Associations of placental weight with maternal and cord blood hormones

PurposePlacental weight has been associated with mammographic pattern and coronary heart disease in the adult offspring, but the mechanisms are unknown. We evaluated the associations of maternal and cord blood hormones with placental weight in normal pregnancies.MethodsProspective study of 167 normal singleton pregnancies in Boston, USA and 256 in Shanghai, China. Maternal hormone levels at the 27th gestational week were available for all pregnancies. Cord blood measurements were available for 86 pregnancies in Boston and 104 in Shanghai. Pearson partial correlation coefficients of log-transformed hormone levels with placental weight were calculated.ResultsMaternal levels of estriol, testosterone, and progesterone (P < .05) were positively associated with placental weight. There was no such evidence for adiponectin, prolactin, and insulin-like growth factor (IGF)-I. Cord blood steroids tended to be inversely associated with placental weight, the results being statistically significant for testosterone (P < .05). There was a marginally significant positive association of cord blood IGF-I with placental weight. Reported results were adjusted for study center.ConclusionsPlacental weight appears to be positively correlated with maternal steroids. Its correlation with cord blood steroids, however, appears inverse, compatible with negative feedback mechanisms. There is also a suggestion for placental weight to be positively associated with cord blood IGF-I.     

Pathological Uterine Perfusion in the Second Trimester Is Not Associated with Neutrophil Activation

Objective: Preeclampsia and intrauterine growth retardation (IUGR) are associated with elevated concentrations of myeloperoxidase (MPO) and polymorphonuclear (PMN) elastase, which indicate maternal neutrophil activation. The aim of the study was to measure maternal MPO and PMN elastase plasma concentrations in second trimester pregnancies with pathological uterine perfusion that are a high risk group for preeclampsia and IUGR, and compare them to normal controls. Methods: The study includes 25 pregnancies with normal and 25 pregnancies with pathological uterine perfusion. In both groups, doppler‐sonographic measurement of uterine perfusion was performed in the twenty‐first week of gestation. Maternal plasma concentrations of MPO and PMN elastase were measured using a specific ELISA for both enzymes. Results: The plasma MPO concentration of pregnant women with normal perfusion did not differ significantly from that of the group with pathological perfusion (27.4 ± 3.3 vs. 23.7 ± 2.0 ng/mL). Likewise, the plasma PMN elastase‐concentration also did not show a significant difference between the groups (5.7 ± 0.5 ng/mL normal vs. 8.0 ± 1.0 ng/mL pathological). Patients with pathological perfusion that later developed preeclampsia or IUGR (9/25) showed unchanged MPO and PMN elastase values in the second trimenon compared to those with pathological perfusion and normal outcome. Conclusions: Pathological uterine perfusion in the second trimester was not associated with maternal neutrophil activation. The measurement of the MPO and PMN elastase concentration suggested that neutrophil activation in preeclampsia or IUGR is a secondary effect of the disease rather than a primary pathophysiological factor.     

Prevention of cardiovascular risk in women who had hypertension during pregnancy after 36 weeks gestation

Objective. The aim of our study was to investigate a possible correlation between the expression of the placenta-secreted hormones, β-subunit of human chorionic gonadotrophin (βhCG) and pregnancy-associated plasma protein A (PAPP-A), during the first trimester screening and the development of preeclampsia. Methods. A total of 155 patients between 11 + 0 and 13 + 6 weeks of gestation were enrolled in this study. PAPP-A and βhCG levels were measured using the KRYPTOR® system. Results. The serum levels of βhCG were significantly higher in pregnancies which subsequently developed preeclampsia. The PAPP-A concentration did not differ significantly in pregnancies complicated by preeclampsia than in uncomplicated pregnancies. Conclusion. These results might contribute to developing new tests in the prediction of preeclampsia.     

In-vivo stretch of term human fetal membranes

IntroductionFetal membranes (FM) usually fail prior to delivery during term labor, but occasionally fail at preterm gestation, precipitating preterm birth. To understand the FM biomechanical properties underlying these events, study of the baseline in-vivo stretch experienced by the FM is required. This study's objective was to utilize high resolution MRI imaging to determine in-vivo FM stretch.MethodsEight pregnant women (38.4 ± 0.4wks) underwent abdominal-pelvic MRI prior to (2.88 ± 0.83d) caesarean delivery. Software was utilized to determine the total FM in-vivo surface area (SA) and that of its components: placental disc and reflected FM. At delivery, the SA of the disc and FM in the relaxed state were measured. In-vivo (stretched) to delivered SA ratios were calculated. FM fragments were then biaxially stretched to determine the force required to re-stretch the FM back to in-vivo SA.ResultsTotal FM SA, in-vivo vs delivered, was 2135.51 ± 108.47 cm² vs 842.59 ± 35.86 cm²; reflected FM was 1778.42 ± 107.39 cm² vs 545.41 ± 22.90 cm², and disc was 357.10 ± 28.08 cm² vs 297.18 ± 22.14 cm². The ratio (in-vivo to in-vitro SA) of reflected FM was 3.26 ± 0.11 and disc was 1.22 ± 0.10. Reflected FM re-stretched to in-vivo SA generated a tension of 72.26 N/m, corresponding to approximate pressure of 15.4 mmHg. FM rupture occurred at 295.08 ± 31.73 N/m corresponding to approximate pressure of 34 mmHg. Physiological SA was 70% of that at rupture.DiscussionFM are significantly distended in-vivo. FM collagen fibers were rapidly recruited once loaded and functioned near the failure state during in-vitro testing, suggesting that, in-vivo, minimal additional (beyond physiological) stretch may facilitate rapid, catastrophic failure.     

Reproductive outcomes after surgical treatment of asherman syndrome: A systematic review

In this systematic review, we analysed the reproductive outcomes of hysteroscopic adhesiolysis in women with Asherman syndrome (AS). We searched PubMed, Web of Science and Cochrane Library (from database inception to April 2018) and selected studies that quantitatively described the reproductive outcomes. We assessed study quality and pooled rate data for each outcome.There were 54 studies (4640 women) of varying quality. The pooled rate of pregnancy was 50.7% (95% CI [confidence interval]: 49.1 to 52.3) in 53 studies, early pregnancy loss was 17.7% (95% CI: 15.9 to 19.6) in 31 studies, ectopic pregnancy (EP) was 4.2% (95% CI: 2.8 to 6.3) in 9 studies, mid-trimester loss (MTL) was 11.5% (95% CI: 7.6 to 17.8) in 7 studies, cervical incompetence was 12.5% (95% CI: 3.3 to 33.5) in 2 studies and placenta accreta syndrome was 10.1% (95% CI: 8.6 to 11.8) in 23 studies. The pregnancy rate in women with severe adhesion was significantly lower than that in women with mild adhesion (P = 0.021).These results can be used to counsel women with AS before surgical treatment and for planning antenatal care after conception.     

Interleukin-34 accelerates intrauterine adhesions progress related to CX3CR1+ monocytes/macrophages

Intrauterine adhesions (IUA) are characterized by endometrial fibrosis and impose a great challenge for female reproduction. IL-34 is profoundly involved in various fibrotic diseases through regulating the survival, proliferation, and differentiation of monocytes/macrophages. However, it remains unclear how IL-34 regulates monocytes/macrophages in context of IUA. Here, we showed that the expression level of IL-34 and the amount of CX3CR1+ monocytes/macrophages were significantly increased in endometrial tissues of IUA patients. IL-34 promoted the differentiation of monocytes/macrophages, which express CX3CR1 via CSF-1R/P13K/Akt pathway in vitro. Moreover, IL-34-induced CX3CR1+ monocytes/macrophages promoted the differentiation of endometrial stromal cells into myofibroblasts. Of note, IL-34 caused endometrial fibrosis and increased the amount of CX3CR1+ monocytes/macrophages in endometrial tissues in vivo. IL-34 modulated endometrial fibrosis by regulating monocytes/macrophages since the elimination of endometrial monocytes/macrophages significantly suppressed the profibrotic function of IL-34. Finally, blocking of IL-34 in the LPS-IUA model resulted in the improvement of endometrial fibrosis and decreased number of CX3CR1+ monocytes/macrophages. Our studies uncover the novel mechanism of interaction between IL-34-induced CX3CR1+ monocytes/macrophages and endometrial stromal cells in endometrial fibrosis pathogenesis, and highlight IL-34 as a critical target for treating IUA.     

不同宫内节育器与妇女生殖道感染情况调查分析

目的调查放置不同宫内节育器妇女生殖道感染及盆腔炎的发生情况。方法统计450例自愿要求放置宫内节育器的育龄妇女发生生殖道感染的情况,宫内节育器种类有3种,其中元宫300组150例,Tcu380A组150例,活性165组150例。结果放置宫内节育器术后6、12个月分别对450例患者进行随访,3组患者在术后6个月阴道炎、宫颈炎、盆腔炎的发生率比较,差异无统计学意义,P〉0.05,其中,盆腔炎的发生率元宫300组和活性165组均为0,Tcu380A组发生率为0.68%;术后12个月阴道炎、宫颈炎、盆腔炎的发生率比较,差异无统计学意义,P〉0.05,其中,盆腔炎的发生率元宫300组和活性165组均为0,Tcu380A组发生率为0.71%。结论不同类型的宫内节育器不增加生殖道感染的发生率,且发生生殖道感染的几率均较低。     

男性射精障碍行宫腔内人工授精的临床研究

目的：探讨对男性射精障碍所致不育夫妻进行宫腔内人工授精（Intrauterine insemination， IUI）的临床疗效。方法：对14例男性射精障碍所致不育夫妻进行宫腔内人工授精的临床资料进行回顾性分析，其中2例为逆行射精，12例为不射精。逆行射精者，取精前常规口服碳酸氢钠碱化尿液，排尿后手淫取精，收集标本；对于不射精者，常规手淫取精收集标本。采用密度梯度离心法处理精液，随后进行IUI。根据IUI精液处理后精子前向运动总数（Processed total motile sperm count，PTMS），将IUI周期分为三组：PTMS＜10×10^6（A组）、PTMS＜10×10^6～20×10^6（B组）和PTMS≥20×10^6（C组），统计每组的妊娠率，并对妊娠周期与非妊娠周期处理后注入宫腔内精液参数进行统计学分析。结果：14例男性射精障碍的不育夫妻经30个周期IUI治疗，10例女方怀孕，临床周期妊娠率为33．33％，临床累积妊娠率为71．43％。PTMS＜10×10^6（A组）、10×10^6～20×10^6（B 组）和≥20×106（C 组），这三组周期妊娠率分别25．00％、40．00％和33.33％。妊娠周期与非妊娠周期处理后注入宫腔内精液参数均无统计学差异（P均＞0.05）。结论：对男性射精障碍所致不孕夫妻进行IUI治疗，效果明显、临床实用性强。     

Coûts de l’hypotrophie par retard de la croissance intra-utérine (RCIU) attribuable à la pollution atmosphérique en France

Exposure of pregnant women to fine particulate matter < 2.5 μm in diameter (PM_2.5) is responsible for low birthweight (LBW) and intellectual disabilities, as expressed by a lower intelligence quotient (IQ). We estimated the attributable cost due to PM_2.5 of healthcare at birth and cognitive retardation of children with LBW in metropolitan France in 2012. The cost of specific care of the 8300 (range, 3100–13,300) children born every year in France with a LBW attributable to PM_2.5 exposure is estimated at € 25 million (range, € 9.5–39 million). Among these 8300 children, 1880 will present an intelligence quotient (IQ) lower than the average of the general population. The annual cost of the care of these intellectual deficiencies attributable to PM_2.5 is estimated at € 15 million and that of the mental handicap on the lifespan of the LBW children born in 2012 attributable to PM_2.5 is estimated at € 1.2 billion (range, € 458 million to € 1.9 billion). Beyond the elevated costs borne by future generations and the intellectual impoverishment of our society, it is essential to provide continued minimal monitoring of pregnant women exposed to air pollution. For the decision-makers, it is urgent to take effective measures and actions to protect the health of exposed populations.