Impact of gestational age on risk of cerebral palsy: unravelling the role of neonatal morbidity.
Impact of gestational age on risk of cerebral palsy: unravelling the role of neonatal morbidity.
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DOI：
10.1093/ije/dyab131
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发表时间：
2022-01-06
影响因子：
7.7
通讯作者：
Cnattingius S
中科院分区：
文献类型：
--
作者：
Chen R;Sjölander A;Johansson S;Lu D;Razaz N;Tedroff K;Villamor E;Cnattingius S
早产的不良后果对胎龄相关脑性瘫痪（CP）风险的贡献很少被研究。我们的目的是评估新生儿发病率对胎龄和CP风险之间关系的潜在介导作用。在这项基于瑞典人群的研究中，1998-2016年期间出生于22-40孕周的1402240例单胎婴儿从出生后第28天开始接受CP诊断，直至2017年。潜在介质包括出生后0-27天内的窒息、窒息相关、感染/炎症相关和神经系统相关疾病。使用考克斯回归估计风险比（HR）和95%置信区间（CI）。因果关系的中介分析，估计比例的协会介导的途径，涉及四个连续介质。我们发现胎龄与CP风险之间存在反向剂量反应关系，其中22-24周（HR 47.26，95% CI 34.09-65.53）与39-40周观察到最强的相关性。与非患病同龄人相比，新生儿发病的儿童，特别是那些与神经系统相关的疾病（HR 31.34，95%CI 26.39-37.21），有更高的风险CP。在24周时，CP风险增加几乎完全由新生儿发病率（91.7%）解释;在32周和36周时，这一比例分别降至46.1%和16.4%。窒息是22 ~ 34周的主要介导途径，34周以后，神经系统相关的新生儿疾病是主要介导途径。新生儿发病率介导了早产对CP的大部分影响，但随着胎龄的增加，影响程度下降。
The contribution of adverse consequences of preterm birth to gestational-age-related risk of cerebral palsy (CP) has rarely been studied. We aimed to assess the potential mediating roles of neonatal morbidity on the association between gestational age and risk of CP. In this Swedish population-based study, 1 402 240 singletons born at 22–40 gestational weeks during 1998–2016 were followed from day 28 after birth for a CP diagnosis until 2017. Potential mediators included asphyxia, respiratory-related, infection-/inflammatory-related and neurological-related diseases within 0–27 days of life. Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Causal mediation analysis was performed to estimate the proportion of the association mediated through pathways involving the four sequential mediators. We found an inverse dose–response relationship between gestational age and risk of CP, where the strongest association was observed for 22–24 weeks (HR 47.26, 95% CI 34.09–65.53) vs 39–40 weeks. Compared with non-diseased peers, children with neonatal morbidity, particularly those with neurological-related diseases (HR 31.34, 95% CI 26.39–37.21), had a higher risk of CP. The increased risk of CP was, at 24 weeks, almost entirely explained by neonatal morbidity (91.7%); this proportion decreased to 46.1% and 16.4% at 32 and 36 weeks, respectively. Asphyxia was the main mediating pathway from 22 to 34 weeks, and neurological-related neonatal diseases led the mediating pathways from 34 weeks onwards. Neonatal morbidity mediates a large proportion of the effect of preterm birth on CP, but the magnitude declines as gestational age increases.