistic regression was used to evaluate aggravating factors. Overall, 16,838 respondents were included in the final analysis (age 30.9±24.1years). The proportion of severe AD was the highest in patients with AD onset at ≥60 years (26.73%). Allergic rhinitis and hypertension were the most common atopic and metabolism-related non-atopic comorbidities, respectively. AD severity was significantly associated with chronic urticaria, food allergies, and diabetes. Aggravating factors including foods, seasonal changes, and psychological factors were also linked to AD severity. The cross-sectional survey implied that severe AD may be related to the undertreatment of effective systemic or topical interventions. To enhance the management of AD, it is crucial to consider both aggravating factors and the increased utilization of systemic immunotherapy. ClinicalTrials.gov Identifier: NCT05316805, CORNERSTONE.

Oral Administration of Apple Pectin Solution Improves Atopic Dermatitis in a Mouse Model.

The development of atopic dermatitis (AD) involves multiple factors. Three such factors are particularly important in AD onset: immune abnormalities, skin barrier dysfunction, and itching. Many studies report that an imbalance between helper T (Th)1 and Th2 cells causes AD. Apple pectin, a prebiotic, has preventative effects in other allergic diseases (e.g., bronchial asthma and AD), but its potential benefits in AD are unclear. In this study, we investigated the effect of oral apple pectin administration on skin inflammation in an AD mouse model and examined changes in T cells involved in AD. To induce AD, a picryl chloride solution was applied to the shaved back skin of male NC/Nga mice. AD mice then received an oral apple pectin solution (0.4% or 4%) for 35 d. Compared with untreated AD mice, mice in both apple pectin-treated groups showed improvement in AD-induced inflammation and skin symptoms. Histological evaluation showed that apple pectin treatment attenuated epidermal thickening and decreased the number of mast cells and CD4+ cells in AD-induced mice. Apple pectin treatment also reduced serum IgE concentration, as well as expression of the inflammation indicator cyclooxygenase-2 and the Th2-related factors thymic stromal lymphopoietin, interleukin-4, and GATA3. Additionally, increased mRNA expression of the genes that encode interferon-γ and T-bet, which are Th1-related factors, and forkhead box protein P3, were observed in the apple pectin-treated groups. Our findings suggest that apple pectin treatment ameliorates AD by increasing regulatory T cells and improving the Th1/Th2 balance in the skin of AD model mice.

Stratum corneum and microbial biomarkers precede and characterize childhood atopic dermatitis.

Atopic dermatitis (AD) is the most common paediatric inflammatory skin disease. There are currently no robust biomarkers that could reliably predict its manifestation, and on the molecular level, it is less well characterized than adult AD. This study aimed to extend previous findings and provide evidence for distinct changes of the epidermal proteome and microbiome preceding the onset of AD as well as characterizing early AD. We longitudinally analysed epidermal biomarker levels and microbial profiles in a cohort of 50 neonates at high risk for AD, who had participated in a randomized controlled trial on early emollient use for AD prevention. About 26% of the infants developed AD until month 24 with an average age of 10 month at disease onset. In children with later AD, IL-1Ra, TNFβ, IL-8, IL-18, IL-22, CCL2, TARC, TSLP and VEGFa showed increased levels prior to disease manifestation with levels of IL-1Ra, TNFβ and VEGFa already increased shortly after birth. Further, children with later AD displayed a delayed maturation and differentially composed skin microbiome prior to AD onset. At manifestation, levels of multiple Th2, Th17/22 and Th1-associated biomarkers as well as innate immunity markers were elevated, and abundances of commensal Streptococcus species were reduced in favour of Staphylococcus epidermidis. Our results indicate that elevations of proinflammatory stratum corneum biomarkers and alterations of the skin microbiome precede paediatric AD and characterize the disease at onset.

Unraveling Atopic Dermatitis: Insights into Pathophysiology, Therapeutic Advances, and Future Perspectives.

Atopic dermatitis (AD) is an inflammatory skin condition that frequently develops before the onset of allergic rhinitis or asthma. More than 10% of children are affected by this serious skin condition, which is painful for the sufferers. Recent research has connected the environment, genetics, the skin barrier, drugs, psychological factors, and the immune system to the onset and severity of AD. The causes and consequences of AD and its cellular and molecular origins are reviewed in this paper. The exploration of interleukins and their influence on the immunological pathway in AD has been facilitated by using relevant biomarkers in clinical trials. This approach enables the identification of novel therapeutic modalities, fostering the potential for targeted translational research within the realm of personalized medicine. This review focuses on AD's pathophysiology and the ever-changing therapeutic landscape. Beyond the plethora of biologic medications in various stages of approval or development, a range of non-biologic targeted therapies, specifically small molecules, have emerged. These include Janus kinase (JAK) inhibitors like Baricitinib, Upadacitinib, and Abrocitinib, thus expanding the spectrum of therapeutic options. This review also addresses the latest clinical efficacy data and elucidates the scientific rationale behind each targeted treatment for atopic dermatitis.

517 - Lebrikizumab demonstrates significant efficacy versus placebo across racial and ethnic subgroups in patients with moderate-to-severe atopic dermatitis

Abstract Introduction/Background The efficacy of monotherapy lebrikizumab to treat moderate-to-severe atopic dermatitis (AD) has been established in phase 3 studies. Disease characteristics and efficacy outcomes may vary among racial and ethnic subgroups. Objectives To report the week 16 efficacy results of lebrikizumab-treated patients by racial and ethnic subgroups from ADvocate1 (NCT04146363) and ADvocate2 (NCT04178967). Methods Eligible patients were randomized 2:1 to receive lebrikizumab or placebo every 2 weeks. Other AD treatments during this induction period were prohibited. The week 16 efficacy endpoints reported here include Investigator’s Global Assessment 0 or 1 with ≥2-point improvement from baseline (IGA 0/1), ≥75% improvement in the Eczema Area and Severity Index from baseline (EASI 75), ≥90% improvement in EASI from baseline (EASI 90), and ≥4-point Pruritus Numeric Rating Scale (NRS) improvement from baseline. Race and ethnicity were self-reported. Data were collected globally. Data were pooled from ADvocate1 (Intent to Treat [ITT]) and ADvocate2 (modified ITT). Subsequent data from patients who received topical or systemic rescue medication or discontinued treatment due to lack of efficacy were imputed as nonresponders. Subsequent data from patients who discontinued treatment for other reasons were set to missing. Missing data were handled with multiple imputation. Logistic regression tested the interaction between the treatment by subgroup. P&amp;gt;0.1 indicated consistent treatment effect of lebrikizumab versus placebo across subgroups. For each outcome, the Cochran-Mantel-Haenszel method evaluated treatment effect within each subgroup after adjusting for stratification factors. Results Most patients (818/851 [96.1%]) were Asian (192 [22.6%]), Black/African American (84 [9.9%]), or White (542 [63.7%]). Due to the low proportion of patients identifying as another racial category (33/851 [3.9%]) including American Indian or Alaska Native, Native Hawaiian or other Pacific Islander, multiple, other, and not reported, only results of Asian, Black/African American, and White subgroups are reported. In patients with completed ethnicity data (N=839), 10.8% (91/839) identified as Hispanic/Latino and 89.2% (748/839) identified as not Hispanic/Latino. At baseline, Asian patients reported a numerically earlier mean age of AD onset (8.3 years) compared to White (16.5 years) and Black/African American (16.9 years) patients. A numerically greater proportion of Asian patients presented with severe (IGA 4) disease at baseline (49.5%) and prior use of systemic treatment for AD (75.5%) compared with White (35.1% and 51.1%, respectively) and Black/African American (33.3% and 36.9%, respectively) patients. At week 16, no significant treatment differences were observed for the proportion of patients achieving or reporting IGA 0/1, EASI 75, EASI 90, or ≥4-point Pruritus NRS improvement across racial or ethnic subgroups (p&amp;gt;0.1). In Asian patients, a higher proportion treated with lebrikizumab vs placebo (p&amp;lt;0.001) achieved or reported IGA 0/1 (25.1%, 4.1%), EASI 75 (45.5%, 8.5%), EASI 90 (26.5%, 4.3%), and Pruritus NRS ≥4-point improvement (36.4%, 5.7%). In Black/African American patients, a greater proportion treated with lebrikizumab versus placebo achieved or reported IGA 0/1 (33.2%, 13.2%) EASI 75 (51.7%, 18.8%), EASI 90 (26.9%, 13.2%), and ≥4-point Pruritus NRS improvement (41.7%, 17.4%). No statistical comparisons were performed due to limited sample size. In White patients treated with lebrikizumab, statistical significance was observed versus placebo (p&amp;lt;0.001) for IGA 0/1 (43.3%, 14.1%), EASI 75 (59.7%, 20.4%), EASI 90 (38.3%, 10.9%), and Pruritus NRS ≥4-point improvement (45.9%, 14.8%). Significant and similar differences with lebrikizumab-treatment versus placebo were observed among IGA 0/1, EASI 75, and ≥4-point Pruritus NRS improvement in Hispanic/Latino (p&amp;lt;0.05) and non-Hispanic/Latino (p&amp;lt;0.001) patients. The proportion of lebrikizumab-treated patients achieving EASI 90 versus placebo was numerically greater in Hispanic/Latino patients (p=0.057) but only reached statistical significance in non-Hispanic/Latino patients (p&amp;lt;0.001). Conclusions In ADvocate1 and ADvocate2, lebrikizumab was effective across racial and ethnic subgroups for the treatment of moderate-to-severe AD after 16 weeks of monotherapy treatment.

The skin microbiome in pediatric atopic dermatitis and food allergy.

The skin microbiome is an extensive community of bacteria, fungi, mites, viruses and archaea colonizing the skin. Fluctuations in the composition of the skin microbiome have been observed in atopic dermatitis (AD) and food allergy (FA), particularly in early life, established disease, and associated with therapeutics. However, AD is a multifactorial disease characterized by skin barrier aberrations modulated by genetics, immunology, and environmental influences, thus the skin microbiome is not the sole feature of this disease. Future research should focus on mechanistic understanding of how early-life skin microbial shifts may influence AD and FA onset, to guide potential early intervention strategies or as microbial biomarkers to identify high-risk infants who may benefit from possible microbiome-based biotherapeutic strategies. Harnessing skin microbes as AD biotherapeutics is an emerging field, but more work is needed to investigate whether this approach can lead to sustained clinical responses.

Heterogeneity in cutaneous infection prevalence and frequency by timing of childhood atopic dermatitis onset

Heterogeneity in cutaneous infection prevalence and frequency by timing of childhood atopic dermatitis onset