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咳嗽变异性哮喘患者诱导痰P物质与气道反应性的关系研究 被引量:26

Relationship between the level of SP in the induced sputum and airway reactivity in patients with cough variant asthma
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摘要 目的:研究咳嗽变异性哮喘(CVA)患者诱导痰P物质(SP)和气道反应性的关系,探讨SP在CVA发病机制中的作用。方法:选择CVA组35例,正常对照组35例,计数两组诱导痰嗜酸性粒细胞(EOS)百分比,ELISA法检测两组诱导痰SP水平;测定两组FEV1,FEF50,比较治疗前后CVA组PD20FEV1。结果:CVA组诱导痰EOS百分比和SP水平显著高于对照组(P<0.05),两者在CVA组治疗后较治疗前显著下降(P<0.05);SP水平与EOS百分比呈正相关(r=0.490,P<0.05)。治疗后CVA组FEF50%和PD20FEV1显著高于治疗前(P<0.05);SP水平与PD20FEV1呈负相关(r=-0.508,P<0.05)。结论:SP的升高可能参与CVA的发病过程,其与气道高反应性密切相关,糖皮质激素联合长效β2受体激动剂吸入能显著降低诱导痰SP水平和气道高反应性。 Objective To examine the relationship between the level of SP in the induced sputum and airway reactivity in patients with cough variant asthma (CVA), and to investigate the role of SP in the pathogenesis of CVA. Methods 35 patients with CVA and 35 healthy controls were enrolled in the study. After the induced sputum was obtained, the percentage of eosinophil (EOS) was detected and the level of SP were determined by ELISA ; FEVI and FEF50 had been obtained by pulmonary function machine, and Histamine brochoprovocational test was done in CVA group, the change of PD20FEVI before and after treatment was compared. Results The percentage of EOS and the level of SP in the induced sputum in CVA group were significantly higher than those in control group (P 〈 0.05), and were significantly reduced after treatment (P 〈 0.05 ). The level of SP was positively correlated with the percentage of EOS (r = 0.490, P 〈 0.05 ). FEF50% and PD20FEVI in CVA group were significantly increased after treatment (P 〈 0.05); and the level of SP was negatively correlated with PD20FEV1 (r = -0.508,P 〈 0.05). Conclusions The increased expression of SP may probably participate in the pathogenesis of CVA, and was closely correlated with airway hyperreactivity, the joint inhaled long-acting beta agonist and glucocorticoids can significantly decrease the level of SP in the induced sputum and airway hyperreactivity.
出处 《实用医学杂志》 CAS 北大核心 2013年第16期2605-2607,共3页 The Journal of Practical Medicine
基金 浙江省卫生厅医药卫生科学研究基金资助课题(编号:2012KYA011)
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