Search

Background. Allergen immunotherapy (AIT) is a pathogenetic substantiated method for the allergic disease’s treatment, which allows reducing the symptom severity and decreasing the medication use. Uncontrolled severe asthma is a contraindication for AIT. The appointment of biological therapy helps to improve the asthma control, but their cancellation is impossible. The combined use of the biological therapy and AIT makes it possible to achieve the long-term symptoms control in patients with severe asthma, increase the AIT safety, and probably stop biological therapy. Aim. To evaluate the efficacy and safety of combination therapy with dupilumab and AIT in patients with severe asthma. Materials and methods. The study involved 30 adult patients with moderate to atopic severe asthma. Patients was randomized for 3 groups: group 1: standard therapy (0–52 weeks) + dupilumab (0–16 weeks) + AIT (12–16 weeks); group 2: standard therapy without biological therapy (0–52 weeks) + AIT (12–16 weeks); group 3: standard therapy without biological therapy, without AIT (0–52 weeks). We evaluated the asthma control and comorbidities using questionnaires (ACQ, AQLQ, TNSS, SNOT-22, DQLQ), respiratory function (FEV1), the number of exacerbations and adverse events At control points (initially, after 12, 20 and 52 weeks). Results. As a result of the appointment of dupilumab it was possible to quickly achieve asthma control and comorbidities (12 wk), which made it possible to successfully conduct AIT. In the first group, symptom control is maintained even after discontinuation of both dupilumab and AIT. ACQ-6 52 wk: 1 group – 0.30±0.21; 2 group – 1.62±0.51; 3 group – 2.76±0.85. FEV1 52 wk: group 1 – 81.47±7.48%; group 2 – 73.99±6.17%; group 3 – 65.02±7.23% for 3 group (р

Abstract Asthma exacerbations in children are associated with respiratory viral infection and atopy, resulting in systemic immune activation and infiltration of immune cells into the airways. The gene networks driving the immune activation and subsequent migration of immune cells into the airways remains incompletely understood. Cellular and molecular profiling of PBMC was employed on paired samples obtained from atopic asthmatic children (n = 19) during acute virus-associated exacerbations and later during convalescence. Systems level analyses were employed to identify coexpression networks and infer the drivers of these networks, and validation was subsequently obtained via independent samples from asthmatic children. During exacerbations, PBMC exhibited significant changes in immune cell abundance and upregulation of complex interlinked networks of coexpressed genes. These were associated with priming of innate immunity, inflammatory and remodelling functions. We identified activation signatures downstream of bacterial LPS, glucocorticoids and TGFB1. We also confirmed that LPS binding protein was upregulated at the protein-level in plasma. Multiple gene networks known to be involved positively or negatively in asthma pathogenesis, are upregulated in circulating PBMC during acute exacerbations, supporting the hypothesis that systemic pre-programming of potentially pathogenic as well as protective functions of circulating immune cells preceeds migration into the airways. Enhanced sensitivity to LPS is likely to modulate the severity of acute asthma exacerbations through exposure to environmental LPS.

Background: Non-communicable diseases are often associated with chronic inflammation, placing patients suffering from these conditions at a higher risk of thrombosis and other complications. The pathophysiology of asthma and/or atopic asthma is also linked to chronic inflammation, which consequently may alter blood parameters including erythrocyte structure and function. Methodology: The objective of this study was to evaluate differences in erythrocytes between patients with atopic asthma (n = 30) and healthy individuals (n = 30) by evaluating routine haematological parameters; structures and axial ratios of erythrocytes using light microscopy; erythrocyte membrane elasticity using atomic force microscopy; and erythrocyte ultrastructure using scanning electron microscopy. Results: The haematological findings of healthy participants and patients suffering from asthma were within normal clinical ranges together with significantly higher levels of circulating monocytes (p = 0.0066), erythrocytes (p = 0.0004), haemoglobin (p = 0.0057), and haematocrit (p = 0.0049) in asthma patients. The analysis of eosin-stained erythrocytes by light microscopy showed more echinocytes, acanthocytes, and ovalocytes compared to controls and a significant difference in axial ratios (p < 0.0001). Atomic force microscopy findings showed reduced erythrocyte membrane elasticity in asthmatic erythrocytes (p = 0.001). Ultrastructural differences in erythrocytes were visible in the asthma group compared to controls. Conclusion: Altered erythrocyte ultrastructural morphology and a significant change in the haematological profile are evident in atopic asthma and may influence common complications associated with asthma. The impact of these changes on the physiological mechanisms of coagulation and the pathophysiology of asthma needs to be further elucidated.

Asthma exacerbations in children are associated with respiratory viral infection and atopy, resulting in systemic immune activation and infiltration of immune cells into the airways. The gene networks driving the immune activation and subsequent migration of immune cells into the airways remains incompletely understood. Cellular and molecular profiling of PBMC was employed on paired samples obtained from atopic asthmatic children (n = 19) during acute virus-associated exacerbations and later during convalescence. Systems level analyses were employed to identify coexpression networks and infer the drivers of these networks, and validation was subsequently obtained via independent samples from asthmatic children. During exacerbations, PBMC exhibited significant changes in immune cell abundance and upregulation of complex interlinked networks of coexpressed genes. These were associated with priming of innate immunity, inflammatory and remodelling functions. We identified activation signatures downstream of bacterial LPS, glucocorticoids and TGFB1. We also confirmed that LPS binding protein was upregulated at the protein-level in plasma. Multiple gene networks known to be involved positively or negatively in asthma pathogenesis, are upregulated in circulating PBMC during acute exacerbations, supporting the hypothesis that systemic pre-programming of potentially pathogenic as well as protective functions of circulating immune cells preceeds migration into the airways. Enhanced sensitivity to LPS is likely to modulate the severity of acute asthma exacerbations through exposure to environmental LPS. [ABSTRACT FROM AUTHOR]

Background: Non-communicable diseases are often associated with chronic inflammation, placing patients suffering from these conditions at a higher risk of thrombosis and other complications. The pathophysiology of asthma and/or atopic asthma is also linked to chronic inflammation, which consequently may alter blood parameters including erythrocyte structure and function. Methodology: The objective of this study was to evaluate differences in erythrocytes between patients with atopic asthma (n = 30) and healthy individuals (n = 30) by evaluating routine haematological parameters; structures and axial ratios of erythrocytes using light microscopy; erythrocyte membrane elasticity using atomic force microscopy; and erythrocyte ultrastructure using scanning electron microscopy. Results: The haematological findings of healthy participants and patients suffering from asthma were within normal clinical ranges together with significantly higher levels of circulating monocytes (p = 0.0066), erythrocytes (p = 0.0004), haemoglobin (p = 0.0057), and haematocrit (p = 0.0049) in asthma patients. The analysis of eosin-stained erythrocytes by light microscopy showed more echinocytes, acanthocytes, and ovalocytes compared to controls and a significant difference in axial ratios (p < 0.0001). Atomic force microscopy findings showed reduced erythrocyte membrane elasticity in asthmatic erythrocytes (p = 0.001). Ultrastructural differences in erythrocytes were visible in the asthma group compared to controls. Conclusion: Altered erythrocyte ultrastructural morphology and a significant change in the haematological profile are evident in atopic asthma and may influence common complications associated with asthma. The impact of these changes on the physiological mechanisms of coagulation and the pathophysiology of asthma needs to be further elucidated. [ABSTRACT FROM AUTHOR]

Introduction. Taking into account the prevalence of asthma and especially severe atopic asthma which requires carefully selected and expensive therapy, the appearance of the domestic biosimilar omalizumab among biological therapy drugs makes the choice of treatment for this category more affordable. The article presents the results of an observational open prospective clinical trial of the omalizumab biosimilar in severe athopic asthma patients.The purpose of this study was to evaluate the efficacy and safety of the domestic production biosimilar in the real clinical practice.Materials and methods. The study involved 10 adult patients aged 19 to 55 years with a diagnosis of moderate to severe uncontrolled persistent asthma treated with mediun to high dose ICS and second&more controller (ACQ-5 ≥ 1,5, FEV1 < 80% of the predicted normal value). For 26 weeks all patients received the omalizumab. The evaluation of the efficacy was provided taking into account asthma symptoms improvement the results of ACQ-5, FEV1, PEF, asthma exacerbations and the use of health resources.Results. According to the results of data analysis due to omalizumab all patients demonstrated reducing daily asthma symptoms, nocturnal awakening and night time symptom, shortness of breath and SABA using. An asthma control improvement was observed after 1 month treatment (Δ ACQ-5 1.6 [1.2; 2.4], p = 0.0002 compared to the baseline data) with a continued tendency to further increase during 6 months of the study. A statistically significant increase in FEV1 was noted (initially, FEV1 56.7% [51.25; 61.8] of the predicted; after 1 month, FEV1 67.5% [63.45; 70.6] of the predicted, p = 0.00003; after 6 months, FEV1 80.6% [80.55; 84.05] of the predicted, p < 0.001). Omalizumab biosimilar used allowed to reduce the background asthma therapy. No asthma exacerbation was registered due to 26 weeks omalizumab treatment.Conclusions. Based on the results of the study, it was shown that the administration of the omalizumab biosimilar to patients with severe atopic asthma improves control over the symptoms, lung function and reduces the amount of asthma exacerbations, and has a good safety.

Abstract Background Eosinophilia is a significant factor in asthma severity; however, the prevalence of severe eosinophilic asthma in Saudi Arabia is largely unknown. We aimed to determine the prevalence of the eosinophilic (defined in this study as ≥ 300 cells/mm3 in blood), atopic (atopic phenotype 1, defined in this study as > 100 IU/mL total serum IgE; atopic phenotype 2, defined in this study as > 150 IU/mL), and overlap phenotypes among patients with severe asthma in Saudi Arabia. Methods A cross-sectional study was conducted in centers specialized in severe asthma management. Patients aged ≥ 12 years with severe asthma were enrolled. Study patients responded to the Global Initiative for Asthma 2018 assessment of asthma control questionnaire and provided study investigators with current information related to the study objectives. Additional medical record data and a blood sample for total serum IgE and complete blood count were collected. Results A total of 101 patients were enrolled; 83% were female and the mean (standard deviation) age was 48.7 (13.2) years. Forty-five (45%) patients had the eosinophilic phenotype, 50 (50%) had atopic phenotype 1, and 25 (25%) had phenotypic overlap (eosinophilic and atopic 1). Forty-one (41%) patients had atopic phenotype 2 and 23 (23%) had phenotypic overlap (eosinophilic and atopic 2). Asthma control and oral corticosteroid use patterns were similar and there were no significant differences in number of asthma exacerbations across phenotypes. Conclusions In Saudi Arabia, 45% of patients with severe asthma had the eosinophilic phenotype, which is most likely an underestimation as no clinical features of eosinophilia were taken into account in the definition of eosinophilia. Approximately half of them had phenotypic overlap with the atopic phenotype. Trial registration NCT03931954; ClinicalTrials.gov, April 30, 2019.

A 45-year-old man, used to work in a cement factory, presented to us with a history of adult-onset sub-optimally controlled asthma and was initially managed as a case of acute exacerbation of allergic asthma. However, his repeated evaluation revealed raised eosinophil count, raised serum total IgE and persistent chest infiltrates on imaging. He was provisionally managed empirically with a short course of oral steroids and advised follow-up on an out-patient basis to rule out the possibility of idiopathic eosinophilic pulmonary syndromes. The patient was then lost to follow-up, and after four years, he presented with a vasculitic presentation and was diagnosed with Eosinophilic Granulomatosis with Polyangiitis (EGPA). He improved with corticosteroids and cyclophosphamide pulse therapy. This case depicts the importance of evolving nature of EGPA wherein the eosinophilic phase of the disease can mimic other pulmonary eosinophilic diseases and vasculitic symptoms can be delayed as much as by four years.

Abstract Background Asthma is a chronic inflammatory disorder of the airways involving many different factors. This study aimed to screen for the critical genes using DNA methylation/CpGs and miRNAs involved in childhood atopic asthma. Methods DNA methylation and gene expression data (Access Numbers GSE40732 and GSE40576) were downloaded from the Gene Expression Omnibus database. Each set contains 194 peripheral blood mononuclear cell (PBMC) samples of 97 children with atopic asthma and 97 control children. Differentially expressed genes (DEGs) with DNA methylation changes were identified. Pearson correlation analysis was used to select genes with an opposite direction of expression and differences in methylation levels, and then Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed. Protein–protein interaction network and miRNA–target gene regulatory networks were then constructed. Finally, important genes related to asthma were screened. Results A total of 130 critical DEGs with DNA methylation changes were screened from children with atopic asthma and compared with control samples from healthy children. GO and KEGG pathway enrichment analysis found that critical genes were primarily related to 24 GO terms and 10 KEGG pathways. In the miRNA–target gene regulatory networks, 9 KEGG pathways were identified. Analysis of the miRNA–target gene network noted an overlapping KEGG signaling pathway, hsa04060: cytokine-cytokine receptor interaction, in which the gene CCL2, directly related to asthma, was involved. This gene is targeted by eight asthma related miRNAs (hsa-miR-206, hsa-miR-19a, hsa-miR-9,hsa-miR-22, hsa-miR-33b, hsa-miR-122, hsa-miR-1, and hsa-miR-23b). The genes IL2RG and CCl4 were also involved in this pathway. Conclusions The present study provides a novel insight into the underlying molecular mechanism of childhood atopic asthma.

Background: Atopic asthma is one of the most common asthma phenotypes and is generally opposed to the non-atopic counterpart. There have been very few large-scale studies comparing atopic and non-atopic asthmatics in terms of systemic and airway inflammation across the age spectrum. Methods: Here, we have undertaken a retrospective study investigating 1626 patients (924 atopic and 702 non-atopic asthmatics) recruited from our university asthma clinic who underwent extensive clinical investigations including induced sputum. Atopy was defined by any positive specific IgE to common aeroallergens (>0,35 kU/L). We performed direct comparisons between the groups and sought to appreciate the influence of age on the airway and systemic inflammatory components. The study was approved by the ethics committee of the University Hospital of Liege (Ref. 2016/276). Informed consents were obtained from healthy subjects. Results: Atopic asthmatics were younger (P

A 45-year-old man, used to work in a cement factory, presented to us with a history of adult-onset sub-optimally controlled asthma and was initially managed as a case of acute exacerbation of allergic asthma. However, his repeated evaluation revealed raised eosinophil count, raised serum total IgE and persistent chest infiltrates on imaging. He was provisionally managed empirically with a short course of oral steroids and advised follow-up on an out-patient basis to rule out the possibility of idiopathic eosinophilic pulmonary syndromes. The patient was then lost to follow-up, and after four years, he presented with a vasculitic presentation and was diagnosed with Eosinophilic Granulomatosis with Polyangiitis (EGPA). He improved with corticosteroids and cyclophosphamide pulse therapy. This case depicts the importance of evolving nature of EGPA wherein the eosinophilic phase of the disease can mimic other pulmonary eosinophilic diseases and vasculitic symptoms can be delayed as much as by four years. [ABSTRACT FROM AUTHOR]

Background: Eosinophilia is a significant factor in asthma severity; however, the prevalence of severe eosinophilic asthma in Saudi Arabia is largely unknown. We aimed to determine the prevalence of the eosinophilic (defined in this study as ≥ 300 cells/mm3 in blood), atopic (atopic phenotype 1, defined in this study as > 100 IU/mL total serum IgE; atopic phenotype 2, defined in this study as > 150 IU/mL), and overlap phenotypes among patients with severe asthma in Saudi Arabia.Methods: A cross-sectional study was conducted in centers specialized in severe asthma management. Patients aged ≥ 12 years with severe asthma were enrolled. Study patients responded to the Global Initiative for Asthma 2018 assessment of asthma control questionnaire and provided study investigators with current information related to the study objectives. Additional medical record data and a blood sample for total serum IgE and complete blood count were collected.Results: A total of 101 patients were enrolled; 83% were female and the mean (standard deviation) age was 48.7 (13.2) years. Forty-five (45%) patients had the eosinophilic phenotype, 50 (50%) had atopic phenotype 1, and 25 (25%) had phenotypic overlap (eosinophilic and atopic 1). Forty-one (41%) patients had atopic phenotype 2 and 23 (23%) had phenotypic overlap (eosinophilic and atopic 2). Asthma control and oral corticosteroid use patterns were similar and there were no significant differences in number of asthma exacerbations across phenotypes.Conclusions: In Saudi Arabia, 45% of patients with severe asthma had the eosinophilic phenotype, which is most likely an underestimation as no clinical features of eosinophilia were taken into account in the definition of eosinophilia. Approximately half of them had phenotypic overlap with the atopic phenotype. Trial registration NCT03931954; ClinicalTrials.gov, April 30, 2019. [ABSTRACT FROM AUTHOR]

Background: Thymic stromal lymphopoietin (TSLP) is recognized for its key role in promoting asthma, hence drawing considerable clinical interest as a potential therapeutic target. Population-based studies found association between single nucleotide polymorphisms (SNPs) located in the TSLP promoter region, and asthma; however, discrepancies have been also reported. Aims and Objectives: To determine whether rs1837253, rs2289276, and rs3806933 SNPs of TSLP gene are associated with asthma predisposition in a Saudi population. Materials and Methods: A total of, 272 asthmatic patients and 398 normal controls, all of Saudi citizenship, were recruited. The TSLP target DNA sequences were polymerase chain reaction (PCR) amplified using specific primers and allelic determination was performed by Sanger sequencing and capillary electrophoresis. Results: The relative frequencies for the minor allele, “T,” in all three SNPs, were smaller in asthmatics although not significant. When testing for genotypes, the homozygous T/T of all three SNPs was less frequent in asthmatic patients, but not to statistically significant levels. Both the recessive and dominant genetic models were tested. Homozygous T/T individuals for each SNP had lower odds of being asthmatics, thus suggesting a “protective” effect, although none of the SNPs in either model reached a statistical significance. Conclusion: Three SNPs in TSLP's promoter gene were not significantly associated with asthma in the Saudi population.

Introduction: Asthma, a prevalent disease, entails persistent inflammation of the respiratory passages, resulting in symptoms such as wheezing, dyspnea, chest tightness, and coughing. In cases of atopic asthma, exposure to various allergens such as pollen, pet dander, and dust can exacerbate these symptoms, potentially leading to a medical emergency known as status asthmaticus. Diagnosis relies on symptomatology, physical assessment, and pulmonary function testing, confirming expiratory airflow obstruction via reduced FEV1/FVC ratio. Treatment typically involves the administration of short-acting beta-agonists and inhaled corticosteroids. Case Report: We present the case of a 7-year-old boy who presented to the hospital with a persistent dry cough. At 8 months of age, he was initially diagnosed with atopic asthma characterized by fever, dry cough, and wheezing. Allergen testing revealed milk protein, dust mites, cats, dogs, and mold sensitivities .Upon diagnosis, he was discharged with controller therapy consisting of Montelukast, Fluticasone, and Salbutamol. Despite treatment, he experienced multiple exacerbations over the years, necessitating dose adjustments. His most severe exacerbation occurred in 2020 during a measles infection due to a lack of MMR vaccination, resulting in respiratory insufficiency with an oxygen saturation of 60%. He required intensive care unit admission and systemic corticosteroid therapy. Subsequent spirometry indicated obstructive ventilatory dysfunction with an FEV1/FVC ratio of 58%. In addition, he presented with atopic dermatitis and allergic rhinitis, managed with Desloratadine. Although initially screened for cystic fibrosis, the sweat chloride test results were negative. Given the refractory nature of his asthma, biological therapy with Dupilumab was initiated for 2 weeks. At the latest follow-up, the patient reported a significant reduction in exacerbations, down from approximately three episodes per week before initiating Dupilumab therapy. Discussions : Nowadays, the therapeutic approach for asthma includes corticosteroids and beta-agonists. However, their prolonged usage can entail numerous adverse effects, and as evidenced in this case report, they may prove ineffective for moderate to severe asthma. Dupilumab, a human monoclonal antibody targeting the interleukin-4 (IL-4) receptor alpha, approved on 19th of October 2018, operates by antagonizing the activity of IL-4 and IL-13, therefore attenuating T helper 2 cell (Th2)-mediated inflammation, a pivotal mechanism in moderate-to-severe asthma pathogenesis. Conclusions: In summary, this case underscores the management of a juvenile patient with a chronic disease, in which the enduring doctor-patient relationship played a significant role in identifying the appropriate medication to improve his quality of life. [ABSTRACT FROM AUTHOR]

Background: Asthma is a chronic inflammatory disorder of the airways involving many different factors. This study aimed to screen for the critical genes using DNA methylation/CpGs and miRNAs involved in childhood atopic asthma.Methods: DNA methylation and gene expression data (Access Numbers GSE40732 and GSE40576) were downloaded from the Gene Expression Omnibus database. Each set contains 194 peripheral blood mononuclear cell (PBMC) samples of 97 children with atopic asthma and 97 control children. Differentially expressed genes (DEGs) with DNA methylation changes were identified. Pearson correlation analysis was used to select genes with an opposite direction of expression and differences in methylation levels, and then Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed. Protein-protein interaction network and miRNA-target gene regulatory networks were then constructed. Finally, important genes related to asthma were screened.Results: A total of 130 critical DEGs with DNA methylation changes were screened from children with atopic asthma and compared with control samples from healthy children. GO and KEGG pathway enrichment analysis found that critical genes were primarily related to 24 GO terms and 10 KEGG pathways. In the miRNA-target gene regulatory networks, 9 KEGG pathways were identified. Analysis of the miRNA-target gene network noted an overlapping KEGG signaling pathway, hsa04060: cytokine-cytokine receptor interaction, in which the gene CCL2, directly related to asthma, was involved. This gene is targeted by eight asthma related miRNAs (hsa-miR-206, hsa-miR-19a, hsa-miR-9,hsa-miR-22, hsa-miR-33b, hsa-miR-122, hsa-miR-1, and hsa-miR-23b). The genes IL2RG and CCl4 were also involved in this pathway.Conclusions: The present study provides a novel insight into the underlying molecular mechanism of childhood atopic asthma. [ABSTRACT FROM AUTHOR]

Moumita Bhowmik,1,* Sreyashi Majumdar,2,* Angira Dasgupta,3 Swati Gupta Bhattacharya,1 Sudipto Saha2 1Division of Plant Biology, Bose Institute, Kolkata, West Bengal, India; 2Division of Bioinformatics, Bose Institute, Kolkata, West Bengal, India; 3BR Singh Hospital and Centre for Medical Education and Research, Kolkata, West Bengal, India*These authors contributed equally to this workCorrespondence: Swati Gupta BhattacharyaDivision of Plant Biology, Main Campus, Bose Institute, 93/1 APC Road, Kolkata 700009, IndiaTel +91 33 2303 1129Email swatigb2929@yahoo.comSudipto SahaDivision of Bioinformatics, Centenary Campus, Bose Institute, P-1/12 CIT Scheme VII-M, Kolkata 700054, IndiaTel +91 33 2569 3333Email ssaha4@jcbose.ac.inBackground: The pathobiology of atopic asthma is complex and the symptoms similar to other respiratory diseases. As such, identification of biomarkers of atopic asthma is of prime importance for better diagnosis and control of the disease.Objectives: We sought to study the changes in plasma proteome and cytokine-expression profile across healthy and atopic asthmatics for identifying biomarkers and exploring aberrant pathways for atopic asthma.Methods: A pilot-scale study in humans was performed to identify differentially expressed proteins in blood plasma of healthy controls (n=5) and treatment-naïve atopic asthma patients (n=5) using quantitative label-free liquid chromatography–tandem mass spectrometry proteomics and ELISA.Results: Mass spectrometry–based proteomic analysis revealed ApoE to be significantly downregulated in atopic asthmatics compared to healthy volunteers. Decreased expression of ApoE in atopic asthmatics was validated by immunoblotting (50.74% decrease). Comparison with atopic asthmatics and COPD patients showed that ApoE was decreased (36.33%) in atopic asthma compared to COPD. IL33 was significantly upregulated in atopic asthmatics compared to healthy subjects (3.84-fold).Conclusion: ApoE was downregulated and IL33 upregulated in atopic asthma patients compared to healthy volunteers. These two proteins’ profiles were distinct in atopic asthma from healthy and COPD plasma samples. Differential expression of these proteins could serve as a probable candidate for a two-protein classifier–based prognostic biomarker of atopic asthma.Keywords: atopic asthma, LC-MS/MS, apolipoprotein E, ApoE, interleukin 33, IL33, biomarkers

Background: Individuals with severe atopic asthma are poorly controlled with standard treatments, including corticosteroids. A humanized monoclonal antibody binding immunoglobulin E (IgE), omalizumab, is approved to treat patients that are managed poorly despite optimal therapy and that have elevated serum levels of IgE. Objective: The purpose of this study was to determine omalizumab’s effectiveness in a real-world setting. The primary outcome was the number of exacerbations of asthma requiring oral corticosteroid treatment in the 2 year pre-treatment period compared to 2 years post-treatment. The secondary outcome was cumulative dose of prednisone used before and after treatment. Other outcomes that were measured included: reduction in maintenance therapy, change in spirometry (FEV1) data, the stratification of patient population based on smoking status, and average exacerbation number and prednisone use as a function of IgE level and blood eosinophilia count. Methods: Patient data were retrieved (n=41) through the hospital records of patients treated at the Montreal Chest Institute of the McGill University Health Center. Data were gathered and analyzed for the 2 years before the treatment start date and compared to data 2 years after. Results: There was a significant reduction in average exacerbation number from 6.4 pre-treatment to 3.2 post-treatment (p=0.003). There was also a reduction in cumulative prednisone use from 2504mg to 1423mg (p=0.04) following the institution of omalizumab treatment. There was no correlation between either the initial IgE levels and blood eosinophilia and the reduction in exacerbations Conclusion: Omalizumab was effective in reducing exacerbation number and prednisone use for patients with severe refractory asthma.

Background Asthma is a chronic airway disease that is characterized by persistant airway inflammation and remoldeing with bronchial hyperactivity in resulted from one allergen or more leading to episodic airflow obstruction. Periostin can be detected in serum of asthmapatients which largly reflected to its level production in airway. Periostin is secreted by airway epithlialcellin response to iL-13 stimulation and easly leak into the airway capillary. Serum periostin could be aperdector ofairway esinophilliato patients with severeasthma. Aim of the work Is estimating the serum periostin level in patients with bronchial asthma to evaluate its role in diagnosis. Methodology This study was carried out on 25 normal healthy individual serveing as control (Group I), 25 patients diagnosed as atopic asthmatic patient regarding to skin prick test (its postive>3) (Group II) and 25 patients diagnosed as non-atopic asthmatic patient regarding to skin prick test (its negative 420 and sensitivity and specifity was 40.0, 100.0 resepctivily. Conclusion Serum periostin can be used in dignosis of asthma and differntiation of atopic asthma from non atopic asthma.

Both allergic and non-allergic asthma phenotypes are thought to vary by specific housing and other indoor environmental conditions. This study evaluated risk factors for allergic asthma phenotypes in First Nation children, an understudied Canadian population with recognized increased respiratory morbidity. We conducted a cross-sectional survey with a clinical component to assess the respiratory health of 351 school-age children living on two rural reserve communities. Asthma was defined as parental report of physician diagnosed asthma or a report of wheeze in the past 12 months. Atopy was determined by a ≥3-mm wheal response to any of six respiratory allergens upon skin prick testing (SPT). Important domestic and personal characteristics evaluated included damp housing conditions, household heating, respiratory infections and passive smoking exposure. Asthma and atopy prevalence were 17.4% and 17.1%, respectively. Of those with asthma, 21.1% were atopic. We performed multivariate multinomial logistic regression modelling with three outcomes: non-atopic asthma, atopic asthma and no asthma for 280 children who underwent SPT. After adjusting for potential confounders, children with atopic asthma were more likely to be obese and to live in homes with either damage due to dampness (p < 0.05) or signs of mildew/mold (p = 0.06). Both natural gas home heating and a history of respiratory related infections were associated with non-atopic asthma (p < 0.01). Domestic risk factors for asthma appear to vary by atopic status in First Nations children. Determining asthma phenotypes could be useful in environmental management of asthma in this population. [ABSTRACT FROM AUTHOR]

Asthma is a chronic inflammation of the respiratory tract characterized by coughing, shortness of breath, wheezing and limited expiratory airflow. Interleukin 10 (IL-10) is a cytokine produced by T regulators which functions to suppress pro-inflammatory production and development. Interleukin 5 (IL-5) is glycoprotein produced by Th2 which acts as a proinflammatory agent. This study aimed to analyze how to balance between IL-10 and IL-5 levels on persistent atopic asthma. The study design was an experimental research method with invitro study used isolation and cell culture of Peripheral Blood Mononuclear Cell (PBMC) with negative control Roswell Park Memorial Institute (RPMI) medium, positive control Phytohaemaglutinin (PHA) and house dust mite allergen stimulation 10 µl. This study involved 39 samples asthmatic. There was a significant increase in IL-5 levels after stimulation of house dust mite allergens with p: 0.000; there was a significant decrease in IL-10 levels after house dust mite allergen stimulation with p: 0.000. Our study suggests that IL-5 and IL-10 balance is related to persistent atopic asthma after house dust mite allergen Der p stimulation. [ABSTRACT FROM AUTHOR]

Background: GB001 is an oral antagonist of the prostaglandin D2 receptor that may inhibit recruitment and activation of airway eosinophils, reducing airway inflammation. Objective: To assess GB001 safety, efficacy and pharmacokinetics from a Phase 2 study and explore the association between type 2 biomarkers (fractional exhaled nitric oxide and blood eosinophils) and asthma control markers following GB001 administration. Methods: A randomized, placebo‐controlled, double‐blind study evaluating 36 patients with mild‐to‐moderate atopic asthma. Patients receiving fluticasone propionate ≤500 mcg/day or equivalent were randomized (2:1) to GB001 (30 mg) or placebo once daily for 28 days. Safety, pharmacokinetics, forced expiratory volume in 1 second, asthma control questionnaire and rescue medication use were assessed. Clinical outcomes were analysed post hoc by baseline fractional exhaled nitric oxide (<35 and ≥35 ppb) and blood eosinophil (<250 and ≥250 cells/µL) subgroups. Results: GB001 was well tolerated and rapidly absorbed with a 14.5‐hour terminal half‐life. Overall, GB001 demonstrated greater improvement relative to placebo in forced expiratory volume in 1 second at Day 28 (102 mL [95% CI: −110, 314]). Greater effects on forced expiratory volume in 1 second were observed in the high baseline fractional exhaled nitric oxide and blood eosinophil subgroups (207 mL [95% CI: −283, 698];133 mL [95% CI: −422, 687], respectively). These effects were observed as early as Day 2 (229 mL [95% CI: −170, 628]; 163 mL [95% CI: −223, 550] for the high baseline fractional exhaled nitric oxide and blood eosinophil subgroups, respectively) and were sustained through treatment completion. Conclusion and clinical relevance: GB001 was well tolerated, with the estimated half‐life supporting once‐daily (QD) dosing. GB001 may have a rapid and sustained effect on lung function, particularly in patients with type 2 phenotype. Further studies are needed to confirm these findings. [ABSTRACT FROM AUTHOR]

Asthma is a chronic inflammatory disorder of airways that involves in many cells and factors. This study aimed to screen critical genes and miRNAs involved in childhood atopic asthma. DNA methylation and gene expression data (access numbers GSE65163 and GSE65204) were downloaded from Gene Expression Omnibus (GEO) database, which included 72 atopic asthmatic subject samples and 69 healthy samples. The differentially expressed genes (DEGs) with DNA methylation changes were identified, followed by Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Gene coexpression network and miRNA–target gene regulatory networks were then constructed. Besides, we screened critical drug molecules that have high correlation with atopic asthma in children. A total of 146 critical DEGs with DNA methylation changes were screened from atopic asthmatic samples compared with healthy control samples. GO and KEGG pathway enrichment analysis showed that the critical genes were mainly related to 20 GO terms and 13 KEGG pathways. In the coexpression network, tumor necrosis factor (TNF) and major histocompatibility complex, class II, DP alpha 1 (HLA-DPA1) were identified that were significantly related to immune response process. Analysis of miRNA–target gene network showed that hsa-miR-148b had the highest number of target genes(degree = 21). Besides, we found that Alsterpaullone had a correlation value closest to −1 (correlation = −0.884, p = 0.0031), which indicated that the agent might be considered as a potential agent that antagonized to asthma. The dysregulation of TNF, HLA-DPA1, and miR-148b might be related to the immune response of childhood atopic asthma. [ABSTRACT FROM AUTHOR]

The efficacy of a gut microbiota control was investigated for patients with atopic asthma. 45 patients with atopic asthma were included in the study. The results of our clinical and lab tests, pulmonary function tests and the lactulose hydrogen breath tests have been presented to evaluate small intestine bacterial overgrowth (SIBO). Under the standard SIBO’s therapy (long-acting beta-agonists, inhaled glucocorticoids), the first group (15 patients) had being tested with Rifaximin for the SIBO therapy during 7 days. The second group (15 patients) had been tested with Rifaximin and with a succeeding probiotics therapy for three months (B. bifidum, B. longum, B. infantis, L. rhamnosus). SIBO was diagnosed for 30 (67%) patients. We have detected a higher IgE level (P

Several biomarkers have been studied to diagnose or to detect the phenotype of asthma. Clusterin is a sensitive cellular biosensor of oxidative stress and has been studied as a biomarker for inflammatory diseases. We aimed to study serum clusterin level in atopic versus non-atopic childhood asthma and its relation to disease severity. This case-control study included 160 children; 120 stable asthmatic children and 40 apparently healthy children. Asthmatic children were further subdivided into atopic and non-atopic. All children were subjected to medical history taking, clinical examination, and laboratory investigations including complete blood count, serum IgE, serum clusterin level and spirometry before and after bronchodilator therapy. In comparison to controls, patients had significantly higher eosinophils count which was higher in atopic than non-atopic group, also serum IgE level was higher in the atopic asthmatics (118.1 ± 16.2 U/ml) than in both the non-atopic asthmatics (81.2 ± 6.1 U/ml) and the controls (76.3 ± 11.6 U/ml). There was statistical significant difference in serum levels of Clusterin which were highest in the atopic group (182.5 ± 33.5 ng/l), followed by the non-atopic patients (127.5 ± 32.5 ng/l) and lowest in the controls (46.09 ± 7.01 ng/l). Moreover, the higher the severity of asthma, the higher was the level of serum clusterin. In conclusion serum level of clusterin was higher in atopic than non-atopic asthmatic children and it increases significantly with increased severity of the disease. [ABSTRACT FROM AUTHOR]

Background: Antigen‐specific IgE binds the Fcε receptor I (FcεRI) expressed on several types of immune cells, including dendritic cells (DCs). Activation of FcεRI on DCs in atopics has been shown to modulate immune responses that potentially contribute to asthma development. However, the extent to which DC subsets differ in FcεRI expression between atopic children with or without asthma is currently not clear. This study aimed to analyse the expression of FcεRI on peripheral blood mononuclear cells (PBMCs) from atopic children with and without asthma, and non‐atopic/non‐asthmatic age‐matched healthy controls. Methods: We performed multiparameter flow cytometry on PBMC from 391 children across three community cohorts and one clinical cohort based in Western Australia. Results: We confirmed expression of FcεRI on basophils, monocytes, plasmacytoid and conventional DCs, with higher proportions of all cell populations expressing FcεRI in atopic compared to non‐atopic children. Further, we observed that levels of FcεRI expression were elevated across plasmacytoid and conventional DC as well as basophils in atopic asthmatic compared to atopic non‐asthmatic children also after adjusting for serum IgE levels. Conclusion: Our data suggest that the expression pattern of FcεRI on DC and basophils differentiates asthmatic from non‐asthmatic atopic children. Given the significant immune modulatory effects observed as a consequence of FcεRI expression, this altered expression pattern is likely to contribute to asthma pathology in children. [ABSTRACT FROM AUTHOR]

Objective: Interleukin 13 (IL-13) plays a critical pro-inflammatory role in asthma. Several single nucleotide polymorphisms (SNPs) are associated with asthma susceptibility in specific populations; however, further replicative studies in other ethnic groups are mandatory. Methods: The association between IL-13 SNPs rs762534, rs20541, rs1295686, and rs1800925 (risk alleles A, A, T, and A, respectively) and asthma predisposition in a Saudi Arabian cohort was examined via a case-control cross-sectional study. Results: The frequencies of alleles between asthmatics and control populations were significantly different for rs20541 and rs1295686 SNPs (p < 0.001), whereas the frequencies of genotypes between asthmatics and controls were significantly different only for rs20541. The association of the risk (minor) alleles with asthma was examined using the dominant genetic model. Individuals with at least one copy of the risk alleles A (for rs20541) and T (for rs1295686) had significantly greater odds of being asthmatic (OR = 2.13, 95% CI = 1.39-3.26, p < 0.0001; OR = 1.69, 95% CI = 1.12-2.54, p = 0.008) relative to their most common homozygous genotypes. On the other hand, the minor A alleles for rs762534 and rs1800925 were not significantly associated with asthma risk. Regarding haplotype association analysis, individuals with at least one copy of the minor "risk" allele for both rs20541 and rs1295686 (CATG and CATA, respectively) had greater odds of being asthmatic relative to CGCG haplotype; however, this trend was not statistically significant (p > 0.3). Conclusions: IL-13 minor T and A alleles for rs1295686 and rs20541, respectively, were associated with significantly higher risk of asthma in the Saudi Arabian population. [ABSTRACT FROM AUTHOR]

Both allergic and non-allergic asthma phenotypes are thought to vary by specific housing and other indoor environmental conditions. This study evaluated risk factors for allergic asthma phenotypes in First Nation children, an understudied Canadian population with recognized increased respiratory morbidity. We conducted a cross-sectional survey with a clinical component to assess the respiratory health of 351 school-age children living on two rural reserve communities. Asthma was defined as parental report of physician diagnosed asthma or a report of wheeze in the past 12 months. Atopy was determined by a ≥ 3-mm wheal response to any of six respiratory allergens upon skin prick testing (SPT). Important domestic and personal characteristics evaluated included damp housing conditions, household heating, respiratory infections and passive smoking exposure. Asthma and atopy prevalence were 17.4% and 17.1%, respectively. Of those with asthma, 21.1% were atopic. We performed multivariate multinomial logistic regression modelling with three outcomes: non-atopic asthma, atopic asthma and no asthma for 280 children who underwent SPT. After adjusting for potential confounders, children with atopic asthma were more likely to be obese and to live in homes with either damage due to dampness (p < 0.05) or signs of mildew/mold (p = 0.06). Both natural gas home heating and a history of respiratory related infections were associated with non-atopic asthma (p < 0.01). Domestic risk factors for asthma appear to vary by atopic status in First Nations children. Determining asthma phenotypes could be useful in environmental management of asthma in this population.

The efficacy of a gut microbiota control was investigated for patients with atopic asthma. 45 patients with atopic asthma were included in the study. The results of our clinical and lab tests, pulmonary function tests and the lactulose hydrogen breath tests have been presented to evaluate small intestine bacterial overgrowth (SIBO). Under the standard SIBO's therapy (long-acting beta-agonists, inhaled glucocorticoids), the first group (15 patients) had being tested with Rifaximin for the SIBO therapy during 7 days. The second group (15 patients) had been tested with Rifaximin and with a succeeding probiotics therapy for three months (B. bifidum, B. longum, B. infantis, L. rhamnosus). SIBO was diagnosed for 30 (67%) patients. We have detected a higher IgE level (P<0.01), a higher eosinophils level (P<0.001) in sputum and more significant decrease of FEV1 (P<0.01) in SIBO(+). The IgE level in patients was decreased (P<0.01) after the complex SIBO therapy both for the Rifaximin therapy group (P<0.05) and for the Rifaximin + Probiotic therapy group (P<0.05). A dramatic decrease of the IgE level (P<0.05) had been induced by probiotics and it was confirmed by the control testing results with a high statistical accuracy for the observed groups of patients. We did not detect any changes for the patients without SIBO (P=0.46), those who had been treated with a standard therapy. A decrease in the number of patient hospitalization was defined by the treatment with probiotics after SIBO therapy (P<0.05). So, SIBO is a significant factor aggravating the atopic asthma in patients. The gut microflora correction with probiotics therapy has been accompanied by a statistical reliability improvement for the immune response and spirometry, as well as by a decrease in the number of hospitalizations for these patients during the year. [ABSTRACT FROM AUTHOR]

Purpose Physical activity is an important part of life, and exercise-induced asthma (EIA) can reduce the quality of life. A standardized exercise challenge is needed to diagnose EIA, but this is a time consuming, effortful and expensive method. Exhaled nitric oxide (eNO) as a marker of eosinophil inflammation is determined rapidly and easily. The aim of this study was to investigate eNO as surrogate marker for predicting a positive reaction in an exercise challenge in a cold chamber (ECC). Methods A total of 143 subjects aged 6–45 years with suspected EIA were recruited for the study. The subjects underwent an eNO measurement, an ECC and a skin prick test (SPT). To define the sensitivity and specificity of eNO as predictor, a receiver-operating characteristic (ROC) curve was plotted. The individual probability of the occurrence of a positive reaction after ECC based on an eNO value was calculated using a logistic regression model. Results An eNO cut-off value of 18.5 ppb (area under the curve (AUC) 0.71, p < 0.001) showed the best combination of sensitivity and specificity for a positive reaction (forced expiratory volume in 1 s (FEV 1 ) decrease ≥ 10% after ECC) for the whole group. An eNO cut-off value of 46.0 ppb had a specificity of 100.0% to predict a significant FEV 1 decrease and may save exercise testing in 22.4% of patients. A negative predictive level with a high sensitivity and negative predictive value (NPV) could not be defined. In the subgroup that was house dust might (HDM) allergy positive (HDM pos; n = 68, 45.5% of all subjects), an eNO cut-off value of 35.5 ppb (AUC 0.79, p < 0.01) showed the best combination of sensitivity and specificity for a positive reaction after the ECC with a specificity 100.0% and may save exercise testing in 45.6% of HDM pos patients. Using logistic regression, a 95% probability for a positive FEV 1 decrease after ECC was estimated at 53 ppb for the whole group and at 47 ppb for the HDM pos subgroup. Conclusions Exhaled NO measurement is a screening tool for EIA, especially in HDM pos subjects. In a real-life setting, a cut-off value of 46.0 ppb detects EIA at 100% in all suspected patients, and a cut-off level of 35.5 ppb is valuable marker of EIA in patients with an HDM allergy. These levels can save time and costs in a large proportion of patients and will be helpful for clinicians. [ABSTRACT FROM AUTHOR]

Background Given the strong environmental influence on both epigenetic marks and allergic asthma in children, the epigenetic alterations in respiratory epithelia might provide insight into allergic asthma. Objective We sought to identify DNA methylation and gene expression changes associated with childhood allergic persistent asthma. Methods We compared genomic DNA methylation patterns and gene expression in African American children with persistent atopic asthma (n = 36) versus healthy control subjects (n = 36). Results were validated in an independent population of asthmatic children (n = 30) by using a shared healthy control population (n = 36) and in an independent population of white adult atopic asthmatic patients (n = 12) and control subjects (n = 12). Results We identified 186 genes with significant methylation changes, differentially methylated regions or differentially methylated probes, after adjustment for age, sex, race/ethnicity, batch effects, inflation, and multiple comparisons. Genes differentially methylated included those with established roles in asthma and atopy and genes related to extracellular matrix, immunity, cell adhesion, epigenetic regulation, and airflow obstruction. The methylation changes were substantial (median, 9.5%; range, 2.6% to 29.5%). Hypomethylated and hypermethylated genes were associated with increased and decreased gene expression, respectively ( P < 2.8 × 10 −6 for differentially methylated regions and P < 7.8 × 10 −10 for differentially methylated probes). Quantitative analysis in 53 differentially expressed genes demonstrated that 32 (60%) have significant methylation-expression relationships within 5 kb of the gene. Ten loci selected based on the relevance to asthma, magnitude of methylation change, and methylation-expression relationships were validated in an independent cohort of children with atopic asthma. Sixty-seven of 186 genes also have significant asthma-associated methylation changes in nasal epithelia of adult white asthmatic patients. Conclusions Epigenetic marks in respiratory epithelia are associated with allergic asthma and gene expression changes in inner-city children. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and objective Fractional exhaled nitric oxide ( FeNO) has been used as a marker for airway inflammation. We evaluated the association between FeNO levels and asthma exacerbations ( AEs) in Thai children and young adults. Methods This was a prospective cohort study in patients with atopic asthma aged 7-20 years. Asthma control level and management were evaluated every 3 months for 1 year. Spirometry and FeNO measurements were performed at baseline, and 6 and 12 months. Results In all, 70 patients (median age: 12.6 (7.2-19.8) years) were enrolled, of whom 18% had an AE during the study period. Median FeNO levels were significantly higher in patients with an AE than in those without an AE (35.6 ppb vs 16.5 ppb; P = 0.012). FeNO of 31 ppb provided optimal sensitivity (92.3%) and specificity (75.4%) for AE prediction. Sensitivity and specificity of FeNO levels were higher than those of forced expiratory volume in 1 s and forced expiratory flow at 25-75% of forced vital capacity bronchodilator reversibility for the prediction of an AE, but the difference was not significant ( P = 0.121). None of the patients with FeNO level of 0-20 ppb had an AE within 12 months. Percentage of patients with FeNO of 21-40 ppb who suffered an AE was 20% and 30% at 6 and 12 months, respectively. Conclusion The optimal cut-off point of FeNO level for the prediction of AE is 31 ppb. AE within the next 12 months was significantly more common in patients with higher FeNO levels and in patients with a higher rate of previous 12-month exacerbations. [ABSTRACT FROM AUTHOR]

There is a difficulty in asthma management regarding to unclear mechanism of asthma, and a variety of asthma phenotypes that individually require individual therapy and approach. The asthmatic phenotype atopic and nonatopic was clinically difficult to distinguish. The study was analytical descriptive with cross-sectional design. The study aim was to explore the differences of atopic and non-atopic asthmatic characteristics. The study subjects were newly asthmatic patients who were out-patients of An-Nur Lung-Asthmatic Clinic, Bandung, in 2007–2008. In patients examined total IgE, spirometry and skin prick test. There were 198 asthmatic patients comprising 149 (75.3%) atopic and 40 (24.7%) non-atopic asthma. The median of the non-atopic age was 39 years, while the atopic was 34 years (p=0.039). There was a significant difference between atopic (68.5%) and non-atopic (44.9%) in complaint of short breath (p=0.003), but non significant in spirometric examination. The history of atopy were present in atopic asthma group (p=0.011), with significance in rhinitis (81.2 vs 61.2 OR=2.7) and urticaria (14.8 vs 4.1 OR=4.0). Non-atopic asthma was not more severe that atopic asthma was known from examination of forced expiratory volume first second (FEV1). Rhinitis patient, having urticaria, have greater risk for atopic asthma. There were no difference in skin prick test results between both groups. The clinical symptoms of atopic group were in line with the positivenes results of IgE examination. Clinical condition of rhinitis and urticaria direct to the diagnosed towards atopic asthma compared than other clinical features or spirometric result.

Xenobiotics can trigger degranulation of eosinophils and mast cells. In this process, the cells release several substances leading to bronchial hyperactivity, the main feature of atopic asthma (AA). GSTM1 and GSTT1 genes encode enzymes involved in the inactivation of these compounds. Both genes are polymorphic in humans and have a null variant genotype in which both the gene and corresponding enzyme are absent. An increased risk for disease in individuals with the null GST genotypes is therefore, but this issue is controversial. The aim of this study was to investigate the influence of the GSTM1 and GSTT1 genotypes on the occurrence of AA, as well as on its clinical manifestations. Genomic DNA from 86 patients and 258 controls was analyzed by polymerase chain reaction. The frequency of the GSTM1 null genotype in patients was higher than that found in controls (60.5% versus 40.3%, p = 0.002). In individuals with the GSTM1 null genotype the risk of manifested AA was 2.3-fold higher (95%CI: 1.4-3.7) than for others. In contrast, similar frequencies of GSTT1 null and combined GSTM1 plus GSTT1 null genotypes were seen in both groups. No differences in genotype frequencies were perceived in patients stratified by age, gender, ethnic origin, and severity of the disease. These results suggest that the inherited absence of the GSTM1 metabolic pathway may alter the risk of AA in southeastern Brazilian children, although this must be confirmed by further studies with a larger cohort of patients and age-matched controls from the distinct regions of the country.

The lymphotoxin-α (LT-α) gene is located on chromosome 6 (6p21.1–6p21.3) and it may regulate tumor necrosis factor (TNF) production. TNF is a potent cytokine in the airway inflammatory response. Polymorphisms of TNF-associated genes have been related to asthma. This study investigated an LT-α-NcoI polymorphism in the first intron of the LT-α gene (LT-α-NcoI*1 allele, as a variant type; and LT-α-NcoI*2 allele), which may predispose individuals to asthma and atopy. Methods: Polymerase chain reaction-based assays were performed to determine LT-α-NcoI genotypes among our subjects. A genetic case control analysis was then performed on 114 atopic asthmatic and 155 non-asthmatic unrelated children. Results: There was a statistically higher frequency of LT-α-NcoI*1 allele carriers (1/1 + 1/2) in the subjects with atopic asthma than in controls (OR = 1.923; 95% CI = 1.061–3.484; p = 0.031). Conclusion: The results indicate that LT-α-NcoI*1 may be a risk factor for atopic asthma in Taiwanese children.