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Associations between obesity and asthma in a low-income, urban, minority population

机译:肥胖与哮喘在低收入,城市少数群体中的关联

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Background: Community-based studies of obesity, asthma, biomarkers of oxidative stress, and adipokines among low-income, urban, minority populations are lacking. Oxidative stress, perhaps modulated by adipokines, may increase airway inflammation in obese individuals. Objectives: To characterize associations between obesity and asthma in a low-income, urban, minority community and evaluate adipokines, biomarkers of inflammation, and oxidant-antioxidant balance in association with asthma and obesity. Methods: A door-to-door evaluation of asthma and obesity prevalence was performed in a low-income housing development. Nonsmoking adults and children underwent additional evaluation, including allergy skin testing, and measures of serum adipokines, and indicators of oxidative stress in blood and exhaled breath. Results: The prevalences of current asthma and a body mass index in the 85th percentile or higher were 15.8% and 35.3%, respectively, among 350 nonsmokers older than 4 years. Asthma and obesity were not associated with one another (odds ratio, 1.0; 95% confidence interval, 0.55-1.84). Among 116 nonsmoking participants who underwent biomarker evaluation, obesity was not associated with exhaled nitric oxide. In multivariate logistic models that adjusted for age category, sex, and a body mass index in 85th percentile or higher, leptin concentrations in the highest quartile were associated with asthma (odds ratio, 8.34; 95% confidence interval, 1.29-50.2) but not with atopy. Adiponectin was associated with total antioxidant capacity in exhaled breath. Conclusion: Asthma and obesity, although both common in a low-income, minority community, were not associated with one another. Nevertheless, adipokines were associated with asthma status and with markers of oxidative stress in the lungs, providing some support for an adipokine-inflammatory mechanistic link between the two conditions.
机译:背景:缺乏针对肥胖,哮喘,氧化应激的生物标志物和低收入,城市,少数民族人群的脂肪因子的社区研究。可能由脂肪因子调节的氧化应激可能增加肥胖个体的气道炎症。目的:鉴定低收入,城市,少数民族社区中肥胖与哮喘之间的关联,并评估与哮喘和肥胖相关的脂肪因子,炎症生物标志物和氧化剂-抗氧化剂平衡。方法:在低收入房屋开发中进行了门到门的哮喘和肥胖患病率评估。不吸烟的成年人和儿童进行了其他评估,包括过敏性皮肤测试,血清脂肪因子的测定以及血液和呼出气中氧化应激指标。结果:在350名4岁以上的非吸烟者中,当前哮喘的患病率和体重指数在85%或更高的百分率分别为15.8%和35.3%。哮喘和肥胖没有相互关联(优势比为1.0; 95%置信区间为0.55-1.84)。在接受生物标志物评估的116位非吸烟参与者中,肥胖与呼出气一氧化氮无关。在针对年龄,性别和体重指数在85%或更高的人群进行调整的多变量Logistic模型中,最高四分位数的瘦素浓度与哮喘相关(优势比为8.34; 95%置信区间为1.29-50.2),但无相关性与特应性。脂联素与呼气中的总抗氧化能力有关。结论:哮喘和肥胖症虽然在低收入的少数族裔社区中很常见,但是却没有相互联系。然而,脂肪因子与哮喘状态和肺中氧化应激的标志物相关,这为这两种情况之间的脂肪因子-炎症机制联系提供了支持。

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