Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia.

Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia.
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DOI:
10.1515/jpm.2011.098
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发表时间:
2011-11
影响因子:
2.4
通讯作者:
Hassan SS
Hassan SS
中科院分区:
医学4区
文献类型:
--
作者:
Ogge G;Chaiworapongsa T;Romero R;Hussein Y;Kusanovic JP;Yeo L;Kim CJ;Hassan SS

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子痫前期(PE)分为早发型和晚发性两类。这两种PE的表型变异被认为具有不同的病理生理机制。然而,在不同的研究中,定义“早期”和“晚期”PE的胎龄界限是不同的。本研究的目的是确定PE患者中母体胎盘灌注不足的病变发生率与胎龄的关系。以队列为基础,对8,307名怀孕20周后分娩的独生子女进行了嵌套式病例对照研究。病例定义为PE患者(n=910),对照组为孕期无高血压疾病的孕妇(n=7,397)。比较两组孕妇胎盘灌注不足的频率(根据儿科病理学会的标准)。采用Logistic回归进行分析。根据调整后的优势比计算估计的相对风险。1)PE患者中与母亲低灌注相一致的病变的发生率高于对照组[43.3%对15.9%;未经调整的优势比4.0(95%CI3.5-4.7);P<0.001];2)PE中母亲低灌注病变的估计相对风险高于对照组;3)分娩时胎龄越低,这些病变的相对风险越高;4)早发性PE,无论用来定义它的胎龄(<32周、33周、34周、35周或37周)的胎盘病变与母体血流灌注不足的发生率显著高于晚发性PE(P<0.001)。1)分娩时先兆子痫的胎龄越早,与母体血流灌注不足一致的胎盘病变的发生率就越高;2)我们的数据表明,在早发型和晚发型先兆子痫中,病理检查所确定的明显的胎盘受累是不同的;以及3)这种现象似乎是连续的,我们无法确定一个明确和明确的胎龄,在哪些胎盘病变与母体血流灌注不足相一致的情况下不会出现。
Preeclampsia (PE) has been classified into early- and late-onset disease. These two phenotypic variants of PE have been proposed to have a different pathophysiology. However, the gestational age cut-off to define ‘early’ versus ‘late’ PE has varied among studies. The objective of this investigation was to determine the prevalence of lesions consistent with maternal underperfusion of the placenta in patients with PE as a function of gestational age. A nested case-control study of 8,307 singleton pregnant women who deliver after 20 weeks of gestation was constructed based on a cohort. Cases were defined as those with PE (n=910); controls were pregnant women who did not have a hypertensive disorder in pregnancy (n=7,397). The frequency of maternal underperfusion of the placenta (according to the criteria of the Society for Pediatric Pathology) was compared between the two groups. Logistic regression was used for analysis. Estimated relative risks were calculated from adjusted odds ratios. 1) The prevalence of lesions consistent with maternal underperfusion was higher in patients with PE than in the control group [43.3% vs. 15.9%; unadjusted odds ratio 4.0 (95% CI 3.5–4.7); P<0.001]; 2) the estimated relative risk of maternal underperfusion lesions in PE was higher than in the control group; 3) the lower the gestational age at delivery, the higher the relative risk for these lesions; 4) early-onset PE, regardless of the gestational age used to define it (<32, 33, 34, 35 or 37 weeks) had a significantly higher frequency of placental lesions consistent with maternal underperfusion than late-onset PE (p<0.001 for all). 1) The earlier the gestational age of preeclampsia at delivery, the higher the frequency of placental lesions consistent with maternal underperfusion; 2) our data suggests that demonstrable placental involvement as determined by pathologic examination differs in early- and late-onset preeclampsia; and 3) this phenomenon appears to be a continuum, and we could not identify a clear and unambiguous gestational age at which lesions consistent with underperfusion would not be present.
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