Prematurity Is Related to High Placental Cortisol in Preeclampsia
Prematurity Is Related to High Placental Cortisol in Preeclampsia
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DOI：
10.1203/pdr.0b013e31818d6c24
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发表时间：
2009-02-01
影响因子：
3.6
通讯作者：
Mohaupt, Markus G.
中科院分区：
文献类型：
--
作者：
Aufdenblatten, Myriam;Baumann, Marc;Mohaupt, Markus G.
在皮质醇可获得性高的动物模型中，在健康怀孕的情况下，胎儿生长受到影响。胎盘11β-羟基类固醇脱氢酶2型(11β-HSD2)保护胎儿免受高循环皮质醇水平的影响，这种酶在先兆子痫中会减少。我们假设先兆子痫患者胎盘皮质醇供应增加，其缺失的环节与胎儿生长受限和早产有关。胎盘组织取自39例正常孕妇(n=16)和子痫前期孕妇(n=23)。用气相色谱-质谱法分析胎盘类固醇激素代谢产物。表观11β-HSD2酶活性以底物与产物之比计算。雌二醇、孕二醇与胎龄呈正相关。在93.8%的对照组中几乎没有皮质醇，但在79.3%的先兆子痫样本中可检测到皮质醇，导致胎盘皮质醇存在的优势比(OR)为0.019(95%可信区间0.002-0.185)。表观11β-HSD2活性与出生体重(R-2=0.16：P<；0.02)和胎龄(R-2=0.11：P<；0.04)直接相关，从而降低早产风险(OR 0.12；95%CI 0.02-0.58)。我们得出结论，血压正常的妊娠以几乎完全失活的胎盘皮质醇为特征。根据我们的假设，先兆子痫患者11β-HSD2活性降低并不能消除胎盘皮质醇，它发现与早产和低出生体重明显相关。(儿科65：198-202,2009)
Fetal growth is compromised in animal models with high cortisol availability, In healthy pregnancies. the fetus is protected from high circulating, cortisol levels by the placental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2), which is reduced in preeclampsia. We hypothesized increased placental cortisol availability in preeclampsia its missing link to fetal growth restriction and prematurity. Placental tissue was obtained from 39 pregnant women dichotomized normotensive (n = 16) or preeclamptic (n = 23). Placental steroid hormone metabolites were analyzed by gas chromatography-mass spectrometry. Apparent 11 beta-HSD2 enzyme activity was Calculated as Substrate to product ratio. Estradiol and pregnandiol positively correlated with gestational age. Cortisol was virtually absent in 93.8% of controls, yet detectable in 79.3% of preeclamptic samples resulting in an odds ratio (OR) of 0.019 (95% Cl 0.002-0.185) for the presence of placental cortisol. Apparent 11 beta-HSD2 activity directly correlated with birth weight (R-2 = 0.16: P < 0.02) and gestational age (R-2 = 0.11: p < 0.04) ensuing a reduced risk, of premature delivery (OR 0.12; 95% Cl 0.02-0.58). We conclude that normotensive pregnancies are characterized by all almost completely inactivated placental cortisol. In line with our hypothesis, reduced 11 beta-HSD2 activity in preeclampsia is unable to abolish placental cortisol, it finding clearly associated with prematurity, and low birth weight. (Pediatr 65: 198-202, 2009)