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目的 探讨毛细支气管炎 (以下简称毛支 )与儿童哮喘的相关性 ,为对毛支患儿行早期干预 ,提供实验室依据。方法 应用瑞典法玛西亚公司的UniCAP10 0全自动变应原体外检测系统检测 32例毛支患儿急性期及缓解期血清嗜酸性粒细胞阳离子蛋白 (ECP)、总IgE的含量 ,并追踪半年观察喘息的再发情况。结果 (1)毛支患儿急性期血清ECP、总IgE浓度明显高于一般肺炎组 (P <0 .0 1)。 (2 )毛支患儿急性期ECP浓度明显高于缓解期 (P <0 .0 1)。而总IgE的变化无意义 (P >0 .0 5 )。 (3)毛支组中合胞病毒感染与非合胞病毒感染比较ECP、总IgE的变化有显著意义 (P <0 .0 5 )。 (4)追踪半年 ,毛支组再发喘息者明显高于一般肺炎组。结论 毛支与哮喘存在部分相同的发病机理。ECP检查可作为毛支患儿过敏性炎症消长的指标 ,总IgE水平可作为毛支患儿过敏素质的预测指标。随访并监测血清ECP、总IgE浓度 ,可作为对毛支患儿施行早期干预的实验室依据。以免其发展为哮喘 ,造成气道的慢性损害。
Objective To investigate the correlation between bronchiolitis (hereinafter referred to as the branch of hair) and childhood asthma, and provide a laboratory basis for early intervention in children with branch of branch of hair. Methods UniCAP10 0 automated in vitro detection system was used to detect serum eosinophil cationic protein (ECP) and total IgE levels in 32 cases of children with bronchiectasis during the acute and remission stages, and to follow up for 6 months Breathing recurrence. Results (1) Serum ECP and total IgE concentrations were significantly higher in children with bronchiolitis than those in normal pneumonia group (P <0.01). (2) The ECP concentration in children with bronchiolitis was significantly higher than that in remission (P <0.01). Changes in total IgE were insignificant (P> 0.05). (3) Compared with non-syncytial virus infection in syncytial virus group, the changes of ECP and total IgE in the branch of hair were significant (P <0.05). (4) After six months of follow-up, the patients in hair branch group recurred more evidently than the general pneumonia group. Conclusion The branch of hair and asthma exist some of the same pathogenesis. ECP examination can be used as indicators of the rise and fall of allergic inflammation in children with bronchiolitis, total IgE levels can be used as predictors of allergic quality in children with bronchiectasis. Follow-up and monitoring of serum ECP and total IgE concentrations may be used as a laboratory basis for early intervention in children with bronchiectasis. Lest its development of asthma, causing chronic airway damage.