背景:在囊性纤维化(pwCF)患者中,除过敏性支气管肺曲霉病(ABPA)外,没有关于曲霉感染对肺功能影响的确切数据。这里,我们旨在确定由曲霉属引起的临床表型。使用实验室和免疫学参数,并前瞻性比较肺功能测试(PFT)方面的曲霉表型。
方法:包括去年从呼吸道培养物中分离曲霉的23例pwCF(病例组)和痰中不分离曲霉的20例pwCF(对照组)。曲霉IgG,曲霉IgE,曲霉菌PCR,半乳甘露聚糖,血液样本中的总IgE,以及来自痰液的曲霉PCR和半乳甘露聚糖,和皮肤点刺试验对曲霉抗原的反应性用于区分不同的曲霉表型。在一年的随访中评估了肺功能和肺加重的频率。
结果:在23个pwCF中,11人(47.8%)有曲霉定植,9人(39.1%)患有曲霉菌支气管炎,3人(13%)患有ABPA。曲霉菌感染与第1秒用力呼气量(FEV1)的z评分较差无关(p=0.612),强迫肺活量(FVC)(p=0.939),和中位数FEV1%下降(0.0%/年对-4.7%/年,p=0.626)。曲霉感染和未感染组的肺部恶化频率相似。
结论:虽然曲霉属。pwCF中的隔离与肺功能下降无关,ABPA亚组进一步下降,以及在一年的随访期间频繁的肺加重。本文受版权保护。保留所有权利。
There are no precise data about the effect of Aspergillus infection on lung function other than allergic bronchopulmonary aspergillosis (ABPA) in patients with cystic fibrosis (pwCF). Here, we aimed to determine clinical phenotypes caused by Aspergillus spp. using laboratory and immunologic parameters and to compare Aspergillus phenotypes in terms of pulmonary function tests (PFT) prospectively.
Twenty-three pwCF who had Aspergillus isolation from respiratory cultures in the last year (
case group) and 20 pwCF without Aspergillus isolation in sputum (control group) were included. Aspergillus immunoglobulin (Ig)-G, Aspergillus IgE, Aspergillus polymerase chain reaction (PCR), galactomannan, total IgE from blood samples, and Aspergillus PCR and galactomannan from sputum, and skin prick test reactivity to Aspergillus antigen were used to distinguish different Aspergillus phenotypes. Pulmonary functions and frequency of pulmonary exacerbations were evaluated during a 1-year follow-up.
Of 23 pwCF, 11 (47.8%) had Aspergillus colonization, nine (39.1%) had Aspergillus bronchitis, and three (13%) had ABPA. Aspergillus infection was not associated with worse z-scores of forced expiratory volume in the first second (FEV1) (p = 0.612), forced vital capacity (p = 0.939), and the median FEV 1% decline (0.0%/year vs. -4.7%/year, p = 0.626). The frequency of pulmonary exacerbations in the Aspergillus infected and noninfected groups was similar.
Although Aspergillus spp. Isolation in pwCF was not associated with decreased lung function, a further decline was seen in the ABPA subgroup, and frequent pulmonary exacerbations during the 1-year follow-up.