RT杂志文章SR Electronic T1呼出一氧化氮:慢性肺移植物功能障碍的生物标志物?《欧洲呼吸学会学报》(JF European Respiratory Journal) 2016。188bet官网地址PA4639 VO 48增刊60 A1格里尔,马克A1 Fuehner,托马斯•A1 Welte Tobias A1 Gottlieb, Jens年2016 UL //www.qdcxjkg.com/content/48/suppl_60/PA4639.abstract AB简介:呼出一氧化氮(eNO)被认为是一个标记辅助细胞类型2介导气道炎症,尤其是哮喘。关于肺移植后慢性肺异体移植物功能障碍(CLAD)存在矛盾的数据1,2。这项前瞻性研究比较了eNO与CLAD表型和结果。方法:回顾2009年7月1日至2016年1月31日期间所有门诊患者的eNO测量结果。≥3个测量值(包括基线测量值≤6 mts)，行双侧肺/心肺移植并发生包衣的患者纳入研究。单个基线值作为控制。纵向比较采用Wilcoxon秩次检验C，组间分析采用Mann-Whitney U检验或Kruskal-Wallis H检验。结果:CLAD发展80pts，每个6 [IQR 5-9] eNO测量。62名患者(78%)出现闭塞性毛细支气管炎综合征(BOS)， 18名患者(22%)出现限制性同种异体移植综合征(RAS)。 Treatment refractory CLAD developed in 32pts (40%). Significant increases in eNO were evident at CLAD onset, but did not persist. This was independent of CLAD phenotype or treatment response NeNO baseline vs CLAD onseteNO baseline vs. established CLADBOS62p=0.001p=0.575RAS18p=0.031p=0.586CLAD progress32p=0.003p=0.881CLAD stable32p=0.079p=0.822CLAD improved16p=0.044p=0.532Change in eNO at CLAD-onset and subsequent control.TABLE 1 Conclusions: Individual variation in baseline eNO is considerable. Significant, albeit transient rises nevertheless occurred in 71% of patients at CLAD onset. Similar courses were evident in both phenotypes, arguing against mutually exclusive pathophysiology. eNO does not appear to predict treatment response.