Different Phenotypes Of Asthma Research Articles

T-cell receptor diversity and allergen sensitivity in childhood asthma and atopic dermatitis.

Childhood allergies of asthma and atopic dermatitis (AD) involve an overactive T-cell immune response triggered by allergens. However, the impact of T-cell receptor (TCR) repertoires on allergen sensitization and their role in mediating different phenotypes of asthma and AD in early childhood remains unclear. A total of 78 children, comprising 26 with asthma alone, 26 with AD alone, and 26 healthy controls (HC), were enrolled. TCR repertoire profiles were determined using a unique molecular identifier system for next-generation sequencing. Integrative analyses of their associations with allergen-specific IgE levels and allergies were performed. The diversity in TCR alpha variable region (TRAV) genes of TCR repertoires and complementarity determining region 3 (CDR3) clonality in TRAV/TRBV (beta) genes were significantly higher in children with AD compared with those with asthma and HC (p < .05). Compared with HC, the expression of TRAV13-1 and TRAV4 genes was significantly higher in both asthma and AD (p < .05), with a significant positive correlation with mite-specific IgE levels (p < .01). In contrast, TRBV7-9 gene expression was significantly lower in both asthma and AD (p < .01), with this gene showing a significant negative correlation with mite-specific IgE levels (p < .01). Furthermore, significantly higher TRAV8-3 gene expression, positively correlated with food-specific IgE levels, was found in children with AD compared with those with asthma (p < .05). Integrated TCR repertoires analysis provides clinical insights into the diverse TCR genes linked to antigen specificity, offering potential for precision immunotherapy in childhood allergies.

Investigation analysis of the acute asthma risk factor and phenotype based on relational analysis with outdoor air pollutants in Xi'an, China.

Asthma is a common chronic heterogeneous disease. Outdoor air pollutants are an important cause of acute asthma. Until now, the association between the risk of acute asthma and outdoor air pollutants is unclear. And the relationship between the different phenotypes of asthma and outdoor air pollutants has not been reported. Thus, an analysis of the association between outdoor air pollutants and daily acute asthma inpatient and outpatient visits in Xi'an, China, from January 1 to December 31, 2018, was conducted. A total of 3395 people were included in the study. The statistical analysis and relational analysis based on the logistic regression were used for illustrating the relatedness of the acute asthma risk factor and phenotype with outdoor air pollutants, while the age, gender, pollen peak and non-pollen peak periods, high type 2 (T2) asthma and non-high T2 asthma were also stratified. Results showed that particulate matter with particle size below 10μm and 2.5μm (PM10 and PM2.5), sulfur dioxide(SO2), nitrogen dioxide(NO2), and carbon monoxide(CO) increase the risk of acute asthma and that air pollutants have a lagged effect on asthma patients. PM10, NO2, CO, and Ozone (O3) are associated with an increased risk of acute attacks of high T2 asthma. PM10, PM2.5, SO2, NO2 and CO are associated with an increased risk of acute asthma in males of 0-16years old. PM10 and PM2.5 are more harmful to asthma patients with abnormal lung function.

Different Characteristics and Clinical Outcomes between Early-Onset and Late-Onset Asthma: A Prospective Cohort Study.

Late-onset asthma (LOA) differs from early-onset asthma (EOA) in terms of prognosis and the treatment response because it has a much worse prognosis and a poorer response to standard asthma treatment. This study sought to investigate the characteristics and clinical outcomes of asthma patients with phenotypes distinguished by age at onset and atopy status. We prospectively recruited patients with asthma who were registered in a pay-for-performance program operated by Taiwan's National Health Insurance Administration (NHIA). These patients received regular outpatient treatment for at least 1 year at every outpatient clinic visit since 2019. Baseline characteristics and clinical outcomes were compared between patients with LOA (≥40 years) and those with EOA (&lt;40 years). Of the consecutive 101 patients with asthma, 21 patients (20.7%) had EOA and 80 (79.3%) had LOA. In the 12-month period, patients with EOA had higher declines in forced expiratory volume in one second (FEV1; -2.1 ± 8.4 vs. 6.8 ± 13.1, % of predicted value, p = 0.037) and forced vital capacity (FVC; -4.6 ± 12.0 vs. 6.1 ± 13.6, % of predicted value, p = 0.023) than patients with LOA. Patients with nonatopic EOA had a significantly higher exacerbation rate at 12 months than patients with nonatopic LOA (50% vs. 11.8%, p = 0.012). Identification of different phenotypes of asthma is important in clinical practice because treatment responses may differ.

Human Lung Mast Cells: Therapeutic Implications in Asthma.

Mast cells are strategically located in different compartments of the lung in asthmatic patients. These cells are widely recognized as central effectors and immunomodulators in different asthma phenotypes. Mast cell mediators activate a wide spectrum of cells of the innate and adaptive immune system during airway inflammation. Moreover, these cells modulate the activities of several structural cells (i.e., fibroblasts, airway smooth muscle cells, bronchial epithelial and goblet cells, and endothelial cells) in the human lung. These findings indicate that lung mast cells and their mediators significantly contribute to the immune induction of airway remodeling in severe asthma. Therapies targeting mast cell mediators and/or their receptors, including monoclonal antibodies targeting IgE, IL-4/IL-13, IL-5/IL-5Rα, IL-4Rα, TSLP, and IL-33, have been found safe and effective in the treatment of different phenotypes of asthma. Moreover, agonists of inhibitory receptors expressed by human mast cells (Siglec-8, Siglec-6) are under investigation for asthma treatment. Increasing evidence suggests that different approaches to depleting mast cells show promising results in severe asthma treatment. Novel treatments targeting mast cells can presumably change the course of the disease and induce drug-free remission in bronchial asthma. Here, we provide an overview of current and promising treatments for asthma that directly or indirectly target lung mast cells.

Heterogeneity of asthma with nasal polyposis phenotypes: Acluster analysis.

Chronic rhinosinusitis with nasal polyposis (CRSwNP) affects a significant number of asthmatic patients and is notably associated with a more difficult-to-control asthma and marked inflammation. We need more studies on this specific asthma phenotype and its possible subphenotypes, in order to better individualize treatments. The aim of this study is to identify and characterize subphenotypes of asthma patients with CRSwNP using clinical, physiological and inflammatory variables. K-means cluster analysis was performed on 17 clinical, physiological, and inflammatory variables from 1263 patients of all asthma severity and on a subpopulation of patients with asthma and CRSwNP. Study was registered on ClinicalTrials.gov (NCT03694847). On the overall population, three groups were identified. Cluster T1 (n=708) are young, have a short asthma duration and a low prevalence of CRSwNP. Cluster T2 (n=263) have the longest asthma duration and Cluster T3 (n=292) are older with the shortest asthma duration. Patients in Clusters T2 and T3 have similar prevalences of CRSwNP. On the subpopulation of asthma with CRSwNP, three clusters were also identified. Cluster S1 (n=83) have mild-to-moderate asthma with normal lung function. Clusters S2 (N=53) and S3 (N=42) include patients with severe asthma and decreased lung function, but those in Cluster S2 have a longer asthma duration, whereas those Cluster S3 have late-onset asthma. Despite coexistence of asthma and CRSwNP, not all patients have the same evolution of their asthma. Different phenotypes of asthma with CRSwNP can be identified and exploration of the characteristics of these subgroups could lead to a better individualized, targeted management.

Obesity and Asthma.

Obesity is a major risk factor for the development of asthma, and the prevalence of obesity is higher in people with asthma than in the general population. Obese people often have severe asthma-recent studies in the United States suggest that 60% of adults with severe asthma are obese. Multiple mechanisms link obesity and asthma, which are discussed in this article, and these pathways contribute to different phenotypes of asthma among people with obesity. From a practical aspect, changes in physiology and immune markers affect diagnosis and monitoring of disease activity in people with asthma and obesity. Obesity also affects response to asthma medications and is associated with an increased risk of co-morbidities such as gastroesophageal reflux disease, depression, and obstructive sleep apnea, all of which may affect asthma control. Obese people may be at elevated risk of exacerbations related to increased risk of severe disease in response to viral infections. Interventions that target improved dietary quality, exercise, and weight loss are likely to be particularly helpful for this patient population.

Phenotype and severity of asthma determines bronchial epithelial immune responses to a viral mimic.

Asthma is characterised by an aggravated immune response to respiratory viral infections. This phenomenon is a clinically well-recognised driver of acute exacerbations, but how different phenotypes of asthma respond immunologically to viruses is unclear. To describe the association between different phenotypes and severity of asthma and bronchial epithelial immune responses to viral stimulation. In the Immunoreact study, healthy subjects (n=10) and 50 patients with asthma were included; 30 (60%) were atopic, and 34 (68%) were eosinophilic; 14 (28%) had severe asthma. All participants underwent bronchoscopy with collection of bronchial brushings. Bronchial epithelial cells (BECs) were expanded and stimulated with the viral replication mimic poly (I:C) (Toll-like receptor (TLR)3 agonist) in vitro. The expression of TLR3-induced pro-inflammatory and antiviral responses of BECs were analysed using reverse transcriptase quantitative PCR and multiplex ELISA and compared across asthma phenotypes and severity of disease. Patients with atopic asthma had increased induction of interleukin (IL)-4, interferon (IFN)-β, IL-6, tumour necrosis factor-α, and IL-1β after poly (I:C) stimulation compared to non-atopic patients, whereas in patients with eosinophilic asthma only IL-6 and IL-8 induction was higher than in non-eosinophilic asthma. Patients with severe asthma displayed a decreased antiviral IFN-β, and increased expression of IL-8, most pronounced in atopic and eosinophilic asthmatics. Furthermore, induction of IL-33 in response to poly (I:C) was increased in severe atopic and in severe eosinophilic asthma, but thymic stromal lymphopoietin only in severe eosinophilic asthma. The bronchial epithelial immune response to a viral mimic stimulation differs between asthma phenotypes and severities, which may be important to consider when targeting novel asthma treatments.

Proximity to Heavy Traffic Roads and Patient Characteristics of Late of Onset Asthma in an Urban Asthma Center

Background: Traffic-related pollution is associated with the onset of asthma and the development of different phenotypes of asthma. Few studies have investigated the association between traffic proximity and late-onset of asthma (LOA) and early-onset asthma (EOA). This study was conducted to investigate the associations of LOA phenotypes with a function of the distance between residence and heavy traffic roads (HTRs).Methods: The study group consisted of 280 patients who were (LOA: 78.4%) recruited consecutively from a pay-for-performance asthma program to clarify the patient characteristics and proximity to HTRs within 1,000 m from their residences between EOA and LOA in three urban centers in Taiwan. The subsequent analysis focused on patients with LOA (n = 210) linking phenotypes and distance to HTRs.Results: Subjects with LOA tended to be older than those with EOA and had shorter asthma duration, poorer lung function, lower atopy, and less exposure to fumes or dust at home. Patients with LOA were more likely than those with EOA to live within 900 m of two or more HTRs (14.3 vs. 3.4%, p = 0.02). Among patients with LOA, minimum distance to an HTR was negatively associated with numbers of specific IgE as well as positively associated with the age of onset and body weight significantly. A higher proportion of patients with atopy (26.3 vs. 20.6%, p = 0.001. odds ratio [OR]: 2.82) and anxiety/depression (21.0 vs. 18.1%, p = 0.047. OR: 1.81) and a trend of lower proportion of patients with obese (5.7 vs. 12.4%, p = 0.075) were found to be living within 900 m from HTRs.Conclusions: Late-onset of asthma (LOA) tended to live in areas of higher HTR density compared to EOAs. Among patients with LOA living close to HTRs, the interaction between traffic-related pollution, allergy sensitization, and mood status were the factors associated with asthma onset early. Obesity may be the factor for later onset who live far from HTRs.

Type 2 immunity-driven diseases: Towards a multidisciplinary approach.

Asthma, atopic dermatitis and chronic rhinoconjunctivitis are highly heterogeneous. However, epidemiologic associations exist between phenotypic groups of patients. Atopic march is one such association but is not the only common point. Indeed, beyond such phenotypes, hallmarks of type 2 immunity have been found in these diseases involving immune dysregulation as well as environmental triggers and epithelial dysfunction. From the canonical Th2 cytokines (IL‐4, IL‐5, IL‐13), new cellular and molecular actors arise, from the epithelium's alarmins to new innate immune cells. Their interactions are now better understood across the different environmental barriers, and slight differences appeared. In parallel, the development of type 2‐targeting biotherapies not only raised hope to treat those diseases but also raised new questions regarding their true pathophysiological involvement. Here, we review the place of type 2 immunity in the different phenotypes of asthma, chronic rhinitis, chronic rhinosinusitis and atopic dermatitis, highlighting nuances between them. New hypotheses rising from the use of biotherapies will be discussed along with the uncertainties and unmet needs of this field.

Arachidonic Acid 15-Lipoxygenase: Effects of Its Expression, Metabolites, and Genetic and Epigenetic Variations on Airway Inflammation

Arachidonic acid 15-lipoxygenase (ALOX15) is an enzyme that can oxidize polyunsaturated fatty acids. ALOX15 is strongly expressed in airway epithelial cells, where it catalyzes the conversion of arachidonic acid to 15-hydroxyeicosatetraenoic acid (15-HETE) involved in various airway inflammatory diseases. Interleukin (IL)-4 and IL-13 induce ALOX15 expression by activating Jak2 and Tyk2 kinases as well as signal transducers and activators of transcription (STATs) 1/3/5/6. ALOX15 up-regulation and subsequent association with phosphatidylethanolamine-binding protein 1 (PEBP1) activate the mitogen-activated extracellular signal-regulated kinase (MEK)-extracellular signal-regulated kinase (ERK) pathway, thus inducing eosinophil-mediated airway inflammation. In addition, ALOX15 plays a significant role in promoting the migration of immune cells, such as immature dendritic cells, activated T cells, and mast cells, and airway remodeling, including goblet cell differentiation. Genome-wide association studies have revealed multiple ALOX15 variants and their significant correlation with the risk of developing airway diseases. The epigenetic modifications of the ALOX15 gene, such as DNA methylation and histone modifications, have been shown to closely relate with airway inflammation. This review summarizes the role of ALOX15 in different phenotypes of asthma, chronic obstructive pulmonary disease, chronic rhinosinusitis, aspirin-exacerbated respiratory disease, and nasal polyps, suggesting new treatment strategies for these airway inflammatory diseases with complex etiology and poor treatment response.

The enigmatic role of TIPE2 in asthma.

Unlike other members of the tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8/TIPE) family that play a carcinogenic role and regulate apoptosis, TNFAIP8-like 2 (TIPE2) can not only maintain immune homeostasis but also regulate inflammation. TIPE2 mainly restrains the activation of T cell receptor (TCR) and Toll-like receptors (TLR), regulating its downstream signaling pathways, thereby regulating inflammation. Interestingly, TIPE2 is abnormally expressed in many inflammatory diseases and may promote or inhibit inflammation in different diseases. This review summarizes the molecular target and cellular function of TIPE2 in immune cells and inflammatory diseases and the underlying mechanism by which TIPE2 regulates inflammation. The function and mechanism of TIPE2 in asthma is also explained in detail. TIPE2 is abnormally expressed in asthma and participates in the pathogenesis of different phenotypes of asthma through regulating multiple inflammatory cells' activity and function. Considering the indispensable role of TIPE2 in asthma, TIPE2 may be an effective therapeutic target in asthma. However, the available data are insufficient to provide a full understanding of the complex role of TIPE2 in human asthma. Further study is still necessary to explore the possible mechanism and functions of TIPE2 in different asthma phenotypes.

IL-17 regulates DC migration to the peribronchial LNs and allergen presentation in experimental allergic asthma.

IL-17 is associated with different phenotypes of asthma, however, it is not fully elucidated how it influences induction and maintenance of asthma and allergy. In order to determine the role of IL-17 in development of allergic asthma, we used IL-17A/F double KO (IL-17A/F KO) and WT mice with or without neutralization of IL-17 in an experimental allergic asthma model and analyzed airway hyperresponsiveness, lung inflammation, T helper cell polarization, and DCs influx and activation. We report that the absence of IL-17 reduced influx of DCs into lungs and lung draining LNs. Compared to WT mice, IL-17A/F KO mice or WT mice after neutralization of IL-17A showed reduced airway hyperresponsiveness, eosinophilia, mucus hypersecretion, and IgE levels. DCs from draining LNs of allergen-challenged IL-17A/F KO mice showed a reduction in expression of migratory and costimulatory molecules CCR7, CCR2, MHC-II, and CD40 compared to WT DCs. Moreover, in vivo stimulation of adoptively transferred antigen-specific cells was attenuated in lung-draining LNs in the absence of IL-17. Thus, we report that IL-17 enhances airway DC activation, migration, and function. Consequently, lack of IL-17 leads to reduced antigen-specific T cell priming and impaired development of experimental allergic asthma.

Asthma, asthma control and risk of ischemic stroke: The HUNT study

BackgroundAsthma, a chronic inflammatory airway disease, shares common pathophysiological mechanisms with ischemic stroke. The aim of the study is to assess the association between asthma, levels of asthma control and ischemic stroke risk in men and women and by smoking habits. MethodsThis prospective population-based cohort study utilized data on 58 712 adults from HUNT Study in Norway free from stroke. Self-reported asthma was categorized as ever asthma, non-active asthma and active asthma (i.e., being on asthma medication within 12 months of the baseline). Asthma control was defined according to the Global Initiative for Asthma questionnaire and was categorized into controlled and not controlled asthma. Stroke was ascertained by linking HUNT data with Nord-Trøndelag hospital records and the Norwegian Patient Registry. ResultsDuring a mean follow-up of 17.3 ± 5.3 years, 2619 participants (4.5%) had a first stroke. Not controlled asthma was associated with a modest increased risk of stroke (adjusted HR 1.34, 95%CI 1.03–1.73). Subgroup analyses revealed that the respective association was stronger among those with history of smoking (HR 1.48, 95%CI 1.10–2.00) and males (HR 1.55, 95%CI 1.12–2.16) while absent in non-smokers (HR 1.02, 95%CI 0.61–1.70) and females (HR 1.05, 95%CI 0.69–1.60). Likewise, active asthma was associated with similar increased stroke risk among smokers and males and absent in non-smokers and females. ConclusionsSymptomatic and active asthma was associated with a modest increased relative risk for ischemic stroke in smokers and males. Future studies should clarify the difference in risks and mechanisms between different phenotypes of asthma.

Analysis of lncRNA Expression in Patients With Eosinophilic and Neutrophilic Asthma Focusing on LNC_000127.

Long non-coding RNA (lncRNA) is important in many diseases. Some studies have shown that lncRNA affects the pathogenesis of systemic inflammation of asthma. lncRNA regulates gene transcription, protein expression, and epigenetic regulation. However, lncRNAs associated with different airway phenotypes, such as eosinophilic (Eos) and neutrophilic (Neu) asthma have not been identified. The goal of this study was to determine the differences in circulating lncRNA signatures in Eos and Neu samples. Using RNA-sequencing (RNA-seq), lncRNA expression was evaluated in peripheral whole blood samples among Eos patients, Neu patients, and healthy individuals (Control). Bioinformatic analysis was used to predict relevant biological pathways. Quantitative PCR (qPCR) was used to measure gene expression in whole blood samples, Jurkat cells, and human CD4+ T cells. Finally, a novel lncRNA, LNC_000127, was inhibited by transfection of Jurkat cells with a lentiviral vector, and the effect was examined by Human Asthma RT2 Profiler™ PCR Array and western blotting. Compared to control samples, Eos samples contained 190 unique lncRNAs and Neu samples had 166 unique lncRNAs (difference ≥2-fold). KEGG pathway annotation data and GO terms revealed that different lncRNAs are involved in different mechanisms. LNC_000127, was highly expressed in Eos samples before treatment; its expression was increased in Jurkat cells and human CD4+ T cells following stimulation with PMA/CD28. Subsequent analyses revealed that LNC_000127 functions in the Th2 inflammation pathway. The results suggest that lncRNAs are involved in different phenotypes of asthma. Whether the different phenotypes of asthma can be recognized based on these lncRNAs (as biomarkers) requires further analysis. Targeting LNC_000127 may be effective for reducing Th2 inflammation in Eos asthma.

Relation of systemic comorbidities in asthma with disease: control, severity and phenotype

Asthma is a heterogeneous and chronic inflamatory disease that can accompany many comorbidities during the course. It is thought that different comorbidities are seen in different phenotypes of asthma. Our aim is to establish the relationship between systemic comorbidities seen in asthmatic patients and asthma control, severity and phenotypes. Patients who were followed up with asthma diagnosis in Polyclinics of Ankara University Faculty of Medicine Department of Immunology and Allergy Diseases were questioned about demographic characteristics. Their control status and disease severity were determined. They were classified whether r atopic, eosinophilic or obese. Systemic comorbidities were questioned and Charlson comorbidity indices (CCI) were calculated. The difference between the groups in the terms of CCI was evaluated. Two hundred and twenty-nine patients (29E/200K, 12.7%/87.3%) with a mean age of 51.25 ± 12.02 were included in the study. CCI was significantly higher in patients without asthma control than in those with partial control and well control (CCI: 2.22, 1.69, 1.50, respectively) (p= 0.03). There was also a linear correlation between asthma severity and CCI (CC: 0.22, p= 0.001). Allergic comorbidities were more frequent in the eosinophilic phenotype (p= 0.01) (OR: 2.20, 95% CI: 1.2-3.8) but did not increase the likelihood of accompanying systemic comorbidity (OR: 1.05, 95% CI: 0.8-1.2) (p> 0.05). The likelihood of systemic comorbidity, especially HT, coroner artery diseases, depression, was higher in nonatopics than in atopic patients (OR: 2.039 95% CI: 1.04.11) (p= 0.03). Obesity was found to be a risk factor for systemic comorbidities (OR: 1.36 %95 C1: 1.09-1.84) (p= 0.04). Severe, uncontrolled, obese or nonatopic asthma patients should be examined for systemic comorbidities. There is a need for further study to assess the relationship between treatment of established comorbidities and asthma course.

Improving care for people with asthma: building capacity across a European network of primary care organisations – the IPCRG’s Teach the Teacher Programme

# Background The International Primary Care Respiratory Group (IPCRG) is a global network of organisations committed to improving assessment/treatment of chronic respiratory disease (CRD) in primary care. As a charity IPCRG supports improvements in health systems within member countries by disseminating research evidence and offering evidence-based resources, such as the U-BIOPRED (Unbiased BIOmarkers in PREDiction of respiratory disease outcomes) research into different phenotypes of asthma and IPCRGs desktop helper - which is short practical guidance distilled from the evidence on structured asthma review -- termed SIMPLES. # Methods We ran a pilot educational programme -- called Teach the Teacher: Difficult to Manage Asthma designed to build capacity for teaching knowledge and skills in asthma management to primary healthcare workers in eight member countries. We used a cascade approach, which allowed for adaptation to local contexts to address local challenges, overcome barriers and optimise facilitators within various political, financial and healthcare systems. We explored impact using an educational evaluation framework. # Results Seven in-country programmes were delivered within project timescales March - December 2015. An important feature of the programme level evaluation shows considerable variation in the design and focus of in-country events. Over 230 health professionals participated in these educational events in seven countries, including specialist nurses, physiotherapists, general practitioners (GP), early career GPs, and GPs with a special interest in respiratory disease. Findings from a survey of in-country leads showed the importance of local needs assessment to ensure it was responsive to local social and healthcare context and allowed local variation and needs to be highlighted. Needs assessment also engaged the potential audience and ensured their buy-in to the programme at an early stage. Evidence based resources were adapted to different contexts which allowed them to be integrated to the routine training of primary care clinicians thus ensuring sustainability. # Conclusions Variation in the design and focus of in-country events was crucial to local implementation. Teams encountered, and found local solutions for, challenges in assessing learning needs, setting up education programmes and in supporting clinical practice change. Project funding enabled national programmes, but sustainability will require additional resource and a longer-term strategy.

Does asthma affect school performance in adolescents? Results from the Swedish population-based birth cohort BAMSE.

Asthma is common among schoolchildren and may influence quality of life and school attendance. However, it is unclear if asthma affects school performance. The aim of this study was to examine whether different phenotypes of asthma affect school performance during adolescence. The study population consisted of 1715 adolescents from a population-based birth cohort, followed up to age 16 with questionnaires and clinical examinations. Asthma was defined as at least 4 wheeze episodes or at least 1 wheeze episode in combination with inhaled steroids in the last 12months. School grades were obtained from Statistics Sweden, and logistic regression analysis was performed to investigate the association between the final overall grade from secondary school and asthma phenotypes. Among the adolescents, 20.8% have had ever asthma; 24.2% early transient, 47.2% school-age onset, and 24.2% persistent asthma. At 16years, 7.8% had asthma; 71.7% multimorbidity and 73.9% allergic asthma. A statistically significant association for performing less well was seen for ever asthma (ORadj =1.43, 95% CI=1.09-1.88). In analyses of asthma onset, an association was seen for school-age onset (ORadj =1.49, CI=1.02-2.16) and a tendency for persistent asthma (ORadj =1.61, CI=0.98-2.66), although with overlapping confidence intervals. Further, adolescents with uncontrolled asthma tended to perform less well (ORadj =2.60, CI=0.87-7.80) compared to adolescents with partly controlled (ORadj =1.12, CI=0.68-1.83) and fully controlled (ORadj =1.29, CI=0.55-3.01) asthma. Our results indicate that asthma impairs school performance in adolescence. Moreover, some evidence suggests the adolescents with asthma during school age and with poorer asthma control to be more likely to perform less well.

Sensitization to dust mite defines different phenotypes of asthma: A multicenter study.

Indoor allergens are risk factors for asthma: Thus, the characterization of indoor air quality is important for studying environment-health relationships in children. In particular, Dermatophagoides pteronyssinus is the dominant allergen for asthma. We cross-sectionally investigated the relationships among respiratory symptoms and function, airway inflammation, allergen sensitization, and indoor allergen concentration. One hundred and thirty-two children aging 10-14years and living in a Southern Mediterranean area were evaluated by parental questionnaires. Spirometry, exhaled nitric oxide (FeNO), skin prick tests, total, and specific serum IgE analyses were performed along with the evaluation of home dust samples for the content in Der p 1 allergen. Three clusters were created on the basis of the presence/absence of wheeze in the last 12months (Wh12m) and Der p 1-specific IgE level. Cluster 1 (Wh12m+/high Der p 1 IgE) presented higher FeNO and poorer pulmonary function (lower FEV1 and FEF25%-75% ), while its symptom score was not different from Cluster 2 (Wh12m+/low Der p 1 IgE). Cluster 3 (Wh12m-/low IgE) showed the lowest FeNO values and pulmonary function similar to Cluster 2. Within Cluster 1, both Der p 1-specific IgE and FeNO were positively correlated with dust Der p 1. Similar asthma phenotypes may occur in children despite differences in their atopic state. In atopic children, sensitizing allergens in the indoor environment may increase airway inflammation worsening pulmonary function. Moreover, environmental exposures may contribute to the development of asthma-like symptoms also in the absence of atopic sensitization, thus contributing to asthma overdiagnosis.

Challenges and errors in the diagnosis and treatment of asthma in children

Bronchial asthma (BA) in children is a difficult diagnosis, and that is especially true for patients in the first six years of life. According to the GINA experts, among the reasons for difficult asthma diagnosis are high prevalence of wheezing, especially under the age of 3 years; limited availability or absence of pulmonary function tests, wherefore asthma diagnosis is based on complaints, medical history and examination, and often on a third-party impression; the existence of different phenotypes of asthma. Both the medical community and parents mistakenly believe that up to 6 years of age the diagnosis can not be established. As a result, for many years patients are followed-up with alternative diagnoses and do not receive the necessary treatment. That means poor control of the disease, repeated exacerbations and hospitalizations. The review presents findings which dispel the afore-mentioned medical myths about the predictors, diagnostic criteria of asthma in children, under-diagnosis, treatment difficulties and errors.

The Asthma&amp;ndash;Obesity Epidemic

Obesity is a risk factor for the development of asthma. Understanding this link between obesity and asthma has major public health implications for developing strategies to prevent the development of asthma and to guide the management of such patients. Obese patients with asthma experience poor asthma control, worse asthma-specific quality of life, and limited response to corticosteroids. This review provides a succinct summary of the current body of literature on the epidemiological relationship between asthma and obesity, the different phenotypes of asthma in obesity, and data on the efficacy of weight loss and discusses the potential role of primary prevention efforts for the current asthma epidemic.