肥胖与哮喘的关系是全身炎症与气道炎症的相互作用吗？
2008/09/28
动物研究提示，肥胖可以增强抗原激发后的气道高反应性，但人体中肥胖与哮喘相互作用的确切证据仍缺乏。
新西兰学者对79名女性进行了观察研究（包括肥胖哮喘患者、正常体重哮喘患者、肥胖非哮喘者及正常体重非哮喘者），比较激素撤退后肺功能、肺容积、呼出气NO、诱导痰细胞计数、痰上清及血液中炎症标记物的组间差别并探讨他们的相互关系。结果发现，肥胖人群全身炎症的标记物水平升高，哮喘患者Th2细胞因子水平提高，两者无显著相互作用；肥胖通过功能残气量和残气量的增加影响肺功能。
结论：肥胖对哮喘的影响可能不是通过全身炎症增强气道炎症这一经典方式实现的，与自然免疫相关的可能机制也许可以解释肥胖与哮喘间的关系。
（农英 卫生部中日友好医院呼吸内科 100029 摘译）
（Am J Respir Crit Care Med. 2008 ;178(5):469-475.）
The association between obesity and asthma: interactions between systemic and airway inflammation.
Sutherland TJ, Cowan JO, Young S, Goulding A, Grant AM, Williamson A, Brassett K, Herbison GP, Taylor DR.
Respiratory Research Unit, Department of Medical and Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
RATIONALE: Both obesity and asthma are common conditions, and both are characterized by the presence of inflammation. Animal studies suggest that the development of airway hyperresponsiveness with antigen challenge is exaggerated with obesity. However, clear evidence for either an additive or a synergistic pathologic interaction between obesity and asthma is lacking in humans.
OBJECTIVES: To identify whether an interaction between systemic and local inflammation occurs in obese subjects with asthma in a controlled observational study.
METHODS: We studied 79 women: obese patients with asthma (n = 20), normal-weight patients with asthma (n = 19), obese patients without asthma (n = 20), and normal-weight patients without asthma (n = 20). After corticosteroid withdrawal, between-group differences in spirometric values, lung volumes, exhaled nitric oxide, induced sputum cell counts, and biomarkers of inflammation in sputum supernatant and blood were measured, and interactions explored.
MEASUREMENTS AND MAIN RESULTS: Markers of systemic inflammation were increased with obesity, and Th2 cytokines were increased with asthma, but no important interactions were identified. Obesity adversely affected lung function with increases in functional residual capacity and residual volume in obese but not normal-weight patients with asthma, with a significant obesity by asthma interaction.
CONCLUSIONS: The link between obesity and asthma is unlikely to be explained by enhancement of the "classical" forms of airway inflammation resulting from the systemic inflammatory effects of obesity itself. Other mechanisms, possibly related to innate immunity, may explain the relationship between obesity and asthma.
OBJECTIVES: To identify whether an interaction between systemic and local inflammation occurs in obese subjects with asthma in a controlled observational study.
METHODS: We studied 79 women: obese patients with asthma (n = 20), normal-weight patients with asthma (n = 19), obese patients without asthma (n = 20), and normal-weight patients without asthma (n = 20). After corticosteroid withdrawal, between-group differences in spirometric values, lung volumes, exhaled nitric oxide, induced sputum cell counts, and biomarkers of inflammation in sputum supernatant and blood were measured, and interactions explored.
MEASUREMENTS AND MAIN RESULTS: Markers of systemic inflammation were increased with obesity, and Th2 cytokines were increased with asthma, but no important interactions were identified. Obesity adversely affected lung function with increases in functional residual capacity and residual volume in obese but not normal-weight patients with asthma, with a significant obesity by asthma interaction.
CONCLUSIONS: The link between obesity and asthma is unlikely to be explained by enhancement of the "classical" forms of airway inflammation resulting from the systemic inflammatory effects of obesity itself. Other mechanisms, possibly related to innate immunity, may explain the relationship between obesity and asthma.
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哮喘孕妇的峰流速值监测
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难治性哮喘患者的呼出一氧化氮水平提示肺功能下降程度
