Rationale The respiratory outcomes for adult survivors of preterm birth in the postsurfactant era are wide-ranging with prognostic factors, especially those encountered after the neonatal period, poorly understood. Objectives To obtain comprehensive ‘peak’ lung health data from survivors of very preterm birth and identify neonatal and life-course risk factors for poorer respiratory outcomes in adulthood. Methods 127 participants born ≤32 weeks gestation (64%, n=81 with bronchopulmonary dysplasia (BPD), initially recruited according to a 2 with-BPD:1 without-BPD strategy), and 41 term-born controls completed a lung health assessment at 16–23 years, including lung function, imaging and symptom review. Risk factors assessed against poor lung health included neonatal treatments, respiratory hospitalisation in childhood, atopy and tobacco smoke exposure. Measurements and main results Young adults born prematurely had greater airflow obstruction, gas trapping and ventilation inhomogeneity, in addition to abnormalities in gas transfer and respiratory mechanics, compared with term. Beyond lung function, we observed greater structural abnormalities, respiratory symptoms and inhaled medication use. A previous respiratory admission was associated with airway obstruction; mean forced expiratory volume in 1 s/forced vital capacity z-score was −0.561 lower after neonatal confounders were accounted for (95% CI −0.998 to –0.125; p=0.012). Similarly, respiratory symptom burden was increased in the preterm group with a respiratory admission, as was peribronchial thickening (6% vs 23%, p=0.010) and bronchodilator responsiveness (17% vs 35%, p=0.025). Atopy, maternal asthma and tobacco smoke exposure did not influence lung function or structure at 16–23 years in our preterm cohort. Conclusions Even after accounting for the neonatal course, a respiratory admission during childhood remained significantly associated with reduced peak lung function in the preterm-born cohort, with the largest difference seen in those with BPD. A respiratory admission during childhood should, therefore, be considered a risk factor for long-term respiratory morbidity in those born preterm, especially for individuals with BPD. Data are available on reasonable request. Individual participant data that underlie the results reported in this article would be available after de-identification, assuming participant consent was given, along with the study protocol and analytic code, beginning 3 months after publication. Data would be made available to investigators providing a sound proposal that has been approved by an independent review committee to achieve the aims of the proposal. Proposals should be directed to shannon.simpson{at}telethonkids.org.au; to gain access, data requestors will need to sign a data access agreement.

中文翻译：

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青少年和早产年轻人呼吸系统不良的危险因素


基本原理 后表面活性剂时代早产成年幸存者的呼吸结局多种多样，其预后因素，尤其是新生儿期后遇到的因素，人们知之甚少。目标 获得极早产幸存者的全面“峰值”肺部健康数据，并确定导致成年期呼吸结果较差的新生儿和生命全程危险因素。方法 127 名妊娠 ≤ 32 周出生的参与者（64%，n = 81 患有支气管肺发育不良 (BPD)，最初根据 2 名有 BPD：1 名无 BPD 策略招募）和 41 名足月出生的对照者完成了肺部健康评估16-23 岁，包括肺功能、影像学和症状检查。评估肺部健康状况不佳的危险因素包括新生儿治疗、儿童时期呼吸系统住院、特应性和烟草烟雾暴露。测量和主要结果 与足月相比，早产的年轻人除了气体传输和呼吸力学异常外，还存在更大的气流阻塞、气体滞留和通气不均匀性。除了肺功能之外，我们还观察到更严重的结构异常、呼吸道症状和吸入药物的使用。之前的呼吸道入院史与气道阻塞有关；考虑到新生儿混杂因素后，1 秒用力呼气量/用力肺活量 z 评分的平均用力呼气量降低了 -0.561（95% CI -0.998 至 –0.125；p=0.012）。同样，早产儿入院时的呼吸系统症状负担增加，支气管周围增厚（6% vs 23%，p=0.010）和支气管扩张剂反应性（17% vs 35%，p=0.025）也增加。在我们的早产儿队列中，特应性、孕产妇哮喘和烟草烟雾暴露不会影响 16-23 岁的肺功能或结构。 结论 即使考虑了新生儿病程，儿童时期的呼吸入院仍与早产儿群体中肺功能峰值下降显着相关，其中 BPD 患者的差异最大。因此，儿童时期的呼吸道入院应被视为早产儿长期呼吸道疾病的危险因素，特别是对于 BPD 患者。可根据合理要求提供数据。假设在发表后 3 个月开始获得参与者同意，构成本文报告结果的个体参与者数据以及研究方案和分析代码将在去识别化后可用。数据将提供给研究人员，提供经过独立审查委员会批准的合理提案，以实现提案的目标。提案应发送至 shannon.simpson{at}telethonkids.org.au；要获得访问权限，数据请求者需要签署数据访问协议。