The Predictive Value of Plasma Fibronectin Concentration on Fetal Growth Retardation at Earlier Stage of the Third Trimester

In order to evaluate the predictive value of maternal plasma fibronectin (FN) concentration at 24-34 weeks on fetal intrauterine growth retardation (IUGR), a prospective double-blinded study was performed. The maternal plasma FN concentrations were measured by using a rate nephelometric procedure in the 130 initial normal nulliparous pregnant woman at 24-34 gestational weeks. The outcome of pregnancies and birth weight of their infants were followed up. IUGR was defined as that the birth weight was less than the 10th percentile for gestational age. The receiver operating characteristic curves and predictive values of FN predicting on outcome of pregnancy with IUGR were analyzed. The results showed that: (1) In a cohort of 130 initially normal nulliparous pregnant women, IUGR occurred in 14 cases during the follow-up; (2) The plasma FN levels in the women with IUGR (467.58±104.43 mg/L) were significantly higher than in the normal control group (299.44±105.55 mg/L, P<0.01). However, there was no significant difference in the mean maternal age, gravidity, sampling gestational ages, delivering gestational ages between the two groups (P>0.05); (3) The areas under ROC curve for predicting the outcome of pregnancy in IUGR was 0.893; (4) At the cut point of 475 mg/L FN level, the sensitivity, specificity, positive predictive value, negative predictive value and Kappa index for predicting the outcomes of pregnancy in IUGR were 57.14 %, 95.69 %, 61.54 %, 94.87 %, 0.5455 respectively. It was concluded that the maternal plasma FN might be used as an earlier predictor for screening of IUGR.

Color Doppler Monitoring of Changes ofUtero-placental-fetal Circulation in Normal Pregnancy and Intrauterine Growth Retardation

The utero-placental-fetal circulation (UPFC) of 150 subjects duringsecond and third trimester was examined by using color DOppler. Of them 89 were normal woman and 58 were patients with intrauterine growth retardation (IUGR). Our results showed that UPFC was increased gradually during normal pregnant period. In IUGR patients it was revealed that TAV and Q of UmA,UmV and UtA decreased at 20th week of gestation, especially after 30th week.PI, RI and S/D ratio of UmA were increased, but TAV, Q of UmA and UmV were markly reduced, so was UtA. Pl were increased, but the changes of RI,S/D ratio in UtA were not significant. HemodynamicaI findings of UmA,UmV and UtA were abnormal in 92. 53 % of IUGR patients,Only 81. 03% present abnormal S/D ratio of UmA (P<0. 01) and the difference was statistically significant.Maternal serum E,, HPL level in IUGR were significantly lower than that of thenormal. 6KP level was reduced, TXB,/6KP ratio was significantly increased.TXB2/6KP ratio was markedIy related with TAV, Q of UmA, UmV and UtA.Our results suggested that using color doppler ultrasound for examination of hemodynamical changes of UmA, UmV and UtA could revealed UPFC function directly. It is one of the best methods for monitoring IUGR and might be used forearly diagnosis of IUGR. The main pathophysiological changes of IUGR were UPFC obstruction and placental disfunction.

Helicobacter pylori's virulence and infection persistence define pre-eclampsia complicated by fetal growth retardation

AIM: To better understand the pathogenic role of Helicobacter pylori (H. pylori) in pre-eclampsia (PE), and whether it is associated or not with fetal growth retardation (FGR). METHODS: Maternal blood samples were collected from 62 consecutive pregnant women with a diagnosis of PE and/or FGR, and from 49 women with uneventful pregnancies (controls). Serum samples were evaluated by immunoblot assay for presence of specific antibodies against H. pylori antigens [virulence: cytotoxin-associated antigen A (CagA); ureases; heat shock protein B; flagellin A; persistence: vacuolating cytotoxin A (VacA)]. Maternal complete blood count and liver enzymes levels were assessed at delivery by an automated analyzer. RESULTS: A significantly higher percentage of H. pyloriseropositive women were found among PE cases (85.7%) compared to controls (42.9%, P < 0.001). There were no differences between pregnancies complicated by FGR without maternal hypertension (46.2%) and controls. Importantly, persistent and virulent infections (VacA/ CagA seropositive patients, intermediate leukocyte blood count and aspartate aminotransferase levels) were exclusively associated with pre-eclampsia complicated by FGR, while virulent but acute infections (CagA positive/ VacA negative patients, highest leukocyte blood count and aspartate aminotransferase levels) specifically correlated with PE without FGR. CONCLUSION: Our data strongly indicate that persistent and virulent H. pylori infections cause or contribute to PE complicated by FGR, but not to PE without feto-placental compromise.

Placental Isoferritin Action in Pathogenesis of Pre-eclampsia and/or Intrauterine Growth Retardation and Its Earlier Predictive Value

In order to investigate the role of placental isoferritin (PLF) in pathogenesis of pre-eclampsia and/or intrauterine growth retardation (IUGR) and its earlier predictive value, a prospective double-blinded study was performed. In 120 initial normal pregnant women at earlier third trimester (from 24 to 34 weeks), plasma placental isoferritin and nitric oxide (NO) metabolites (nitrite/nitrate) (NO 2 -/NO 3 -) were examined by using ELISA and Criess assay respectively. The outcome of pregnancies and birth weight of their infants were followed up. The receiver operating characteristic curves (ROC) and predictive values of PLF predicting the outcome of pregnancy with IUGR, pre-eclampsia were analyzed. Results showed that in 120 initial normal pregnant women, IUGR occurred in 15 pregnant women (IUGR group) and pre-eclampsia in 19 (pre-eclampsia group), and the remaining 86 had normal pregnancy (normal group). The levels of plasma placental isoferritin were significantly decreased in IUGR group (260.01±58.95) μg/ml and pre-eclampsia group (285.31±53.73) μg/ml as compared with those in normal group (775.62±89.32) μg/ml at earlier third trimester (both P<0.01). The levels of plasma NO were significantly increased in IUGR group (61.57±46.22) μmol/L and pre-eclampsia group (58.37±30.52) μmol/L as compared with those in the normal group (35.29±24.46) μmol/L (both P<0.01). There was no significant difference in plasma placental isoferritin and NO levels between IUGR group and pre-eclampsic group (both P>0 05). The plasma placental isoferritin was negatively correlated with NO levels (r=0.329,P<0 01). The areas under ROC of PLF predicting IUGR and pre-eclampsia were 0.977 and 0.905 respectively. At the cut point of 400 μg/ml PLF level, the sensitivity, specificity, positive predictive value, negative predictive value and Kappa index of PLF levels predicting the outcome of pregnancy with pre-eclampsia were 100 %, 85.15 %, 55.88 %, 100 % and 0.645 respectively. At the cut point of 390 μg/ml PLF level, the sensitivity, specificity, positive predictive value, negative predictive value and Kappa index of PLF levels predicting the outcome of pregnancy with IUGR were 100 %, 81.9 %, 44.12 %, 100 % and 0.663 respectively. It was concluded that the decrease of plasma placental isoferritin levels at earlier third trimester was associated with IUGR and/or pre-eclampsia, and the endothelial cell damage may be one of its mechanisms. The plasma PLF level can be used as an earlier predictor for screening of IUGR and/or pre-eclampsia.

Perinatal Morbidity, Mortality, and Neurodevelopmental Outcomes of Neonates with Fetal Growth Restriction

Objective: This study aimed to assess perinatal morbidity, mortality rates, and neurodevelopmental outcomes in the management of fetal growth restriction (FGR) at a single tertiary institute. Methods: Among 2465 deliveries between 2013 and 2019, 109 cases of FGR were reviewed retrospectively for causes, indications for pregnancy termination, perinatal death, overall neonatal outcomes, and long-term prognosis. Results: Excluding FGR due to congenital anomalies (n = 17), the mortality rate was 3.3% (3/92). One neonate delivered at 23 weeks developed cerebral palsy (1.1%). Retinopathy of prematurity occurred in four neonates (4.3%). Neurodevelopmental disorders were present in six neonates (6.5%), all of whom were delivered at 32 - 38 weeks. Significantly lower gestational age at delivery, lower birth weight, and higher umbilical artery resistance indices were observed in neonates with neurodevelopmental disorders. Conclusions: Intact survival before 27 weeks of gestation at delivery with FGR is uncommon. Neurodevelopmental disorders may still develop after delivery at 32 - 38 weeks;consideration should be given to the timing of delivery usingfetal ductus venosus Doppler waveforms measurements to reduce neurodevelopmental disorders.

Role of intergenic interactions among folate cycle genes in the development of fetal growth retardation

Objective:Metabolic disturbances in the folate cycle in mothers can lead to fetal growth retardation(FGR).This study was to analyze the role of intergenic interactions among maternal folate cycle genes in the development of FGR.Methods:This case-control study recruited 365 women in the third trimester of pregnancy,including 122 FGR patients and 243 controls.The women were genotyped for 5 polymorphisms of the 4 folate cycle genes:MTR(rs1805087),MTRR(rs1801394),serine hydroxymethyl transferase(SHMT1;rs1979277),and TYMS(rs699517 and rs2790).The SNP×SNP interactions in the two-,three-,and four-locus models were analyzed using the multifactor dimensionality reduction method and a modification of it(the model-based multifactor dimensionality reduction method).Results:Four loci of maternal folate cycle genes(rs1805087 MTR,rs2790 TYMS,rs1801394 MTRR,and rs1979277 SHMT1)were associated with FGR in 3 significant models of single nucleotide polymorphism(SNP)×SNP interactions(two-,three-,and four-locus models)(P<0.05).The highest contribution to FGR was made by polymorphic loci rs1979277 SHMT1(1.70%of entropy),rs1805087 MTR(0.96%),and interactions between rs1979277 SHMT1×rs1805087 MTR(-1.11%)and rs1801394 MTRR×rs1979277 SHMT1(-0.64%).The four-locus maternal genotype combination AG rs1801394 MTRR×AA rs1805087 MTR×CT rs1979277 SHMT1×AG rs2790 TYMS was associated with an increased risk of FGR(β=2.69,P=0.012).FGR-associated SNPs were correlated with the expression of 16 genes(MTR,MTRR,SHMT1,ALKBH5,CTD-2303H24.2,ENOSF1,FAM106A,FOXO3B,LGALS9C,LLGL1,MIEF2,NOS2P2,RP11-806L2.6,SMCR8,TOP3A,and USP32P2)in various tissues and organs related to FGR pathophysiology.Conclusion:SNP×SNP interactions of maternal folate cycle genes(MTR,MTRR,SHMT1,and TYMS)are associated with the development of FGR.

Fetal programming of polycystic ovary syndrome

Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development,possibly even during intrauterine life.This suggests that PCOS is either genetically-transmittedor is due to epigenetic alterations that develop in the intrauterine microenvironment.Although familial cases support the role of genetic factors,no specific genetic pattern has been defined in PCOS.Several candidate genes have been implicated in its pathogenesis,but none can specifically be implicated in PCOS development.Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories.The first is the "thrifty" phenotype hypothesis,which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and,as a compensatory mechanism,insulin resistance.Additionally,an impaired nutritional environment can affect the methylation of some specific genes,which can also trigger PCOS.The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues,causing the PCOS phenotype to develop in adult life.This review aimed to examine the role of fetal programming in development of PCOS.

超声微血管成像联合血管内皮生长因子诊断胎儿生长受限

目的观察超声微血管成像(MV-Flow)联合孕妇血清血管内皮生长因子(VEGF)表达水平诊断胎儿生长受限(FGR)的价值。方法前瞻性纳入87例胎儿生长受限[FGR组,包括43例孕周<28周(<28周亚组)及44例孕周≥28周(≥28周亚组)]孕妇及112名正常孕妇[对照组,55名孕周<28周(对照组1)、57名孕周≥28周(对照组1)],以MV-Flow技术测量胎盘微血管指数(MVI),于同期检测孕妇血清VEGF表达水平,于分娩后即刻检测胎盘母体面VEGF表达水平;绘制受试者工作特征曲线,评价胎盘MVI、母体血清VEGF及二者联合诊断FGR的价值。结果FGR组2亚组胎盘MVI、孕妇血清VEGF表达水平及胎盘组织VEGF表达水平均明显低于对照组(P<0.01)。胎盘MVI、母体血清VEGF及二者联合诊断<28周FGR的曲线下面积(AUC)分别为0.981、0.870和0.997,诊断≥28周FGR的AUC分别为0.991、0.867和0.993。以单一孕妇血清VEGF诊断2亚组FGR的AUC均低于胎盘MVI及其联合孕妇血清VEGF(P均<0.05),而后二者AUC差异均无统计学意义(P均>0.05)。结论胎盘MVI和孕妇血清VEGF可用于筛查FGR,而前者更具价值。

TNF-α和IL-6对胎儿生长受限胎儿骨骼肌的影响

胎儿生长受限(fetal growth restriction,FGR)是一种常见的产科疾病,其可导致新生儿低出生体质量和出生后肌肉量减少。这可能与肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白细胞介素-6(interleukin-6,IL-6)的调控密切相关。研究发现,这两种炎症因子在FGR胎儿中表达水平异常,可通过影响成肌细胞的增殖和分化,干扰正常骨骼肌的发育。此外,TNF-α与IL-6还可以激活特定的信号通路,如核因子κB(nuclear factor-κB,NF-κB)、Janus激酶/信号转导及转录活化因子(Janus kinase/signal transducer and activator of transcription,JAK/STAT)、丝裂原激活的蛋白激酶(mitogen-activated protein kinase,MAPK)等信号通路,调节肌细胞的代谢和功能。如使用特定的抗炎药物或生物制剂来降低TNF-α和IL-6的活性,可能有助于改善FGR胎儿的骨骼肌发育。总的来说,TNF-α和IL-6在FGR胎儿骨骼肌发育中的作用是一个多层面、复杂的过程,需要进一步的深入研究来阐明其具体机制,帮助理解FGR的病理生理学,并为治疗FGR胎儿提供新的思路。

子痫前期血清中血管生成抑制蛋白1水平与胎儿生长受限的相关性分析

目的检测子痫前期(PE)病人血清中血管生成抑制蛋白1(VASH1)的水平,分析其与胎儿生长受限(FGR)的相关性。方法选取2020年3月至2022年3月雅安市人民医院收治的152例PE病人作为研究对象,其中发生FGR的有80例(FGR组),未发生FGR的有72例(非FGR组)。采用酶联免疫吸附法测定血清VASH1水平;受试者操作特征曲线(ROC曲线)分析血清VASH1水平对PE病人发生FGR的预测价值;logistic回归分析PE病人发生FGR的影响因素。结果FGR组PE病人尿蛋白(186.71±11.15)mg/24 h、收缩压(166.66±10.11)mmHg、舒张压(95.52±7.17)mmHg水平均显著高于非FGR组[(167.62±10.51)mg/24 h、(153.62±9.19)mmHg、(89.80±6.11)mmHg](均P<0.05)。FGR组PE病人血清VASH1水平(467.89±111.24)ng/L显著高于非FGR组(328.33±69.54)ng/L(P<0.05)。FGR组PE病人胎儿胫骨长度(5.93±0.20)cm、双顶径(7.87±0.21)cm、头围(28.15±1.27)cm显著低于非FGR组[(6.59±0.38)cm、(8.64±0.47)cm、(31.43±1.36)cm](均P<0.05)。FGR病人血清中VASH1的水平与尿蛋白、收缩压、舒张压水平呈正相关,与胎儿胫骨长度、双顶径、头围水平呈负相关(均P<0.05)。单因素回归分析表明,高水平VASH1、高水平尿蛋白、高水平舒张压是影响FGR发生的危险因素(P<0.05);多因素分析得知,高水平VASH1、高水平尿蛋白、高水平舒张压是影响FGR发生的独立危险因素(P<0.05)。结论FGR组PE病人血清VASH1水平显著高于非FGR组,是影响PE病人发生FGR的独立危险因素,检测血清VASH1水平有利于筛查出PE病人中FGR发生风险较高的病人。

SLRPs在胎盘发育及妊娠相关疾病中的研究进展

小富亮氨酸蛋白聚糖家族(small leucine-rich proteoglycans,SLRPs)是一类富含亮氨酸重复序列的小分子蛋白聚糖,是细胞外基质的关键组成部分,参与调控多项生理功能。SLRPs共分为5类,其中Ⅰ类SLRPs的主要成员decorin、biglycan和Ⅱ类SLRPs的主要成员lumican、fibromodulin在胎盘和子宫中的表达尤为显著,在妊娠过程中起到重要作用。这些蛋白聚糖参与维持妊娠期细胞外基质的稳态平衡,通过介导细胞间信号转导,调节绒毛外滋养层细胞的增殖、迁移和侵袭能力,影响胎盘血管的形成与功能,在维持胎盘和胎膜结构-功能完整性方面发挥重要作用,它们的异常表达或功能改变可能与子痫前期、胎儿生长受限等多种妊娠相关疾病的发病密切相关。综述SLRPs在胎盘发育和妊娠相关疾病中的作用机制,以期为临床防治提供相关理论支持。

胎盘体积结合葡萄糖转运蛋白3对胎儿生长受限的预测价值

目的探讨胎盘体积联合血清中葡萄糖转运蛋白3(GLUT3)对胎儿生长受限的预测价值。方法以我院2018年12月—2020年5月行MRI检查的100例胎儿生长受限的孕妇作为观察组,孕检正常的100例孕妇作为对照组。根据MRI检查获取受试者胎盘体积,并检测受试者血清GLUT3的水平;采用logistics回归模型构建胎盘体积与血清GLUT3联合诊断模型,应用ROC曲线下面积(AUC)评判胎盘体积和血清GLUT3独立或两者联合应用对胎儿生长受限的预测价值。结果两组孕妇胎盘体积和血清GLUT3水平比较差异均具有显著性(t=13.380、54.173,P<0.05)。以胎盘体积联合血清GLUT3预测胎儿生长受限的模型为Logit(P)=-0.647×胎盘体积+0.598×GLUT+0.431;胎盘体积联合血清GLUT3预测胎儿生长受限的灵敏度、特异度及AUC均明显高于单个指标(P<0.05)。结论胎盘体积联合血清GLUT3对胎儿生长受限具有一定的预测价值。

胎儿生长受限的病因及对患儿远期健康的影响

胎儿生长受限(fetal growth restriction,FGR)是指胎儿在妊娠期内无法达到其预期的生长潜力,其是妊娠期常见且较复杂的并发症之一。FGR病因复杂多样,可能是由母体、胎儿或胎盘因素所引起。对于存在FGR的儿童和成年患者,长期的追踪研究揭示了其健康状况的不良后果。生长受限胎儿的出生体质量和身长明显落后于正常儿童,绝大部分患儿在生后早期即开始出现明显的生长追赶,但其存在更高的代谢问题风险。FGR常常伴随着一系列的远期并发症,如神经系统发育障碍和骨骼肌生长代谢异常等问题,甚至是在成年期时更易出现代谢综合征和心血管疾病,这对患儿的身体健康和生活质量产生了严重影响。综述FGR致病因素及对患儿远期健康的影响,以期为临床防治提供相关理论支持。

胎儿生长受限孕妇血清与胎盘Gas6、Endoglin、PLAC-1表达水平及其临床意义

目的分析胎儿生长受限(FGR)孕妇血清及胎盘中生长阻滞特异性蛋白6(Gas6)、Endoglin、胎盘特异性蛋白1(PLAC-1)表达水平,并探讨其临床意义。方法选取2022年5月至2024年9月确山县人民医院收治的81例FGR孕妇为FGR组,按照1∶1配对原则,另选取同期81例无FGR孕妇为对照组。比较两组孕妇的基线资料和胎盘相关指标(Gas6 mRNA、Endoglin mRNA、PLAC-1 mRNA、胎盘厚度、胎盘质量),采用Pearson法分析胎盘各指标表达与胎盘厚度、胎盘质量、新生儿体质量的相关性,比较两组孕妇不同孕期的血清各指标水平,采用Pearson法分析孕妇血清与胎盘各指标表达的相关性,采用受试者工作特征曲线(ROC)分析血清各指标对FGR的预测价值。结果FGR组孕妇的新生儿体质量、PLAC-1 mRNA、胎盘厚度、胎盘质量[(2.13±0.32)kg、0.50±0.11、(1.90±0.66)cm、(0.38±0.10)kg]明显低于对照组[(3.23±0.29)kg、1.00±0.06、(2.51±0.57)cm、(0.59±0.08)kg],胎盘Gas6 mRNA、Endoglin mRNA(1.42±0.24、1.38±0.16)明显高于对照组(1.04±0.05、1.06±0.07),差异均有统计学意义(P<0.05);胎盘Gas6 mRNA、Endoglin mRNA与胎盘厚度、胎盘质量、新生儿体质量呈负相关(P<0.05),PLAC-1 mRNA与胎盘厚度、胎盘质量、新生儿体质量呈正相关(P<0.05);FGR组孕妇孕早、中、晚期的血清Gas6、Endoglin明显高于对照组,PLAC-1明显低于对照组,差异均有统计学意义(P<0.05);孕早、中、晚期血清Gas6、Endoglin、PLAC-1表达与对应指标胎盘中表达量均呈正相关(P<0.05);经ROC分析结果显示,孕早、中、晚期血清Gas6、Endoglin、PLAC-1联合预测FGR的曲线下面积(AUC)分别为0.890、0.913、0.936,均优于单一指标,且血清各指标联合预测FGR的AUC随着孕期的推进依次增大,至孕晚期联合预测AUC为0.936,为最大。结论FGR孕妇血清及胎盘组织中Gas6、Endoglin、PLAC-1表达异常,且血清各指标联合检测对FGR具有一定预测价值,可作为临床早期评估FGR的辅助指标。

孕中期子宫动脉搏动指数联合血清β-HCG水平对孕妇发生晚发型胎儿宫内生长受限的预测价值

【目的】探讨孕中期子宫动脉搏动指数(PI)联合血清β亚单位人绒毛膜促性腺素(β-HCG)水平对孕妇发生晚发型胎儿宫内生长受限的预测价值。【方法】选择2019年1月至2023年12月在西安市人民医院(西安市第四医院)定期产检的179例孕妇,根据是否发生晚发型胎儿宫内生长受限分为晚发型胎儿宫内生长受限组(于妊娠32周以后首次诊断为胎儿生长受限,A组)和非晚发型胎儿宫内生长受限组(B组),检测两组孕妇孕中期PI、β-HCG水平,采用Logistic多因素回归分析孕妇发生晚发型胎儿宫内生长受限的危险因素,分析孕中期子宫动脉PI联合β-HCG水平对孕妇发生晚发型胎儿宫内生长受限的预测价值。【结果】179例孕妇发生晚发型胎儿宫内生长受限31例,发生率为17.32%。两组年龄、孕次、妊娠期高血压家族史、收缩压、总胆固醇(TC)、白蛋白水平比较,差异无统计学意义(P>0.05)。A组PI、β-HCG水平及分娩孕周高于B组(P<0.05)。Logistic多因素回归分析结果显示:PI、β-HCG水平高为孕妇发生晚发型胎儿宫内生长受限的危险因素(P<0.05)。受试者工作特征(ROC)曲线结果显示:PI联合β-HCG水平预测孕妇发生晚发型胎儿宫内生长受限的曲线下面积(AUC)值为0.937,显著高于单独预测值(P<0.05)。【结论】PI、β-HCG与孕妇发生晚发型胎儿宫内生长受限密切相关,两者可用于预测孕妇发生晚发型胎儿宫内生长受限,且联合预测效能更高。

胎儿宫内发育迟缓的孕前高危因素分析

目的:分析胎儿宫内发育迟缓的孕前高危因素。方法:回顾性分析2019年1月—2023年12月肇庆市广宁县人民医院收治的493例产妇的临床资料,追踪其妊娠结局,根据新生儿是否发生宫内发育迟缓进行分组,将发生胎儿宫内发育迟缓的产妇纳入观察组(n=43),未发生胎儿宫内发育迟缓的产妇纳入对照组(n=450)。比较两组产妇一般资料[年龄、身高、文化程度、收入水平、孕前身体质量指数(BMI)、吸烟情况、酗酒情况]、孕次、产次、贫血、合并糖尿病、流产史等指标。采用多因素Logistic回归分析胎儿宫内发育迟缓的孕前独立危险因素。结果:两组产妇身高、文化程度、月收入、吸烟情况、酗酒情况、孕次、产次、合并糖尿病情况比较,差异无统计学意义(P>0.05);观察组年龄<25岁、孕前BMI<18.5 kg/m^(2)、有流产史、贫血占比均高于对照组(P<0.05)。Logistic回归分析显示,年龄<25岁、孕前BMI<18.5 kg/m^(2)、合并贫血、有流产史是影响胎儿宫内发育迟缓的孕前高危因素(P<0.05)。结论:孕妇年龄小、孕前BMI低、贫血、流产史均是影响胎儿宫内发育迟缓的孕前高危因素,对存在相关高危因素的孕妇进行监护,有助于预防胎儿宫内发育迟缓。

Low Expression of FGF23 and Its Effect on Rats with Intrauterine Growth Retardation

Objective:To explore the levels of fibroblast growth factor 23(FGF23)during pregnancy and its relationship with intrauterine growth restriction(IUGR).Methods:Pregnant rats were classified into an ad libitum rat chow group(ad libitum rat chow,AD group,n=25)and an undernutrition group(50%of their daily food requirement,UN group,n=25).The levels of maternal serum FGF23,tissue homogenate FGF23,and bone gla protein in fetal rats,and placental FGF23 mRNA and protein expression were examined by enzyme-linked immunosorbent assay,real-time qPCR analysis respectively.Finally,the effect of recombinant FGF23 on the viability of MG-63 cells was determined by cell proliferation assay.Data were analyzed with independent two-tailed t test and one-way analysis of variance.Spearman rank-order correlation coefficients(continuous variables)was performed to determine the relationship of results.Results:The diet restriction induced IUGR in rat offsprings,and the UN group exhibited a significantly lower FGF23 level(P<0.05,n=5).The FGF23 level was increased and peaked in maternal serum on gestation day(GD)15,but peaked in fetal and placenta on GD20.Moreover,the tissue homogenate levels of FGF23 and bone gla protein in fetal rats in both groups were positively correlated(r=0.923,P<0.05;r=0.925,P<0.05,respectively,n=15),FGF23 was localized to both decidual and labyrinth zones,with remarkably higher expression on GD20,P<0.05,n=5.In vitro,recombinant human FGF23 enhanced MG-63 cell viability,P<0.05,n=5.Conclusion:Prenatal undernutrition could decrease the FGF23 expression in fetal rats caused by the mother through the placenta,and induced the IUGR and hindered the ossification.And the FGF23 levels are peaked on GD15 mother but peaked on GD20 placenta and fetuses,these might be associated with the over compensation of maternal placenta on GD20.

胎儿静脉导管多普勒血流检测在产前诊断中的应用

随着对胎儿血流动力学研究的深入和超声多普勒技术的成熟,分析胎儿静脉系统的血流变化逐渐成为估测宫内胎儿情况的最新手段。其中,胎儿静脉导管(DV)血流的变化更能准确、全面地评价胎儿生长发育状况,预测染色体异常和心脏疾病等的发病风险。本文对DV超声多普勒检测在产前诊断中的应用进行综述。

褪黑素保护细菌脂多糖引起的小鼠宫内胎儿死亡和生长发育迟缓

目的研究褪黑素（MT）对细菌脂多糖（LPS）引起宫内胎儿死亡（IUFD）和生长发育迟缓（IUGR）的保护作用。方法实验1：LPS组小鼠于受孕第15-17天每天经腹腔注射LPS（75μg／kg），LPS＋MT组在LPS处理前和（或）处理后经腹腔注射MT，生理盐水和单纯MT处理作为对照。所有孕鼠于受孕第18天处死，统计活胎、死胎和吸收胎数，称量活胎体重，测量胎鼠身长和尾长，并对胎鼠骨骼发育情况进行评价。实验2：LPS组小鼠于受孕第16天经腹腔一次性注射75μg／kg LPS，LPS＋MT组孕鼠于LPS处理前和（或）处理后经腹腔注射MT，生理盐水和单纯MT处理作为对照。LPS处理后6h处死孕鼠，取母肝和胎盘，检测丙二醛和谷胱甘肽水平。结果LPS＋MT处理组宫内胎儿死亡数显著低于单纯LPS处理组，并呈明显剂量-效应关系；MT预＋后和后处理均显著减轻LPS引起生长发育迟缓，并逆转LPS引起的枕骨骨化不全。MT预＋后处理明显减轻LPS引起的母肝和胎盘脂质过氧化，但对LPS所致GSH含量降低无明显影响。结论MT通过其抗氧化功能保护LPS引起的IUFD和IUGR。

晚发型胎儿生长受限胎盘组织绒毛微循环变化的体视学分析

目的:观察晚发型胎儿生长受限(fetal growth restriction,FGR)患者胎盘绒毛微血管的体视学变化,探讨FGR的发病机制。方法:FGR组和对照组的胎盘组织标本各15例,应用免疫组织化学法抗CD34标记血管内皮细胞显示血管,测试胎盘绒毛内微血管的长度密度和体积密度。结果:抗CD34几乎标记胎盘绒毛所有的血管。两组微血管长度密度的差异无统计学意义(P>0.05),FGR组微血管体积密度小于对照组,差异有统计学意义(P<0.05)。结论:胎盘绒毛微血管管腔缩窄引起胎盘微循环血量减少,可能导致FGR的发生。