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Recent studies suggest that leptin, the product of the obese gene, is produced by the placenta during pregnancy. The present study addressed the question whether second trimester maternal serum leptin could be altered by fetal Down syndrome or Edwards syndrome. Maternal serum leptin concentrations were measured in 18 pregnancies complicated with Down syndrome, six pregnancies complicated with Edwards syndrome and 183 uncomplicated pregnancies during the second trimester of pregnancy. The present results demonstrate that leptin concentrations in uncomplicated pregnancies slightly decrease from the 16th week of pregnancy, reaching a minimum of 18.8 ng/ml around the 20th week, and then rapidly increase to 28.2 ng/ml by the 24th week. Leptin correlation with maternal body weight decreases from r=0.695 at 16–17 week of gestation to r=0.544 at >22 weeks of gestation. There was no significant difference between the mean MoMs of Down syndrome- (0.926) or Edwards syndrome- (0.960) affected pregnancies and normal pregnancies (1.002). A weak correlation (r=0.18, p<0.02) was observed between corrected leptin MoMs and human chorionic gonadotrophin (hCG) MoMs in normal pregnancies. It is assumed that around the 20th week of pregnancy placental leptin production is activated or at least is accelerated and it is added to the amount of leptin produced by maternal adipose tissue. Fetal Down syndrome or Edwards syndrome does not seem to alter maternal leptin concentration and therefore leptin cannot be used as a marker for these chromosomal abnormalities in the early second trimester of pregnancy. Copyright © 2002 John Wiley & Sons, Ltd.  相似文献   
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Increased fetal nuchal translucency (NT) in the first trimester is associated with adverse pregnancy outcomes. Whether the increased NT is also associated with an increased frequency of pregnancy-associated hypertension (PAH) is not known. Seven hundred and seventy-nine pregnant women who received NT-based Down syndrome screening and delivered their babies at our hospital by September 2000 were enrolled into this study. Among these women, there are 46 cases of preeclampsia, 68 cases of gestational hypertension (GH); 665 women without any adverse pregnancy outcomes served as controls. Correlation analysis demonstrated that NT MoM (multiples of median) level had a positive association with maternal diastolic blood pressure at the time of admission for delivery (r = 0.104; p < 0.01). The severity of PAH was concordant with the stepwise increase of mean NT MoM level, which was 0.88 in control, 1.07 in gestational hypertension, and 1.13 in preeclampsia (p < 0.001). Using the 95th (1.52 MoM) and 90th (1.31 MoM) percentiles of NT thickness as cut-offs, the sensitivities and odds ratios of the women at risk for developing GH after 20 weeks of gestation were 8.8%, 19.1% and 1.98, 2.15 respectively, while for preeclampsia were 10.9%, 28.3% and 2.49, 3.58 respectively. It is concluded that the pathological changes in the placenta responsible for the development of PAH may also influence the physiological decrease of NT thickness in late first trimester. However, the sensitivity of fetal NT measurement in first trimester is not sufficient as a single marker for predicting the pregnant women at risk for subsequent PAH. Copyright © 2002 John Wiley & Sons, Ltd.  相似文献   
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Three twin pregnancies, each with one affected fetus (by microcephaly, haemophilia A and spina bifida respectively) were encountered. Selective feticide was performed at the patient's request by injection of filtered air into an umbilical vessel by fetoscopy. The method was successful in all three pregnancies two of which resulted in a live, healthy baby.  相似文献   
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2,3,7,8,-四氯苯噁英对NIH小鼠早期妊娠和生殖激素的影响   总被引:1,自引:0,他引:1  
用不同剂量的2,3,7,8 四氯苯二英(2,3,7,8 tetrachlorodibenzopdioxin,TCDD)对小鼠胚胎附植数量和生长发育情况进行剂量反应评估,分析TCDD对假孕小鼠子宫蜕膜生长状况的影响以及比较胚胎种植前后染毒效果.所有样本采集血液,测定母体血清雌二醇和孕酮的浓度变化.结果表明,50和100ng·(kg·d)-1TCDD处理的孕鼠,胚胎附植数量明显减少(P<0 05),着床后胚胎出现发育迟缓,质量减轻(P<0 05);同等剂量TCDD处理的假孕小鼠,子宫蜕膜生长受到了极显著的抑制(P<0 01);种植前后染毒效果比较发现种植前期染毒的小鼠胚胎对TCDD更为敏感.母体血清雌二醇浓度随剂量和染毒时段有不同程度的升高,而孕酮浓度则极显著下降(P<0 01).由此表明低剂量TCDD可能通过对生殖激素的干扰,强烈影响NIH小鼠妊娠早期生殖生理状态和着床后胚胎的发育.实验同时证明小鼠也可作为早期妊娠毒物研究的供试动物,用以筛选动物和人类早期妊娠的有害化合物.  相似文献   
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