Byrne Bridgette M, Crowley Aoife, Taulo Frank, Anthony John, O'Leary John J, O'Herlihy Colm
Department of Obstetrics and Gynaecology, University College Dublin, Coombe Womens Hospital, Dublin, Ireland.
Hypertens Pregnancy. 2003;22(2):157-64. doi: 10.1081/PRG-120021062.
Trophoblast migration into the maternal circulation is increased in preeclampsia and can trigger the endothelial dysfunction that characterizes the clinical disease. We hypothesised that 'fetal trafficking' is increased in women with severe preeclampsia and that the quantity of trafficking is greater in women with more severe disease.
To test the hypothesis, we used a technique that quantifies a genetic marker specific for the fetomaternal unit, that is, the SRY gene in a pregnant woman carrying a male fetus. Thirty two women with pre-eclampsia and 32 control women (women without preeclampsia) were recruited. Preeclampsia was defined according to the International Society for the Study of Hypertension in Pregnancy (ISSHP). All subjects with preeclampsia had evidence of the multisystemic nature of the disease. DNA was extracted from maternal peripheral blood and RTQ PCR analysis was performed to quantify the fetal DNA (SRY) and the total DNA (beta-actin) in each sample. The ratio of fetal to total DNA was calculated and compared between women with preeclampsia and controls.
The women with preeclampsia and the control women did not differ in parity, blood pressure at booking, and gestational age at sampling. The groups differed significantly in age (29 +/- 5.7 vs 25 +/- 5.1 years; P =.007), diastolic blood pressure (DBP) at sampling (101 +/- 9.5 vs 70 +/- 5.5 mm Hg; P <.0001), gestational age at delivery (33 +/- 4.3 vs 39 +/- 1.8 weeks; P <.001), and fetal weight (1.98 +/- 1 vs 3.35 +/- 0.5 kgs; P <.0001). SRY was detected in 31 out of 32 women with preeclampsia and in 24 out of 32 control women (P <.001). The median SRY copy number per micro L was greater in women with preeclampsia (10.6, interquartile range 12.89) than in the control women (8.6, interquartile range 20.1) but these differences were not statistically significant at P =.75. The median ratio of fetal to total DNA was almost identical in both groups (0.06, interquartile range 0.13) in PET compared to (0.06, interquartile range 0.17) the control women. No correlation was found between the quantity of fetal DNA and disease severity.
Fetal trafficking is more likely to be detected in women with preeclampsia compared to control women but the quantity does not appear to correlate with disease severity.
子痫前期患者的滋养层细胞向母体循环的迁移增加，可引发内皮功能障碍，这是该临床疾病的特征。我们假设重度子痫前期女性的“胎儿细胞转运”增加，且疾病越严重，转运量越大。
为验证该假设，我们采用了一种技术，该技术可对胎儿 - 母体单位特有的遗传标记进行定量，即在怀有男性胎儿的孕妇中检测SRY基因。招募了32例子痫前期女性和32例对照女性（非子痫前期女性）。子痫前期根据国际妊娠高血压研究学会（ISSHP）的标准进行定义。所有子痫前期患者均有该疾病多系统性质的证据。从母体外周血中提取DNA，并进行实时定量PCR分析，以定量每个样本中的胎儿DNA（SRY）和总DNA（β - 肌动蛋白）。计算胎儿DNA与总DNA的比率，并在子痫前期女性和对照组之间进行比较。
子痫前期女性和对照女性在产次、孕早期血压和采样时的孕周方面无差异。两组在年龄（29±5.7岁 vs 25±5.1岁；P = 0.007）、采样时的舒张压（DBP）（101±9.5 vs 70±5.5 mmHg；P < 0.0001）、分娩时的孕周（33±4.3 vs 39±1.8周；P < 0.001）和胎儿体重（1.98±1 vs 3.35±0.5 kg；P < 0.0001）方面存在显著差异。32例子痫前期女性中有31例检测到SRY，32例对照女性中有24例检测到SRY（P < 0.001）。子痫前期女性每微升SRY拷贝数的中位数（10.6，四分位间距12.89）高于对照女性（8.6，四分位间距20.1），但这些差异在P = 0.75时无统计学意义。子痫前期组胎儿DNA与总DNA的中位数比率（0.06，四分位间距0.13）与对照女性（0.06，四分位间距0.17）几乎相同。未发现胎儿DNA数量与疾病严重程度之间存在相关性。
与对照女性相比，子痫前期女性更有可能检测到胎儿细胞转运，但转运量似乎与疾病严重程度无关。
