论文部分内容阅读
目的:探讨肥胖与非肥胖哮喘患儿的临床疗效对比研究。方法:将佛山市南海区第五人民医院2013年1月至2015年8月收治的60例肥胖哮喘患儿,设为肥胖哮喘组,同期将本院收治的60例非肥胖(正常体质量)哮喘患儿设为非肥胖哮喘组。两组患儿均给予西医常规抗哮喘治疗,比较两组患儿临床疗效、肺功能及免疫球蛋白E(Ig E)、干扰素(IFN-γ)、白介素(IL-4)的差异。结果:非肥胖哮喘组患儿临床总有效率为95.0%显著高于肥胖哮喘组81.7%,组间比较,差异具有统计学意义(P<0.05);治疗后3 d、治疗后7 d非肥胖哮喘组患儿FEV1、PEF显著升高,同时其也显著高于同期肥胖哮喘组比较,差异具有统计学意义(P<0.05);治疗后3 d、治疗后7 d非肥胖哮喘组患儿Ig E、IL-4水平显著下降,其也显著低于同期肥胖哮喘组,治疗后3 d、治疗后7 d非肥胖哮喘组IFN-r水平显著升高,其也显著高于同期肥胖哮喘组,差异具有统计学意义(P<0.05);结论:肥胖可降低哮喘患儿治疗反应性,为临床治疗和预防哮喘提供依据,也从分子水平初步阐释肥胖与哮喘患儿的相互作用机制。
Objective: To investigate the clinical efficacy of obese and nonobese children with asthma. Methods: Sixty obese children with asthma who were admitted to the Fifth People’s Hospital of Nanhai District of Foshan City from January 2013 to August 2015 were enrolled as obese asthma group. In the same period, 60 non-obese (normal body weight) Children with asthma were set as non-obese asthma group. The two groups of children were given western medicine conventional anti-asthma treatment, the clinical efficacy, lung function and immunoglobulin E (Ig E), interferon (IFN-γ), interleukin (IL-4) differences between the two groups were compared. Results: The total clinical effective rate in non-obese asthma group was 95.0%, which was significantly higher than that in obese asthma group (81.7%). There was significant difference between the two groups (P <0.05); after 3 days of treatment, FEV1 and PEF in asthmatic children were significantly higher than those in obese asthmatic children at the same time (P <0.05), and the difference was statistically significant (P <0.05). After 3 days of treatment, the IgM of non-obese asthmatic children E and IL-4 levels in asthma group were significantly lower than those in obese asthmatic group. After 3 days of treatment, the level of IFN-γ in non-obese asthmatic group at 7 days after treatment was significantly higher than that in obese asthmatic group, (P0.05) .Conclusion: Obese can reduce the therapeutic response of children with asthma, provide a basis for clinical treatment and prevention of asthma, and also initially explain the interaction mechanism between obesity and asthma children at the molecular level.