Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, NTNU, PO Box 8905, MTFS, N-7491 Trondheim, Norway.
BMJ. 2013 Jul 9;347:f4089. doi: 10.1136/bmj.f4089.
To test the hypothesis that pre-eclampsia is a risk factor for cerebral palsy mediated through preterm birth and being born small for gestational age.
Population based cohort study.
Clinical data from the Norwegian Cerebral Palsy Registry were linked with perinatal data prospectively recorded by the Medical Birth Registry of Norway.
All singleton babies who survived the neonatal period during 1996-2006 (849 children with cerebral palsy and 616,658 control children).
Cerebral palsy and cerebral palsy subtypes.
Children exposed to pre-eclampsia had an excess risk of cerebral palsy (unadjusted odds ratio 2.5, 95% confidence interval 2.0 to 3.2) compared with unexposed children. Among children born at term (≥ 37 weeks), exposure to pre-eclampsia was not associated with an excess risk of cerebral palsy in babies not born small for gestational age (1.2, 0.7 to 2.0), whereas children exposed to pre-eclampsia and born small for gestational age had a significantly increased risk of cerebral palsy (3.2, 1.5 to 6.7). Non-small for gestational age babies born very preterm (<32 weeks) and exposed to pre-eclampsia had a reduced risk of cerebral palsy compared with unexposed children born at the same gestational age (0.5, 0.3 to 0.8), although the risk was not statistically significantly reduced among children exposed to pre-eclampsia and born small for gestational age (0.7, 0.4 to 1.3). Exposure to pre-eclampsia was not associated with a specific cerebral palsy subtype.
Exposure to pre-eclampsia was associated with an increased risk of cerebral palsy, and this association was mediated through the children being born preterm or small for gestational age, or both. Among children born at term, pre-eclampsia was a risk factor for cerebral palsy only when the children were small for gestational age.
检验先兆子痫是通过早产和胎儿小于胎龄导致脑瘫的中间因素，从而导致脑瘫的假说。
基于人群的队列研究。
临床数据来自挪威脑瘫注册中心，与挪威围产期医学出生登记处前瞻性记录的围产期数据相关联。
所有在 1996-2006 年期间新生儿期存活的单胎婴儿（849 例脑瘫患儿和 616658 例对照儿童）。
脑瘫及脑瘫亚型。
与未暴露于先兆子痫的儿童相比，暴露于先兆子痫的儿童脑瘫风险增加（未经调整的优势比 2.5，95%置信区间 2.0 至 3.2）。在足月出生（≥37 周）的儿童中，未暴露于先兆子痫的情况下，出生时小于胎龄儿（SGA）并不增加脑瘫风险（1.2，0.7 至 2.0），而暴露于先兆子痫且出生时 SGA 的儿童脑瘫风险显著增加（3.2，1.5 至 6.7）。极早产（<32 周）且未暴露于先兆子痫的非 SGA 婴儿与同期出生且未暴露于先兆子痫的儿童相比，脑瘫风险降低（0.5，0.3 至 0.8），但暴露于先兆子痫且出生时 SGA 的儿童风险并未显著降低（0.7，0.4 至 1.3）。暴露于先兆子痫与特定的脑瘫亚型无关。
暴露于先兆子痫与脑瘫风险增加相关，这种关联是通过儿童早产或 SGA 或两者共同作用而产生的。在足月出生的儿童中，只有当儿童 SGA 时，先兆子痫才是脑瘫的危险因素。
