PURPOSE:Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory disease in which eosinophil (Eos) infiltration into polyp tissues is associated with disease prognosis. Our previous study found that linoleic acid is an important differential metabolite. However, lipid metabolism in nasal polyps has been insufficiently investigated. This study aimed to explore the characteristics of lipid metabolism in CRSwNP tissue. METHODS:This study employed a multi-omics approach by integrating lipidomics and single-cell transcriptomics. The lipidomics analysis was performed using nasal mucosal tissues obtained from 32 patients with nasal polyps and 20 healthy controls. The sequencing findings were validated by using immunofluorescence staining and Western blotting. RESULTS:Phosphatidylethanolamine and phosphatidylcholine were the most abundant lipids expressed in the sinus mucosa, and lysophosphatidylinositol (LPI) was significantly increased in the eosinophilic CRSwNP group compared to the noneosinophilic CRSwNP and the control groups. The LPI levels showed significant positive correlations with the Eos counts and percentages in nasal polyp tissue. The expressions of membrane-bound O-acyltransferase 7 and receptor G-protein coupled receptor 55 in the LPI metabolic pathway were significantly elevated in eosinophilic nasal polyps, and their expression was mainly localized to Eos in polyp tissues. CONCLUSIONS:There are differences in the lipidomic patterns between healthy individuals and patients with CRSwNP. The LPI metabolic axis may be associated with Eos activation in polyp tissue. These findings could provide new insights into the pathogenesis and endotyping of CRSwNP.
PURPOSE:Specialist cough clinics operate in various countries to address the complex needs of patients with chronic cough. Despite their increasing recognition and the recent establishment of an international consensus, such as the European Respiratory Society NEUROCOUGH initiative, no formal agreement on the goals and standards of chronic cough clinics has been established in South Korea. To address this gap, the Korean Academy of Asthma, Allergy and Clinical Immunology (KAAACI) and its Chronic Cough Working Group initiated a Delphi study to develop an expert consensus on the objectives, roles, and standards of chronic cough clinics tailored to the Korean healthcare context. METHODS:A Task Force endorsed by KAAACI and composed of members of the Chronic Cough Working Group conducted a 2-round Delphi survey involving 113 clinicians with relevant clinical or research expertise. The panel evaluated 12 statements and 17 diagnostic items. A consensus was defined as > 70% agreement and < 20% disagreement. RESULTS:Consensus was achieved for all 12 statements (agreement rates, 93.9%-99%), covering clinical care, research, and education. The key agreements were the provision of evidence-based care to improve the quality of life and reduce disease burden; comprehensive assessment of cough characteristics and treatable traits; careful use of neuromodulators or opioid antitussives; appropriate referral to other specialists; and active participation in research and education. A minimum diagnostic test panel, comprising chest radiography, spirometry, paranasal sinus X-ray, and fractional exhaled nitric oxide measurement/blood eosinophil count, was also established. CONCLUSIONS:This study presents the first national consensus to define the goals and standards of chronic cough clinics in South Korea. The recommendations reflect a balance between internationally suggested approaches and local healthcare realities. This consensus is expected to provide updates to national guidelines, facilitate standardized care, and support future research and educational initiatives in chronic cough.
Topical Streptococcus postbiotic emollient (Strain CX) has shown efficacy for mild-to-moderate atopic dermatitis (AD) in a previous study; however, treatment responses according to allergic comorbidity status have not yet been explored. We conducted a post hoc analysis to evaluate the differential therapeutic effects of Strain CX in patients with AD stratified by the presence or absence of allergic comorbidities. This post hoc analysis was derived from a randomized, double-blind, vehicle-controlled trial (Clinical Research Information Service of South Korea, KCT0007876). A total of 98 patients with mild-to-moderate AD were stratified into placebo (n = 33), AD without allergic comorbidities (n = 29), and AD with allergic comorbidities (n = 36) groups. The primary outcomes were the Investigator's Global Assessment (IGA) score and the proportions of participants achieving 25% or 50% improvement in the Eczema Area and Severity Index (EASI), assessed at weeks 4 and 8. The secondary outcomes included a range of skin-related clinical and molecular measures, along with additional evaluations of serum inflammatory and allergic biomarkers as laboratory measures in the per-protocol analysis set. At week 8, 55.2% (16/29) of participants in the AD without allergic comorbidities group achieved an IGA score of 0 or 1 with ≥ 1 point reduction, compared to 30.6% (11/36) in the AD with allergic comorbidities group (P = 0.0272). Both Strain CX intervention groups showed significant improvements in skin parameters, including EASI, skin moisture, and transepidermal water loss. Notably, the AD with allergic comorbidities group solely exhibited significant reductions in systemic inflammatory markers, including sIL-2R (mean, -231.19; 95% confidence interval [CI], -378.82 to -83.57 pg/mL), CCL17 (-127.05; 95% CI, -251.80 to -2.31 pg/mL), and CCL22 (-578.40; 95% CI, -939.31 to -217.49 pg/mL). Clinical skin responses improved more in patients with AD without allergic comorbidities, while immunomodulatory benefits were observed in those with allergic comorbidities. These findings support patient stratification based on allergic comorbidity status for personalized Strain CX treatment strategies. Trial Registration: Clinical Research Information Service Identifier: KCT0007876.
Periostin is a matricellular protein that binds to its receptors, which include several integrin molecules but mainly αvβ3 integrin on cell surfaces, thereby transducing its signals into cells. Almost 20 years have passed since we found that periostin is involved in the pathogenesis of asthma, which marked the first evidence of its involvement in allergic diseases. Over the past 2 decades, cumulative evidence has demonstrated that periostin plays important roles in the onset or progress of many allergic diseases such as chronic rhinitis with nasal polyp, atopic dermatitis (AD), allergic conjunctivitis, eosinophilic esophagitis, eosinophilic otitis media, allergic rhinitis, and eosinophilic granulomatosis with polyangiitis. Starting from the observation of highly expressed periostin in the lesions of these diseases, periostin studies have expanded to include how periostin contributes to the generation of allergic phenotypes, how measurement of periostin is useful as a biomarker for allergic diseases, and recently how periostin inhibitors can improve allergic diseases. Periostin contributes to the generation of allergic phenotypes by acting as a matricellular protein on many cells, including both non-immune and immune cells. Based on the characteristics of periostin as a surrogate biomarker of interleukin-13, a signature cytokine of type 2 inflammation, serum periostin has been used as a biomarker for stratifying endotypes, estimating disease severity, predicting or monitoring the efficacy of therapeutic drugs, and predicting disease relapse or recurrence. Moreover, a lot of attention is now being paid to periostin in body fluids such as tears and sputum as a biomarker directly reflecting type 2 inflammation. Since it has been shown that periostin evokes itch in AD, we hope to see the development of a novel therapeutic agent for AD targeting periostin/αvβ3 integrin. Here we summarize the discovery and characteristics of periostin, as well as questions and/or problems regarding periostin that remain to be resolved.
PURPOSE:Chronic rhinosinusitis with nasal polyps (CRSwNP) is a common chronic inflammatory disease of the mucosa, which significantly impairs patients' quality of life. Eucalyptol-Limonene-Pinene (ELP) is a plant-derived mucoactive agent used in respiratory diseases, including CRSwNP; however, its underlying mechanisms remain unclear. This study aimed to evaluate ELP's effect on CRSwNP and explore its mechanisms. METHODS:Predicted targets and pathways from network pharmacology were validated in vitro using nasal epithelial cells (NECs) and single-cell suspensions from CRSwNP patients, and in vivo using Aspergillus oryzae protease/ovalbumin-induced mouse CRSwNP model. Quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, Western blot, Luminex, hematoxylin and eosin staining, Alcian blue-periodic acid-Schiff staining, immunofluorescence, and immunohistochemistry were used to quantify inflammatory mediators and mucociliary changes. RESULTS:Network pharmacology revealed that epidermal growth factor receptor (EGFR), hypoxia-inducible factor 1-alpha, interleukin (IL)-2 are core targets and enriched in inflammation pathways. In vitro, ELP inhibited the overexpression of mucin 5AC induced by amphiregulin, hypoxia, IL-2 and IL-13 in NECs. ELP decreased expression of type 2 inflammatory mediators, arachidonate 15-lipoxygenase, C-C motif chemokine ligand 26, periostin and epithelial-derived alarmins thymic stromal lymphopoietin, IL-33 in NECs, reduced the concentrations of cytokines/chemokines and countered lipopolysaccharide-induced inflammation in single-cell suspensions. In vivo, ELP reduced epithelial thickness, inflammatory infiltration, goblet cell hyperplasia and cilia damage. CONCLUSIONS:ELP reduced mucus hypersecretion and inflammatory mediators in vitro and in vivo in CRSwNP by specifically inhibiting EGFR-, hypoxia-, IL-2- and IL-13-mediated pathways, suppressing inflammatory responses, and alleviating ciliary damage, suggesting its potential therapeutic value.
PURPOSE:The pathophysiology and natural course of childhood food allergies (FAs) remains largely elusive. Recent findings have implicated resolvins, omega-3 metabolites, in the pathogenesis and resolution of FAs, highlighting their potential clinical significance. This investigation aimed to elucidate the clinical implications of resolvins in the manifestation and resolution of childhood FAs. METHODS:Serum samples were collected from a cohort of children diagnosed with FA and healthy controls upon their first visit to the Severance Children's Hospital (Seoul, Korea). FA persistence was assessed for each patient based on follow-up records. Resolvin D1 (RvD1) levels were measured and their correlation with total immunoglobulin E (IgE) and allergen-specific IgE levels were evaluated. RESULTS:This study included 278 children (mean age 3.28 ± 3.17 years; 62% male), consisting of 92 children with resolved FA (resolved FA group), 113 children with persistent FA (persistent FA group), and 73 children (control group). RvD1 levels were significantly higher in children with FA than in controls (P < 0.001), and were significantly higher in the persistent FA group than in the resolved FA group (P = 0.045). A positive correlation was found between total IgE and RvD1 levels (r = 0.32, P < 0.001), particularly in the persistent FA subgroup. Furthermore, the correlation between RvD1 and total IgE was stronger in children with multiple FAs (r = 0.367, P < 0.001). RvD1 levels were also positively correlated with egg- and milk-specific IgE levels, especially in the persistent FA group. CONCLUSIONS:Our findings suggest that RvD1 is a candidate metabolite associated with the persistence of childhood FA, across various food allergens and may provide complementary information to existing clinical features.
Epidermal lipids are essential for skin barrier function and actively influence cutaneous immune homeostasis. Recent advances have transformed our understanding of skin lipid dysregulation in allergic diseases, revealing complex bidirectional relationships between barrier dysfunction and immune activation. This review provides a comprehensive analysis of the 2020-2025 literature on skin lipid metabolism in allergic and inflammatory diseases, with a particular focus on molecular mechanisms, diagnostic biomarkers, therapeutic advances, and implications for precision medicine. Key discoveries include the finding that sphingomyelin deacylase, long linked to ceramide (CER) deficiency, is actually the β-subunit of acid ceramidase. In atopic dermatitis, this enzyme shifts its substrate specificity to sphingomyelin, depleting the barrier lipid pool. Type 2 cytokines, particularly interleukin (IL)-4 and IL-13, suppress lipid biosynthesis through Janus kinase (JAK)/Signal Transducer and Activator of Transcription 6-mediated downregulation of fatty acid (FA) elongases. This suppression, particularly affecting elongation of very long-chain fatty acid (ELOVL) enzymes, such as ELOVL1, ELOVL3, and ELOVL6, disrupts the synthesis of ultra-long-chain CERs essential for barrier function. JAK inhibitors effectively reverse T helper 2 (Th2)-mediated lipid suppression, while optimized topical lipid ratios (3:1:1 CER: cholesterol: FA) enhance barrier repair. Innovations, such as lipid nanoparticles and microbiome-modulating therapies, further support personalized treatment strategies. The integration of barrier repair with targeted immunomodulation-guided by lipidomic and genomic profiling-marks a paradigm shift toward predictive and preventive approaches in allergic skin diseases. Early intervention strategies that simultaneously address immune dysregulation and lipid metabolism hold promise for preventing the atopic march and sustaining long-term remission.
PURPOSE:Although around 90% of penicillin allergies are mislabelled, delabeling initiatives have been hindered by limited access to drug allergy services. Asia Pacific Association of Allergy, Asthma, and Clinical Immunology (APAAACI) and PENFAST risk-stratification tools can facilitate non-allergist delabeling, but their comparative real-world performance remains unknown. The purpose of this study was to prospectively evaluate APAAACI and PENFAST against allergist assessment and drug provocation testing (DPT) outcomes. METHODS:In a blinded, head-to-head study, 103 adults with penicillin allergy labels underwent independent risk stratification using both APAAACI and PENFAST tools, followed by allergist evaluation and allergy testing (skin tests, in vitro tests, and DPT). We assessed diagnostic performance (area under the curve [AUC]-receiver operating characteristic, accuracy, sensitivity, specificity, positive and negative predictive values [NPVs]) and agreement (Cohen's κ) of these tools. RESULTS:Overall, allergist assessment demonstrated the highest AUC of 0.82 (95% confidence interval [CI], 0.69-0.95), outperforming APAAACI (AUC, 0.79; 95% CI, 0.66-0.92; P = 0.012) and PENFAST (AUC, 0.75; 95% CI, 0.62-0.89; P = 0.010). Both APAAACI and PENFAST demonstrated high sensitivity (0.88) and NPV (APAAACI, 0.99; PENFAST, 0.98), missing only one non-severe DPT-positive case. APAAACI showed excellent agreement with allergist assessment (κ = 0.96, P < 0.001) versus moderate agreement for PENFAST (κ = 0.43). Allergist evaluation had superior specificity (0.77 vs. 0.71 [APAAACI] and 0.63 [PENFAST]) and overall accuracy (0.78 vs. 0.72 and 0.65). CONCLUSIONS:APAAACI and PENFAST can both effectively identify low-risk patients labelled with penicillin allergy when used by non-allergists, with comparable sensitivity to allergist assessment. APAAACI's stronger agreement with allergist assessment may suggest particular utility in Asian populations. These tools can significantly improve access to delabeling in settings lacking specialist allergy services.
PURPOSE:Respiratory allergies impair children's health-related quality of life (HRQoL) and increase caregiver burden. While allergen-specific subcutaneous immunotherapy (SCIT) is known to improve clinical outcomes, its short-term impact on HRQoL in children and their parental caregivers remains underexplored. We aimed to evaluate the 12-month impact of SCIT on HRQoL, identify the determinants of HRQoL, and assess the correlation between symptom improvements and HRQoL gains. METHODS:This prospective study enrolled children with allergic rhinitis and/or asthma receiving either SCIT or standard pharmacotherapy, alongside their parental caregivers. Validated generic and disease-specific HRQoL instruments were administered at baseline and the 12-month follow-up. HRQoL changes were analyzed using paired t-tests and Cohen's d effect sizes (ESs). Factors influencing HRQoL were identified using multivariable regression, and correlations between symptom changes and HRQoL gains were examined. RESULTS:After 12 months, children in the SCIT group (n = 132) showed significantly greater improvements in HRQoL than those receiving standard pharmacotherapy (n = 120) (ESs: 0.52-1.34 vs. 0.21-1.05), particularly in the domains of "usual activities" and "pain/discomfort." Caregivers in the SCIT group also experienced greater improvements in HRQoL (ESs: 0.54-0.60 vs. 0.23-0.26), particularly in the domains of "exhaustion," "anxiety," and "day-to-day activities." Multivariable regression analysis identified significant factors influencing HRQoL for both children and caregivers, including coexisting allergic conditions, disease control status, SCIT, and caregiver burdens. Symptom improvements with SCIT showed moderate-to-strong correlations with HRQoL gains. CONCLUSIONS:Over a 12-month period, SCIT was associated with significantly greater improvements in HRQoL for children with respiratory allergies and their parental caregivers compared with standard pharmacotherapy. Generic HRQoL instruments demonstrated good sensitivity to short-term treatment-related changes, supporting their utility as complementary outcome measures in SCIT evaluation. TRIAL REGISTRATION:ClinicalTrials.gov Identifier: NCT06535087.
PURPOSE:Coronavirus disease 2019 (COVID-19) mRNA vaccines have reduced the severity and mortality of severe acute respiratory syndrome coronavirus 2 infection. However, several reports of asthma exacerbations following COVID-19 mRNA vaccination have raised safety concerns for patients with obstructive airway diseases. This study aimed to evaluate the risk of mRNA vaccine-associated exacerbations and identify associated clinical factors among patients with asthma and chronic obstructive pulmonary disease (COPD). METHODS:This multicenter historical cohort study enrolled 455 patients (387 with asthma, including 30 with COPD overlap and 68 with COPD) from 13 Japanese institutions between September 2022 and September 2024. Demographic data, pulmonary function, biomarkers, and questionnaire responses were collected. Exacerbation was defined as worsening of respiratory symptoms occurring within 1 week after vaccination. Independent risk factors were identified by multivariate logistic regression. RESULTS:Patients with asthma had a higher COVID-19 mRNA vaccine-associated exacerbation rate than those with COPD (14.5% vs. 0%, P < 0.001). Among patients with asthma, exacerbations were more frequent after COVID-19 mRNA vaccination than after influenza vaccination (14.5% vs. 1.8%, P < 0.001). Younger age, atopic predisposition, lower fractional exhaled nitric oxide levels (< 25 ppb), and poor asthma control (asthma control test < 20 and/or frequent exacerbations ≥ 2/year) were identified as independent risk factors (all P < 0.05). Most exacerbations were mild, with no severe outcomes. CONCLUSIONS:Poorly controlled atopic asthma in younger individuals was associated with increased risk of COVID-19 mRNA vaccine-associated exacerbation. Despite this, the overall benefits of COVID-19 mRNA vaccination support its continued use, with an emphasis on optimizing asthma control beforehand in high-risk patients. TRIAL REGISTRATION:UMIN Clinical Trials Registry Identifier: UMIN000049011.
Purpose: Airway remodeling is a key pathological feature of asthma. The CD30ligand (CD30L), a member of the tumor necrosis factor (TNF) superfamily encoded by the Tnfsf8 gene, has been linked to immune-inflammatory pathologies. Nevertheless, the role of CD30L in airway remodeling has not been elucidated. Methods: We investigated CD30L expression and localization in lung specimens from asthma patients and ovalbumin (OVA)-induced asthmatic mice. Subsequently, we established asthmatic mice with macrophage-specific Tnfsf8 knockout or intranasal administration of recombinant CD30L protein, and analyzed airway pathology using multiple techniques. In vitro, an indirect co-culture system of macrophages and bronchial epithelial cells was employed to investigate the impact of CD30L on airway epithelial remodeling. The mechanisms of CD30L in human bronchial epithelial (HBE) cells were explored using small interfering RNA targeting CD30 (the receptor for CD30L), c-Jun N-terminal kinase (JNK) inhibitor, and p38 inhibitor. Results: CD30L expression was upregulated in asthmatic lung tissues (human/mice) and colocalized with macrophage markers. In vivo, macrophage-specific Tnfsf8 knockout attenuated extracellular matrix (ECM) deposition and epithelial-mesenchymal transition (EMT) during OVA-induced airway remodeling, whereas intranasal CD30L exacerbated these pathologies. Transcriptomic analysis of lung tissues revealed that CD30L regulated ECM deposition, cell adhesion, and epithelial cell migration. In vitro co-culture of macrophages with bronchial epithelial cells demonstrated that macrophage-specific CD30L silencing reversed remodeling-related proteins and EMT in bronchial epithelial cells. Furthermore, we found that CD30L significantly upregulated the JNK/p38 mitogenactivated protein kinase (MAPK) pathway in HBE cells. Silencing CD30 in HBE cells alleviated CD30L-induced remodeling and EMT, accompanied by downregulation of the JNK/p38 MAPK pathway. Treatment with JNK inhibitor (SP600125) or p38 inhibitor (SB203580) reversed the CD30L-induced pathological effects. Conclusions: Collectively, these findings demonstrate that CD30L critically regulates asthma airway remodeling via the JNK/p38 MAPK pathway, strongly suggesting its therapeutic potential as a target for airway remodeling in asthma.
PURPOSE:This study assessed the prevalence, major triggers, and risk factors of food allergy (FA) and food-induced anaphylaxis among Korean school-aged children. METHODS:In 2022, a nationwide school-based survey was conducted using a structured questionnaire. Cluster sampling yielded a representative sample of 12,558 students aged 6-7, 9-10, and 12-13 years from 213 elementary and 103 middle schools in Korea. RESULTS:The prevalence of self-reported perceived FA was 15.3%; recurrent immediate-type (< 4 hours) FA, 7.8%; and physician-diagnosed FA, 5.5%, with food-induced anaphylaxis in 0.7% of cases. The leading allergens for recurrent immediate-type FA were peach (1.13%), milk (0.82%), egg (0.79%), kiwi (0.65%), walnut (0.62%), peanut (0.62%), apple (0.61%), crab (0.59%), shrimp (0.54%), and pineapple (0.33%). By food group, fruits (3.67%) were most frequent, followed by crustaceans (1.20%), and tree nuts (1.18%). Major anaphylaxis triggers included egg (0.19%), milk (0.11%), walnut (0.10%), peanut (0.09%), and peach (0.06%). Fruit allergy was more common in older age groups, accompanied by increased oral allergy symptoms, suggesting a rising burden of pollen FA syndrome. In these groups, crustaceans were also major allergens. Among tree nuts, walnut was the most common. Perilla seed, a uniquely observed allergen in Korea, had prevalences of 0.11% for allergy and 0.02% for perilla seed-induced anaphylaxis. Multiple food allergies were reported by 29.9% of children with FA. Significant risk factors included paternal allergic disease, parental history of FA, delayed complementary food introduction (≥ 7 months), prolonged breastfeeding (≥ 7 months), and current allergic diseases, particularly atopic dermatitis. CONCLUSIONS:In Korean school-aged children, recurrent immediate-type FA and food-induced anaphylaxis affect 7.8% and 0.7%, respectively. Fruits, milk, egg, tree nuts, and peanuts are the most common triggers, with notable age-related differences. These findings underscore the need for continued surveillance, early identification of high-risk groups, and targeted prevention and management strategies.
Hen's egg allergy is one of the most common food allergies worldwide and has a significant impact on children's health. Hen's egg allergy is primarily immunoglobulin E (IgE)-mediated reaction, and Gal d 1-5 are the most common allergens. Filaggrin mutations impair skin barrier function, promoting sensitization and persistent allergy. Family history, early atopic dermatitis, and limited microbial exposure can increase the risk of egg allergy. Additionally, there is a difference in the prevalence of hen's egg allergy between Eastern and Western countries. Egg allergy is closely linked to moderate-to-severe atopic dermatitis and follows the atopic march, with many children outgrowing it by school age; however, the early or persistent IgE sensitization increases the risk of asthma and rhinitis later in childhood. A high initial IgE level, large skin prick test wheals, multiple food allergy, severe eczema, Gal d 1 sensitization, filaggrin gene mutations, and epigenetic changes can be used to predict the risk of persistent egg allergy. Early introduction of allergenic foods, such as eggs, may safely reduce future allergy risk. Oral, sublingual, and epicutaneous immunotherapies offer desensitization options, but they rarely achieve long-term tolerance and raise safety concerns.
Work-related asthma (WRA), encompassing occupational asthma and work-exacerbated asthma, is among the most prevalent yet preventable occupational respiratory diseases, with population-based studies estimating that 10% to 25% of adult asthma cases are attributable to workplace exposure. This review examines epidemiology, causative agents, pathogenesis, clinical evaluation, management, and WRA prevention from an occupational medicine perspective, with emphasis on Korean surveillance data. The Korea Work-related Asthma Surveillance program (2004-2009) identified 236 cases with a crude incidence of 3.31 per million workers, revealing a 40-to 90-fold detection gap when compared to European population-based estimates of 250 to 300 per million workers annually. Korean cases showed a distinctive agent profile, with isocyanates accounting for 46.6%-a figure that far exceeds the 13% to 23% in Western surveillance systems-which reflects the prominence of the furniture manufacturing industry. Temporal trends demonstrated successful prevention, with isocyanate-related cases decreasing from 65.0% to 26.9% during the period 2004-2009. Despite treatment advances, the prognosis remains poor: only 32% of patients achieve symptomatic recovery following the complete avoidance of exposure, and continued exposure increases the symptom burden 10-fold. Workers' compensation data confirm persistent underdiagnosis, with only 0 to 5 cases annually approved during the period 2013-2023 despite expanding recognition of occupational diseases overall. The Korea Occupational Disease Surveillance Center, established in 2022, offers an opportunity to bridge the prolonged surveillance gap. Clinicians treating working adults should maintain a high index of suspicion for the occupational causes of asthma, pursue early diagnosis and exposure cessation, and integrate workplace assessments into their routine clinical evaluations.
Purpose: Upadacitinib is an oral selective Janus kinase (JAK)1 inhibitor that has demonstrated high efficacy in clinical trials for patients with atopic dermatitis (AD). However, clinical trial settings may not always reflect real-world practice. This study aimed to assess the real-world efficacy and safety of upadacitinib in AD patients. Methods: One hundred fifteen AD patients treated with upadacitinib were retrospectively analyzed using medical records. Patients who received treatment for at least 16 weeks were included. In the moderate-to-severe AD group, efficacy was assessed by the proportion of patients achieving Eczema Area and Severity Index (EASI) 50, EASI 75, and EASI 90 at weeks 2 and 16 compared to baseline, whereas efficacy in the mild AD group was evaluated based on the reduction in patient-reported outcomes. Results: The mean EASI score significantly decreased after 16 weeks of upadacitinib treatment. At week 2, 67%, 35%, and 6% of moderate-to-severe AD patients achieved EASI 50, EASI 75 and EASI 90, respectively. At week 16, 88%, 71%, and 31% of moderate-to-severe AD patients achieved EASI 50, EASI 75 and EASI 90, respectively. Patient-reported outcome measures improved rapidly within 2 weeks and were sustained through week 16. The most common adverse event was acne, occurring in 35 patients (41.2%) with mild severity. No serious adverse events occurred. Conclusions: Upadacitinib is effective and safe for AD patients in a real-world clinical setting.
