Occurrence of placental abruption in relatives

Objective  The aim of this study was to assess the recurrence of placental abruption by severity, comparing the risk in a woman with that of recurrence in her sister and in the partner of her brother.
Design  Prospective observational study.
Setting  General population.
Population  Population-based study based on records of pregnancies from the Medical Birth Registry of Norway; 377 902 sisters with 767 395 pregnancies, 168 142 families incorporating 2–10 sisters, and 346 385 brothers with 717 604 pregnancies in their partners were identified.
Methods  Placental abruption with preterm birth, birthweight below 2500 g or perinatal death was defined as severe, other cases as mild. Because of the nested family data structure, multilevel multivariate regression was used.
Main outcome measures  Placental abruption (severe and mild).
Results  Adjusted odds ratios of recurrence of mild and severe abruption were 6.5 (1.7%) and 11.5 (3.8%), respectively, compared with risks of 0.2 and 0.3% in the total population. After a severe abruption, odds ratios in her sisters were 1.7–2.1, whereas mild abruption produced no increased recurrence in sisters. The estimated heritability between sisters of severe abruption was 16%. No excess rate of abruption was observed between sisters and brothers' partners, between brothers' partners, or from brothers' partners to sisters. The odds ratios for a third abruption after a second abruption and a second severe abruption were 38.7 (19%) and 50.1 (24%), respectively.
Conclusions  The recurrence risk of placental abruption in the same woman was higher after severe than mild abruption. Severe abruption was associated with a two-fold risk in sisters. Pregnancies following a second abruption should be considered very high risk.     

The risk of placental abruption when using prostaglandins for cervical ripening in women with preeclampsia: Comparing misoprostol versus dinoprostone

Objective.?Recent data have raised concern about the safety of using misoprostol in women with preeclampsia. We wanted to evaluate the risk of placental abruption in women with preeclampsia undergoing cervical ripening with misoprostol compared to dinoprostone.

Methods.?We evaluated data on 403 preeclamptic women receiving either misoprostol (N?=?235) or dinoprostone (N?=?168) at different regimens and delivering in two university hospitals in Switzerland (Geneva and Basel). The main outcome was the incidence of placental abruption in both groups using two definitions for placental abruption (“clinical” and “post hoc”). We performed univariable and multivariable analysis.

Results.?The overall incidence of placental abruption was 1.5% (six cases); 1.3% (3) in the misoprostol group versus 1.8% (3) in the dinoprostone group; p?=?0.69). When using the post-hoc definition the incidence was higher in the latter group (1.3 versus 5.4%; p?=?0.03). In multivariable analyses, the risk of placental abruption using the “post hoc” definition was associated with the use of dinoprostone.

Conclusions.?The use of misoprotol in preeclamptic women appears to be safe and is not associated with a higher risk of placental abruption when compared with other prostaglandins. Concerns about the use of misoprostol in the case of preeclampsia are not justified.     

脐血内皮祖细胞中整合素连接激酶在子痫前期发病机制中的作用

目的 探讨整合素连接激酶(integrin linked kinase,ILK)在子痫前期患者脐血内皮祖细胞中的表达及其在新生血管形成中的作用. 方法 采用逆转录聚合酶链反应和Western印迹实验分别检测35例正常孕妇(正常妊娠组)和30例子痫前期孕妇(子痫前期组,其中轻度18例,重度12例)的脐血内皮祖细胞中ILK mRNA和蛋白的表达,采用小管形成实验检测内皮祖细胞血管形成能力;分析ILK mRNA和蛋白表达的差异及其与血管管状结构形成的相关性.统计学分析采用方差分析和相关分析. 结果 (1)正常妊娠组内皮祖细胞中ILK mRNA相对吸光度(A)值较子痫前期组显著升高(0.64±0.05与0.45±0.06),轻度子痫前期组较重度者显著升高(0.47±0.07与0.39±0.08)(q=18.76和5.13,P＜0.05);正常妊娠组内皮祖细胞中ILK蛋白A值较子痫前期组明显升高(32±2与26±1),轻度子痫前期组较重度者显著升高(25±2与20±2)(q=18.47和4.72,P均＜0.05).(2)正常妊娠组小管结构形成的数量较子痫前期组显著增多(330±8与135±7),重度子痫前期组的小管形成的数量明显少于轻度者(116±8与148±6)(q=152.70和5.42,P均＜0.05).(3)内皮祖细胞中ILK mRNA及其蛋白表达与其小管形成均呈正相关关系,正常妊娠组相关系数(r)分别为0.69和0.73,子痫前期组分别为0.67和0.72;轻度子痫前期组分别为0.65和0.68,重度组分别为0.63和0.74(P均＜0.05). 结论 子痫前期患者内皮祖细胞中ILK mRNA及其蛋白表达下降可能与子痫前期的发生密切相关.     

Reduction of maternal circulating endothelial progenitor cells in human pregnancies with intrauterine growth restriction

Introduction

Circulating endothelial progenitor cells (EPCs) may play a crucial role during pregnancy by sustaining adequate placentation and fetal growth. Unambiguous demonstration of EPC increase during pregnancy has been hampered so far by lack of standardized methods for EPC quantification. In this study we used the currently most accepted phenotype for EPC detection for investigating whether maternal circulating EPCs might increase during normal pregnancy and whether they may fail to increase in pregnancy complicated by idiopathic intrauterine growth restriction (IUGR), a leading cause of perinatal mortality and morbidity characterized by insufficient placental perfusion.

Methods

Twenty-one non-pregnant women, 44 women during healthy pregnancy progression (9, 13 and 22 women in the first, second and third trimester, respectively) and 11 with pregnancy complicated by idiopathic IUGR were recruited in a cross-sectional study. EPCs in maternal blood were identified as CD45^dim/CD34⁺/KDR⁺ cells by flow cytometry. Plasmatic cytokines were measured by ELISA.

Results

We observed a significant and progressive increase of EPCs in normal pregnancy, yet detectable in early pregnancy but even more pronounced in the third trimester. The increase of EPCs was impaired in IUGR-complicated pregnancies at comparable gestational age. The circulating levels of placental growth-factor and stromal-derived-factor-1 were significantly lower in IUGR than normal pregnancies, possibly contributing to EPC impairment.

Conclusions

EPC count in maternal circulation may have a great potential as a novel biomarker for pregnancy monitoring and may represent the target of novel therapeutic strategies designed to prevent adverse pregnancy outcomes often occurring in IUGR.     

Frequency of selected thrombophilias in women with placental abruption

OBJECTIVE: There is a growing view that inherited or acquired thrombophilia may predispose a woman towards an adverse pregnancy outcome. The aim of this study was to investigate whether risk factors for placental abruption because of such thrombophilias (such as carriership of factor V Leiden (FVL), prothrombin G20210A gene mutation and homozygous MTHFR C677T) might be used as a predictor for placental abruption. METHODS: A retrospective case-control study conducted at the University Hospital, Palacky University, Olomouc, Czech Republic. One hundred and eighty women with placental abruption out of 20,175 deliveries (0.79%) were compared to 196 unselected gravidae. A detailed medical history was taken with special reference to factors related to hypercoagulation and blood was drawn for polymerase chain reaction analysis. The prevalence of FVL, prothrombin G20210A and MTHFR C677T was related to placental abruption. RESULTS: The heterozygous form of FVL was present in 20of 142 cases (14.1%) in the placental abruption group, compared to ten of 196 (5.1%) in the control group (odds ratio 3.0, 95% confidence interval 1.4-6.7). CONCLUSIONS: We found that factor V Leiden is a significant risk factor for placental abruption.     

The risk of placental abruption and placenta previa in pregnant women with chronic hepatitis B viral infection: A systematic review and meta-analysis

Introduction

Several epidemiological studies have found a positive association between chronic hepatitis B virus (CHB) infection and the risk of placental abruption and placenta previa, but various studies have reported conflicting findings. The objective was to systematically review the literature to determine a possible association between CHB infection and these two placental complications.

Methods

We conducted a computerized search in electronic database through March 1, 2014, supplemented with a manual search of reference lists, to identify original published research on placental abruption and placenta previa rates in women with CHB infection. Data were independently extracted, and relative risks were calculated. The meta-analysis was performed using Stata version 10.0 software.

Results

Five studies involving 9088 placenta previa cases were identified. No significant association between CHB infection and placenta previa was identified (OR = 0.98, 95% CI = 0.60–1.62). Five studies involving 15571 placental abruption cases were identified. No significant association between CHB infection and placental abruption was identified (OR = 1.42, 95% CI, 0.93–2.15).

Discussion

The immune response against the virus represents a key factor in determining infection outcomes. No observation of significant increased risk of the placental complications could be partially explained by the complex immune response during CHB infection.

Conclusions

Our meta-analysis found no evidence of significant associations between CHB infection and increased risk of placental abruption as well as placenta previa. Further well-designed studies were warranted to assess any potential association between CHB infection and increased risk of placental abruption as well as placenta previa.     

Risk and risk estimation of placental abruption

OBJECTIVE: Several variables related to increased risk of placental abruption are also risk factors for venous thromboembolism. Prior second trimester-, third trimester, and repeated fetal loss are reported to be associated to thrombophilias. However, it is yet not known if they are also related to placental abruption. STUDY DESIGN: A retrospective case-control study of 161 women with placental abruption and 2371 unselected gravidae without placental abruption. The medical files were scrutinized and the selected variables were investigated in relation to the development of placental abruption. RESULTS: As compared to controls, previous second trimester-, third trimester-, repeated fetal loss, and prior placental abruption were related to a 3-, 13-, 3-, and a 25-fold increased risk of placental abruption, respectively. Several other factors were associated with a roughly three-fold increased risk such as: preeclampsia, IUGR, high maternal age (>35), family history of venous thromboembolism, smoking, and multiple birth. A risk score was created and as compared with those with no risk factors present, the risk of placental abruption was increasing from 2.5-fold for those with risk score=1, to almost 100-fold for risk score 4 or above. CONCLUSION: Easily obtainable information might be used to classify the risk of placental abruption.     

胎盘生长因子与子痫前期发病及一氧化氮关系的研究

目的:探讨胎盘生长因子(PLGF)在子痫前期发病中的作用及其与一氧化氮的关系。方法:选择妊娠期高血压疾病患者45例,其中妊娠期高血压10例,轻度子痫前期12例,重度23例;选择同期正常妊娠妇女20例作为对照组。采用免疫组织化学染色法和逆转录-聚合酶链式反应(RT-PCR)检测两组患者胎盘PLGF蛋白及mRNA的表达。采用硝酸盐还原酶法测定两组胎盘组织NO浓度的变化。结果:(1)免疫组化结果显示,轻度和重度子痫前期的胎盘绒毛合体滋养细胞、绒毛间质PLGF表达均显著低于正常妊娠组(P<0.05),妊娠期高血压组与正常组无差别;PLGF在妊娠期高血压、子痫前期组及正常妊娠组分布范围基本一致,主要分布在绒毛合体滋养细胞和间质细胞胞浆,部分血管合体膜上也有表达;(2)轻、重度子痫前期胎盘组织PLGF mRNA平均灰度分别为3.33±0.39、1.97±0.29,显著低于正常妊娠组的平均灰度4.87±0.60(P<0.01);(3)轻、重度子痫前期胎盘组织中NO浓度分别为8.20±5.56μmol/g、6.46±2.25μmol/g,显著低于对照组18.10±7.12μmol/g(P<0.05);妊娠期高血压组胎盘组织NO浓度与对照组差异无显著性;(4)胎盘组织中胎盘生长因子表达水平与胎盘组织NO浓度呈显著正相关(r=0.54,P<0.05)。结论:子痫前期胎盘组织中胎盘生长因子水平降低,NO浓度下降,可能在子痫前期的发病中起一定作用。     

Maternal pre-gravid body weight and risk for placental abruption among twin pregnancies

Abstract

Objectives.?Placental abruption is a major cause of fetal and neonatal death and has been reported more frequently in twin pregnancies than among singleton gestations. The purpose of this article is to investigate the role of maternal pre-gravid body mass index (BMI) on the risk for placental abruption among twin pregnancies.

Methods.?We used the Missouri maternally linked cohort files (years 1989–1997) consisting of twin live births (gestational age 20–44 weeks). Maternal pre-gravid weight was classified based on the following BMI-based categories: normal (18.5–24.9), underweight (<18.5), overweight (25–29.9), and obese (>30). We used logistic regression for generated adjusted odds ratios with correction for the presence of intra-cluster correlation using generalized estimating equations.

Results.?Overall, 261 cases of placental abruption were registered over the entire study period, yielding a placental abruption rate of 14.9/1000. The frequency of placental abruption correlated negatively with maternal BMI in a dose–effect pattern: underweight (19.3/1000); normal weight (16.1/1000); overweight (13.9/1000); and obese (9.5/1000) mothers (p for trend?<?0.01). After adjusting for confounders, the likelihood of placental abruption was still lower in obese women (OR?=?0.58; 95% CI?=?0.38–0.87). By contrast, women who were underweight had a 20–30% greater likelihood for placental abruption when compared with normal weight mothers, although these findings were statistically not significant.

Conclusions.?There is an inverse relationship between pre-gravid maternal BMI and placental abruption. The mechanism by which obesity impacts the likelihood of placental abruption in twin pregnancies requires further study.     

IFI16在子痫前期孕妇胎盘组织和血清中的表达及其与子痫前期发病的相关性

目的:探讨人γ干扰素诱导蛋白16(IFI16)在子痫前期(PE)孕妇胎盘组织和血清中的表达及其与PE发病的相关性。方法:分别采用免疫组化法、实时荧光定量PCR技术和蛋白印迹法检测胎盘组织中IFI16表达;ELISA法检测血清IFI16及重组IFI16(r IFI16)处理后内皮细胞培养上清液中内皮素-1(ET-1)和可溶性血管内皮黏附分子(s VCAM-1)的浓度,分析PE孕妇血清IFI16水平与临床指标之间的相关性。结果:IFI16在PE组胎盘组织中的阳性表达率明显高于对照组(P0.05);与对照组相比,PE组胎盘组织中IFI16 mRNA和蛋白表达水平明显升高(P0.01);IFI16在PE组孕妇血清中的水平显著高于对照组(P0.01),且与孕妇收缩压(r=0.62,P0.001)、24h尿蛋白定量(r=0.723,P0.001)及相应胎盘组织中IFI16 mRNA表达水平(r=0.527,P0.05)呈正相关;r IFI16处理后,细胞培养上清液中ET-1和s VCAM-1浓度明显升高。结论:IFI16在PE孕妇胎盘组织和血清中的水平明显升高,并与内皮细胞损伤相关,提示IFI16可能通过损伤血管内皮细胞参与了PE的发病。     

Postpartum alterations in circulating endothelial progenitor cells in women with a history of pre-eclampsia

ObjectiveTo characterize persistent postpartum maternal endothelial dysfunction following pre-eclampsia (PE) through the assessment of endothelial progenitor cells as markers of endothelial reparative capacity.Study designMaternal circulating endothelial progenitor cells were measured at 2 months and 6 months postpartum in women who had recently experienced PE pregnancies (n = 17). Normotensive controls (n = 13) with uncomplicated pregnancies served for comparison at the same time points. Progenitor cells were measured by flow cytometry and by colony forming units. Maternal cardiovascular risk was measured at 6 months postpartum.Main outcome measuresLevels of maternal circulating endothelial progenitor cells and cardiovascular risk in the early postpartum period of uncomplicated and PE pregnancies.ResultsCD34 + VEGFR-2+ and CD133 + VEGFR-2+ cells were elevated in PE subjects at 2 months postpartum compared to healthy control subjects, although reduced by 6 months postpartum. PE was associated with reduced colony forming units at 2 and 6 months postpartum. Cardiovascular risk scores were increased in PE compared to normotensive controls.ConclusionsWe have demonstrated that there is a physiological alteration in the number and function of circulating progenitor cells following PE pregnancies. Furthermore, this population of women exhibited elevated cardiovascular risk profiles compared to those with uncomplicated pregnancies. Pregnancy and the development of PE identify an early window for cardiovascular risk screening in women. Cellular markers of vascular health offer an approach to the investigation of postpartum endothelial dysfunction.     

Risk factors for placental abruption in a socio-economically disadvantaged region

Objective. This study was undertaken in order to determine the risk factors for pregnancies complicated by placental abruption in a socio-economically disadvantaged region in metropolitan Adelaide.

Methods. This was a retrospective case–control study including all singleton pregnancies resulting in placental abruption between 2001 and 2005.

Results. The overall incidence of placental abruption was 1.0%; the overall perinatal mortality among the births with abruption was 13%. Univariate analyses showed the following significant risk factors for placental abruption: preterm pre-labor rupture of the membranes (PRE-PROM; odds ratio (OR) 4.79, 95% confidence interval (CI) 1.52–15.08), non-compliance with antenatal care (OR 2.93, 95% CI 1.06–8.90), severe intrauterine growth restriction (IUGR), and elevated homocysteine levels (OR 45.55, 95% CI 7.05–458.93). Severe IUGR was significantly more common in the abruption group compared with the control group (p = 0.032). In the multivariate analysis, PRE-PROM remained a significant independent risk factor for placental abruption. Marijuana use, domestic violence, and mental health problems were more common (borderline significance) in the abruption group. Smoking and preeclampsia were not found to be associated with placental abruption in this study.

Conclusions. In this high-risk population, PRE-PROM and elevated homocysteine levels appear to represent the major risk factors for placental abruption.     

Placental lesions of vascular insufficiency are associated with anti-angiogenic state in women with preeclampsia

Objective: To evaluate if placental histopathological changes of vascular insufficiency correlate with circulating angiogenic factors in patients with preeclampsia. Materials and methods: Subjects were selected from a previous prospective cohort study of preeclampsia based on the availability of plasma anti-angiogenic factor (sFlt1) and pro-angiogenic factor (PlGF) measurements and placental histology specimens. Preeclamptic patients were divided into two groups based on plasma levels of these factors described as a ratio: anti-angiogenic preeclampsia with sFlt1/PlGF ratio ≥85 and normal angiogenic preeclampsia with sFlt1/PlGF?n (%) when appropriate. Results: The anti-angiogenic preeclampsia group (N?=?48) presented at an earlier gestational age (weeks) than the normal angiogenic group (N?=?28); {32 (28, 34) versus 35 (32, 36), p?=?0.002}, had higher systolic blood pressure (mmHg) {154 (147, 168) versus 147 (132, 158), p?=?0.02}, delivered early (weeks) {(32 (29, 34) versus 36 (34, 37), p?p?p?p?=?0.002}, and syncytial knots {81.3% versus 39.3%, p?Conclusion: Preeclamptic patients with imbalance in circulating angiogenic factors have disproportionally higher rates of placental vascular lesions historically associated with severe disease.     

Optimal treatment of hypothyroidism associated with live birth in cases of previous recurrent placental abruption and stillbirth

Objective

To examine the clinical management of and placentas from pregnant women with hypothyroidism and obstetric history of recurrent stillbirth in order to identify possible etiologic mechanisms.

Methods

Two cases involving 26-year-old women with hypothyroidism and history of recurrent stillbirth are reported. Placentas from all of the women’s pregnancies were compared in order to identify histologic similarities.

Results

In both cases, multifocal hemorrhagic infarctions and abruptions were seen, indicating progressive uteroplacental ischemic damage leading to stillbirth. Thrombophilia, infection, and diabetes tests were all negative. With meticulous monitoring and normalization of thyroid function by end of first/early second trimester in subsequent pregnancies, there were live births and no evidence of infarction on placental histology.

Conclusion

The 2 reported cases raise the possibility of uteroplacental ischemia and placental abruption being mechanisms by which hypothyroidism can lead to stillbirth; they also highlight the potential of minimizing this risk via adequate levothyroxine treatment from early pregnancy.     

Circulating Angiogenic Factors and Abnormal Uterine Artery Doppler Velocimetry in the Second Trimester

Objective: Circulating angiogenic growth factors (such as vascular endothelial growth factor [VEGF] and placental growth factor [PlGF]) and their interaction may be associated with vascular remodeling of spiral arteries in normal pregnancy. Soluble Flt-1, an antagonist of both VEGF and PlGF, has been shown to be increased, while PlGF is decreased in women prior to the onset of preeclampsia. The purpose of this study was to compare maternal soluble Flt-1 and PlGF levels in the second trimester with a marker of abnormal placentation, abnormal uterine artery Doppler (UAD). Method: A prospective cohort of women, 16 to 24 weeks estimated gestational age (EGA), with singleton pregnancies, underwent UAD and phlebotomy. Maternal soluble Flt-1 and free PlGF were measured by ELISA in samples from women with abnormal UAD with a group, controlled for EGA, with normal UAD. Mann-Whitney Rank-Sum test was used to compare maternal serum levels of both soluble Flt-1 and PlGF between women with abnormal uterine artery Doppler versus women with normal uterine artery Doppler. Results: Of the 222 study subjects enrolled, 34 (15%) had abnormal UAD. The mean EGA at enrollment of subjects in each group was 18 weeks. There was no difference in PlGF between subjects with abnormal UAD (median, 191 pg/mL; range, 187 to 337 pg/mL) versus controls (median, 171 pg/mL; range, 169 to 289 pg/mL) (p = 0.59) or soluble Flt-1 (median, 780 pg/mL; range, 280 to 3200 pg/mL) or between subjects with abnormal UAD versus controls (median, 720 pg/mL; range, 220 to 1980 pg/mL) (p = 0.36). Conclusion: Concentrations of maternal soluble Flt-1 and free PlGF in the second trimester do not appear to be altered in women with abnormal UAD. This suggests that these biochemical markers are independent of the increased placental resistance seen with abnormal uterine artery Doppler.     

高龄孕妇子痫前期并发胎盘早剥妊娠结局分析

目的 探讨高龄对子痫前期并发胎盘早剥母儿结局的影响.方法 回顾性分析2017年1月至2019年12月在广州医科大学附属第三医院住院分娩的子痫前期并发胎盘早剥、单胎妊娠患者40例,以年龄≥35岁者为高龄组(14例),年龄<35岁者为对照组(26例),比较两组患者的临床资料特点、生化指标及围产儿结局.结果(1)两组孕妇一般...