AIRWAY OBSTRUCTION IN CHILDREN.
Ontology highlight
ABSTRACT:
SUBMITTER: Raman TR
PROVIDER: S-EPMC5529917 | biostudies-other | 1995 Apr
REPOSITORIES: biostudies-other
Similar Datasets
Project description:In the first decade of life, high-asthma risk urban children develop stable phenotypes of respiratory health versus disease that link early life environmental exposures to childhood allergic sensitization and asthma. Moreover, unique patterns of nasal gene expression demonstrate how specific molecular pathways underlie distinct respiratory phenotypes, including allergic and non-allergic asthma.
2021-04-01 | GSE145505 | GEO
Project description:BackgroundBlack and Hispanic children growing up in disadvantaged urban neighborhoods have the highest rates of asthma and related morbidity in the United States.ObjectivesThis study sought to identify specific respiratory phenotypes of health and disease in this population, associations with early life exposures, and molecular patterns of gene expression in nasal epithelial cells that underlie clinical disease.MethodsThe study population consisted of 442 high-risk urban children who had repeated assessments of wheezing, allergen-specific IgE, and lung function through 10 years of age. Phenotypes were identified by developing temporal trajectories for these data, and then compared to early life exposures and patterns of nasal epithelial gene expression at 11 years of age.ResultsOf the 6 identified respiratory phenotypes, a high wheeze, high atopy, low lung function group had the greatest respiratory morbidity. In early life, this group had low exposure to common allergens and high exposure to ergosterol in house dust. While all high-atopy groups were associated with increased expression of a type-2 inflammation gene module in nasal epithelial samples, an epithelium IL-13 response module tracked closely with impaired lung function, and a MUC5AC hypersecretion module was uniquely upregulated in the high wheeze, high atopy, low lung function group. In contrast, a medium wheeze, low atopy group showed altered expression of modules of epithelial integrity, epithelial injury, and antioxidant pathways.ConclusionsIn the first decade of life, high-risk urban children develop distinct phenotypes of respiratory health versus disease that link early life environmental exposures to childhood allergic sensitization and asthma. Moreover, unique patterns of airway gene expression demonstrate how specific molecular pathways underlie distinct respiratory phenotypes, including allergic and nonallergic asthma.
| S-EPMC8429519 | biostudies-literature
Project description:BackgroundThe contribution of environmental tobacco smoke (ETS) exposure to pulmonary morbidity in children with sickle cell anemia (SCA) is poorly understood. We tested the hypothesis that children with SCA and ETS exposure would have an increased prevalence of obstructive lung disease and respiratory symptoms compared with children with SCA and no ETS exposure.MethodsParent reports of ETS and respiratory symptom frequency were obtained for 245 children with SCA as part of a multicenter prospective cohort study. One hundred ninety-six children completed pulmonary function testing. Multivariable regression models were used to evaluate the associations between ETS exposure at different time points (prenatal, infant [birth to 2 years], preschool [2 years to first grade], and current) and lung function and respiratory symptoms.ResultsAmong the 245 participants, a high prevalence of prior (44%) and current (29%) ETS exposure was reported. Of the 196 children who completed pulmonary function testing, those with parent-reported infant and current ETS exposure were more likely to have airway obstruction (defined as an FEV1/FVC ratio below the lower limit normal) compared with unexposed children (22.0% vs 3.1%, P < .001). Those with ETS exposure also had a lower forced expiratory flow, midexpiratory phase/FVC ratio (0.82 vs 0.97, P = .001) and were more likely to have evidence of bronchodilator responsiveness (23% vs 11%, P = .03). Current and prior ETS exposure and in utero smoke exposure were associated with increased frequency of respiratory symptoms.ConclusionsETS exposure is associated with evidence of lower airway obstruction and increased respiratory symptoms in SCA.
| S-EPMC3787918 | biostudies-literature
Project description: Not available
| S-EPMC7808036 | biostudies-literature
Project description:Endotype of Allergic Asthma with Airway Obstruction in Urban Children
| PRJNA607333 | ENA
Project description:Malignant central airway obstruction (MCAO) impacts many patients with advanced primary lung cancers and metastatic disease to the thorax and may cause substantial symptoms and functional limitations in those affected. Making the diagnosis may be challenging as symptoms are often non-specific but identification is improved with a heightened level of suspicion and newer thoracic imaging modalities. Bronchoscopy plays a crucial role in the diagnosis and management of MCAO and therapeutic interventions may be lifesaving and result in palliation of symptoms. This may ultimately improve a patient's candidacy to receive additional systemic or local cancer therapies or potential tumor resection. After initial stabilization, it is important that patients with MCAO undergo prompt evaluation and treatment. Multiple bronchoscopic instruments are available for management depending on tumor characteristics, location of the obstruction, and viability of distal airways, and may be utilized in combination during therapeutic procedures. These modalities include dilation, endobronchial stent placement, thermal and non-thermal ablation, mechanical debulking, and novel endobronchial therapies. While these procedures are not without risk, there is ample evidence showing improvements in patient symptoms, quality of life, and survival following therapeutic bronchoscopy. This review article provides a general overview of the diagnosis and management of MCAO with a focus on bronchoscopic interventions.
| S-EPMC10713238 | biostudies-literature
Project description:BACKGROUND:Differences in asthma severity may be related to inflammation in the airways. The lower airway microbiota has been associated with clinical features such as airway obstruction, symptom control, and response to corticosteroids. OBJECTIVE:To assess the relationship between local airway inflammation, severity of disease, and the lower airway microbiota in atopic asthmatics. METHODS:A cohort of young adult, atopic asthmatics with intermittent or mild/moderate persistent symptoms (n = 13) were assessed via bronchoscopy, lavage, and spirometry. These individuals were compared to age matched non-asthmatic controls (n = 6) and to themselves after six weeks of treatment with fluticasone propionate (FP). Inflammation of the airways was assessed via a cytokine and chemokine panel. Lower airway microbiota composition was determined by metagenomic shotgun sequencing. RESULTS:Unsupervised clustering of cytokines and chemokines prior to treatment with FP identified two asthmatic phenotypes (AP), termed AP1 and AP2, with distinct bronchoalveolar lavage inflammatory profiles. AP2 was associated with more obstruction, compared to AP1. After treatment with FP reduced MIP-1? and TNF-? and increased IL-2 was observed. A module of highly correlated cytokines that include MIP-1? and TNF-? was identified that negatively correlated with pulmonary function. Independently, IL-2 was positively correlated with pulmonary function. The airway microbiome composition correlated with asthmatic phenotypes. AP2, prior to FP treatment, was enriched with Streptococcus pneumoniae. Unique associations between IL-2 or the cytokine module and the microbiota composition of the airways were observed in asthmatics subjects prior to treatment but not after or in controls. CONCLUSION:The underlying inflammation in atopic asthma is related to the composition of microbiota and is associated with severity of airway obstruction. Treatment with inhaled corticosteroids was associated with changes in the airway inflammatory response to microbiota.
| S-EPMC5650135 | biostudies-literature
Project description:There are multiple causes of dyspnea upon exertion in young, healthy patients to primarily include asthma and exercise-induced bronchospasm. Excessive dynamic airway collapse (EDAC) describes focal collapse of the trachea or main bronchi with maintained structural integrity of the cartilaginous rings. It is commonly associated with pulmonary disorders like bronchiectasis, chronic obstructive pulmonary disease and asthma. It is believed to result secondary to airway obstruction in these conditions. While uncommon in young, healthy adults, it has recently been found as a cause of dyspnea in this population. Inducible laryngeal obstruction (ILO) is an umbrella term that describes an induced, intermittent upper airway impediment. While ILO is found in 10% of young patients with exertional dyspnea, it is primarily inspiratory in nature due to paradoxical closure of the glottis or supraglottis. This report highlights the presentation of a United States Army soldier who after a deployment was given a diagnosis of asthma, later found to have ILO and was subsequently diagnosed with concurrent EDAC. We follow up with a literature review and discussion of symptomatology, diagnosis, exercise bronchoscopy, and treatment modalities for both EDAC and ILO.
| S-EPMC6446124 | biostudies-literature
Project description:Congenital high airway obstruction (CHAOS) is a rare lethal fetal malformation characterised by obstruction to the fetal upper airway, which can be partial or complete. Antenatal diagnosis of CHAOS is important due to recent management options. Diagnosis is made with secondary changes such as hyperechoic enlarged lungs resulting in mediastinal compression, ascites, hydrops, flattened or everted diaphragms and dilated distal airways. We reported a case of CHAOS, antenatally on ultrasonography (USG) at 20 weeks of gestation.
| S-EPMC5535577 | biostudies-other
Project description:BACKGROUND: Endothelin-1 (EDN1) has been involved in the development of airway obstruction and inflammation in asthma. Several polymorphisms have been identified among the genes encoding for preproET1, an inactive precursor of ET-1, and for ETA (EDNRA) and ETB (EDNRB), the two receptors for EDN1. In the present work, we hypothesised that molecular variation in these genes could be a major determinant of the degree of bronchial obstruction. The purpose of this study was to investigate whether the genetic polymorphisms of preproET-1, EDNRA and EDNRB genes were associated with the degree of airway obstruction, assessed by FEV1. METHODS: Polymorphisms of preproET-1, EDNRA and EDNRB were first studied in a population of adult asthmatic patients. Results were confirmed in a large population of adults from the general population from the ECRHS II study. RESULTS: In our population of adult asthmatic patients, the EDNRB-30G>A (Leu277Leu) polymorphism (GG genotype) is strongly associated with a low FEV1 and with a higher percentage of patients with FEV1 < 80% of predicted value. No relationship was found between pulmonary function and EDNRA-1363C>T (His323His) or preproET-1-595G>T (Lys198Asp) polymorphism. In the adult population from the ECRHS II, we found a similar association between GG genotype and a low FEV1 or a higher percentage of subjects with FEV1 < 80% predicted, especially in the subgroups of asthmatics subjects (OR = 4.31 (95%CI 1.03 - 18.04)) and smokers (OR = 7.42 (95%CI 1.69 - 32.6)). CONCLUSION: the EDNRB-30G>A polymorphism could be a determinant of airway obstruction in humans with predisposing factors such as tobacco smoke exposure or asthma.
| S-EPMC1871605 | biostudies-literature