水肿胎儿血液常规指标分析

目的检测Barts′（重型α-地贫）、染色体异常、病毒感染、同种免疫性（母Rh-）及其他原因所致水肿胎儿血液常规指标并与相同孕周胎儿血液常规指标比较,分析各种原因所致水肿胎儿血液常规指标变化规律,探讨水肿胎儿病因与病理的内在联系,为胎儿宫内疾病诊治提供线索。方法应用全自动血液分析仪对66例孕19~35w水肿单活胎儿脐血进行染色体,TORCH,胎儿血红蛋白检查和血常规：白细胞总数（WBC）及中性粒细胞分类（NEU%）、淋巴细胞分类（LYM%）、单核细胞分类（MONO%）、嗜酸性白细胞分类（EOS%）、嗜碱性白细胞分类（BASO%）和红细胞数（RBC）、血红蛋白（HGB）、血球压积（HCT）、红细胞平均体积（MCV）、平均体积血红蛋白（MCH）、血小板（PLT）、有核红细胞（NRBC）等检测;并按染色体、TORCH、Bart′s、其他原因的水肿胎儿分为4类和按孕周分组统计与同孕周正常胎儿比较。结果RBC、HGB、HCT、MCV、MCH、NRBC水平在所有水肿胎（包括染色体、TORCH、Bart′s和其他原因）与同孕周正常胎儿中均有显著差异,而WBC、NEU%、LYM%、MONO%、EOS%、BASO%、PLT等数值在各组间无显著差异。结论胎儿血RBC、HGB、HCT、MCV、MCH、NRBC水平,可作为胎儿水肿等发育异常胎儿诊断与评估的参考指标。     

水肿胎儿血液生化指标分析

目的检测水肿胎儿（包括Bart′s、染色体异常、病毒感染、同种免疫性及其他原因所致水肿胎儿）血液生化指标并与相同孕周胎儿血液生化指标比较,分析各种原因所致水肿胎儿血液生化指标变化,探讨水肿胎儿病因与病理,为胎儿疾病诊断与治疗提供线索和依据。方法应用Bayer1650全自动生化分析仪对66例孕19～35周水肿单活胎儿脐静脉穿刺所取脐血进行：碱性磷酸酶（ALP）、谷草转氨酶（AST）、谷丙转氨酶（ALT）、总胆红素（TB）、直接胆红素（DB）、间接胆红素（IB）、总蛋白（TP）、白蛋白（ALB）、球蛋白（GLB）、r-谷氨酰基转酞酶（r-GT）、羟丁氨酸脱氢酶（HBDH）、乳酸脱轻酶（LDH）、肌酸磷酸激酶（CK）、肌酸磷酸激酶同工酶-1（CK-MB）等项生化指标检测,同时进行染色体,TORCH,胎儿血红蛋白和血常规等检查;并按染色体、TORCH、Bart′s、不明原因的水肿胎儿分为四类和按孕周分组统计与同孕周正常胎儿比较。结果除外Bart′s水肿胎其余原因（包括染色体、TORCH、和其他原因）所致水肿胎的心、肝酶及蛋白等水平均与与同孕周正常胎儿的水平有显著差异。结论胎儿在水肿的病理状态时存在血液生化指标异常,可能是水肿的原因或是后果,可作为水肿胎儿诊断与评估及治疗效果观察的参考指标。     

超声诊断胎儿唇腭裂畸形漏诊原因及对策

目的探讨超声诊断胎儿唇腭裂畸形漏诊原因及对策。方法对超声诊断并经引产证实的10例胎儿唇腭裂畸形的超声图像进行回顾性分析。结果复习文献,结合病例,找到超声诊断胎儿唇腭裂的影响因素（1）胎龄的影响;（2）胎位的影响;（3）合并其它因素的影响等。结论总结经验提出防漏诊的对策：（1）正确选择超声筛查时机;（2）掌握正常胎儿唇腭部的超声图像;（3）多切面、多角度、多体位仔细检查以防漏诊;（4）可疑病例复查后诊断。     

影响产前超声诊断胎儿出生缺陷因素的研究

目的探讨影响产前超声诊断胎儿出生缺陷（胎儿先天畸形）的因素。方法对319例分娩证实的胎儿畸形与产前超声诊断结果进行对照分析。结果产前超声诊断胎儿出生缺陷240例,诊断符合率75.23%;漏误诊79例,漏误诊率24.76%。各类出生缺陷漏误诊构成比依次为心脏缺陷25.23%,多指（趾）、并（趾）指畸形15.18%,尿道下裂11.39%,唇腭裂8.86%,肢体关节畸形7.59%,足内（外）翻5.06%,隐性脊柱裂5.06%,两性畸形5.06%,染色体异常3.79%,外耳廓畸形3.79%,无眼球1.26%,双足皮肤缺损1.26%,轻度鱼鳞病1.26%,其它畸形5.06%。结论影响产前超声诊断胎儿出生缺陷的因素,主要为胎儿畸形的类别、超声医师个人专业的差异、产科医师宣教、产前超声检查的时间、次数、仪器条件、母体的情况（肥胖、水肿等）、胎儿的宫内情况（羊水、体位）以及胎儿的宫内情况和产科医师的宣教有关。     

胎儿血清β2-微球蛋白测定的临床意义

目的通过比较检测正常胎儿和发育异常胎儿脐血β2-微球蛋白水平,并探讨其临床意义。方法通过脐带穿刺取得胎儿血,应用免疫比浊法对107例产前诊断结果正常的胎儿以及77例宫内感染、胎儿发育迟缓（SGR）并羊水少和泌尿系畸形等发育异常的胎儿血清β2-MG含量进行测定。结果妊娠18～34周正常胎儿血清β2-MG含量为（4.57±0.56）mg/L,与孕周变化无相关;妊娠34周后β2-MG含量下降,妊娠35～38周胎儿血清β2-MG含量为（3.58±0.69）mg/L,与妊娠18～34周相比差异有统计学意义（P〈0.05）;宫内感染、SGR并羊水少和泌尿系畸形等胎儿β2-MG含量与正常胎儿相比明显升高,差异有统计学意义（P〈0.05）。结论检测胎儿血清β2-微球蛋白水平,可为宫内感染、SGR并羊水少和泌尿系畸形等发育异常胎儿诊断与评估提供参考指标。     

胎儿畸形198例临床分析和预防措施

目的了解胎儿畸形的发生率、发生系统及缺陷分布情况,探讨引起胎儿畸形的相关因素,为临床预防和治疗提供依据。方法我院2006年1月至2009年12月产前检查确诊胎儿畸形并引产的198例病例进行回顾性分析。结果 198例胎儿畸形引产的原因位于前6位的分别为：先天性心脏病（32例,占16.6%）、脑积水（21例,占10.60%）、唇腭裂（20例,占10.10%）、四肢畸形包括四肢短小、并指、并趾（19例,占9.60%）、神经管畸形（18例,占9.09%）、消化道畸形（15例,占7.58%）。结论胎儿畸形的发生与孕妇的年龄、文化程度素质、环境、孕期服药、孕期合并症、并发症及营养等有关。为了减少出生缺陷的发生,应以预防为主,加强孕前及产前咨询,避免孕早期不良因素影响,尽早发现异常,及时行治疗性引产,以免给家庭和社会带来负担。     

不同分娩方式对母婴垂体前叶激素的影响

目的：研究不同的分娩方式对孕妇及胎儿垂体前叶激素分泌的影响。方法：选取25例自然经产道顺产孕妇（顺产组）;25例剖宫产孕妇,手术采取脊麻-硬膜外联合阻滞麻醉（剖宫产组）。以免疫学方法分别测得孕妇外周血及胎儿脐血中泌乳素（PRL）、促甲状腺激素（TSH）、促肾上腺皮质激素（ACTH）浓度。结果：顺产组孕妇及胎儿PRL、TSH、ACTH均比剖宫产组高（P〈0.05）。结论：剖宫产手术可影响孕妇及胎儿垂体激素水平,垂体分泌PRL、TSH、ACTH功能降低。     

超声多普勒检测晚孕期妊娠高血压综合征胎儿静脉导管血流的临床价值

目的探讨超声多普勒对晚孕期妊娠高血压综合征（PIH）胎儿静脉导管血流检测的临床价值。方法将临床确诊为PIH、孕周为32—40周的胎）L85例作为研究组,随机抽取相同孕周正常胎）LI32例为对照组。除外糖尿病、心脏病、胎儿畸形、多胎等影响因素。以超声多普勒检测胎儿静脉导管（DV）血流,分析每例胎儿的频谱波形变化,检测并计算相关的血流参数,并追踪每一例胎儿出生结局。结果研究组胎）LDV搏动指数（PI）、阻力指教（RI）、静脉前负荷指数（PLI）、S／a较对照组增高,两组比较有统计学意义。PIH胎儿不良出生结局组DV血流参数较正常出生结局组增高,两组比较有统计学意义。结论检测PIH胎儿DV血流参数可作为了解胎儿宫内情况及预测出生结局的有效指标,对指导围产期处理有重要临床价值。     

肾上腺髓质素与妊娠合并胎儿生长受限关系的研究进展

胎儿生长受限（fetal growth restriction，FGR）是指胎儿体重低于同孕龄胎儿平均体重两个标准差或第十百分位数，是围产期的主要并发症之一。其发生率占妊娠总数的3％-7％，围产儿的死亡率为正常发育胎儿的4～6倍。FGR与遗传、营养、孕妇患各种慢性疾病及吸烟、环境、胎次、年龄等因素有关，另外，胎儿本身发育缺陷畸形、宫内感染等也可影响胎儿发育。     

彩色多普勒及无应激试验监测胎儿窘迫的临床应用

目的探讨彩色多普勒超声及无应激试验（NST）监测胎儿窘迫的临床价值。方法80例孕龄37-42周的孕妇,其中40例胎儿窘迫及40例胎儿正常。均于产前进行彩色多普勒超声探测及NST。结果胎儿窘迫组其血流阻力指标：胎儿大脑中动脉（MCA）的S/D、血流阻力指数（RI）、搏动指数（PI）明显低于胎儿正常组（P〈0.01）,而母体子宫动脉（UTA）的血流阻力指标均明显高于胎儿正常组（P〈0.01）。此外,胎儿窘迫组与胎儿正常组S/D与NST对胎儿缺氧检测,其灵敏度、特异度、阳性预测值、阴性预测值分别为92.5%、95.0%、94.5%、92.7%,NST为75.0%、62.5%、66.7%、71.4%。S/D对胎儿窘迫的检出率明显高于NST。结论应用彩色多普勒超声检测血流动力学中阻力指标对胎儿窘迫的诊断优于NST。     

重度子痫前期患者肝功能损害与围产儿结局的相关性研究

目的 分析重度子痫前期患者肝功能损害与围产儿结局的相关性.方法 回顾性分析114例重度子痫前期合并肝功能损害患者(观察组)及同时期100例重度子痫前期未合并肝功能损害患者(对照组)、正常住院分娩的100例孕妇(正常组)的临床资料,比较观察组与正常组血清谷氨酸转氨酶(alanine aminotransferase,ALT)、天冬氨酸氨基转移酶(aspartate aminotransferase,AST)、r-谷氨酰转肽(glutamyl transferase,GGT)水平,并比较观察组与对照组的围产儿结局,采用线性回归分析,分析血清ALT、AST、GGT与围产儿结局的相关性.结果 观察组血清ALT、AST、GGT水平均显著高于正常组,差异具有统计学意义(P＜0.05);观察组胎儿生长受限、早产、围产儿死亡、胎盘早剥、死胎的发生率均大于对照组,差异具有统计学意义(P＜0.05);血清ALT、AST、GGT水平与胎儿生长受限、早产和围产儿死亡发生率呈正相关(P＜0.05).结论 重度子痫前期患者肝功能损害与围产儿结局的发生、发展具有明显的相关性,随着肝功能损害程度增大,可能导致胎儿生长受限、早产、围产儿死亡等不良围产儿结局发生.     

Chorangiosis: the potential role of smoking and air pollution

Chorangiosis is considered to be strongly associated with various fetal, maternal, and placental disorders, including pre-eclampsia, diabetes, hypertension, and major congenital anomalies, and has been found to correlate with increased fetal morbidity and mortality. In this study, we investigated the pathologic effects of maternal smoking and air pollution on the pathogenesis of chorangiosis. We investigated 92 placentas macroscopically and microscopically over a 3-month period (March 2006-May 2006) at Denizli State Hospital to identify the frequency of chorangiosis and the potential role of maternal smoking and air pollution. Placental changes were examined by light microscopy after hematoxylin and eosin (H&E) staining and immunohistochemical evaluation of CD 34 and CD 68; muscle-specific actin was used to confirm the diagnosis. Among the 92 mothers included in the study, 33 were smokers (group I), 31 were thought to have been exposed to air pollution (group II), and 28 were living in rural areas free of air pollution and maternal smoking (group III). Chorangiosis was found in 14% (13/92) of all placentas: 7 (53.8%) cases were assigned to group I, 5 (38.5%) to group II, and 1 (7.7%) to group III. Vascular changes were found mainly in the smoking and air pollution groups. There appeared to be no correlation of these vascular changes with placental weight, parity, gestational age, major congenital anomalies, and maternal factors, including diabetes and pre-eclampsia. We presume that smoking and air pollution may contribute to the development of chorangiosis. We suggest that chorangiosis may be an adaptive response to maternal hypoxia, and studies addressing the role of smoking and air pollution in chorangiosis may provide new insights into the pathogenesis of this condition.     

Tracing the origins of “fetal origins” of adult diseases: Programming by oxidative stress?

Too small size at birth (due to poor fetal growth and/or preterm delivery) has been associated with substantially elevated risks of the metabolic syndrome (dislipidemia, insulin resistance, hypertension), type 2 diabetes and cardiovascular disease in adulthood. The mechanisms of such "fetal origins" or "programming" of disease phenomenon remain unresolved. Too large size at birth seems also associated with an increased risk. Many known or suspected causes of or conditions associated with adverse (poor or excessive) fetal growth or preterm birth have been associated with oxidative stress. Plausibly, oxidative stress may be a common link underlying the superficial "programming" associations between adverse fetal growth or preterm birth and elevated risks of certain chronic diseases. The mechanisms of oxidative stress programming may be through directly modulating gene expression or indirectly through the effects of certain oxidized molecules. Experimental investigations have well demonstrated the role of redox balance in modulating gene expression, and recent studies indicate that both the insulin functional axis and blood pressure could be sensitive targets to oxidative stress programming. Adverse programming may occur without affecting fetal growth, but more frequently among low birth weight infants merely because they more frequently experienced known or unknown conditions with oxidative insults. As oxidative stress levels are easily modifiable during pregnancy and early postnatal periods (which are plausible critical windows), the hypothesis, if proved valid, will suggest new measures that could be very helpful on fighting the increasing epidemic of the metabolic syndrome, type 2 diabetes and cardiovascular disease. Currently, there are several ongoing large randomized trials of antioxidant supplementation to counter oxidative stress during pregnancy for the prevention of preeclampsia. It would be invaluable if long-term follow-ups of infants born to women in such trials could be realized to test the oxidative stress programming hypothesis in such experimental trial settings.     

Unexplained fetal death has a biological signature of maternal anti-fetal rejection: chronic chorioamnionitis and alloimmune anti-human leucocyte antigen antibodies

Lee J, Romero R, Dong Z, Xu Y, Qureshi F, Jacques S, Yoo W, Chaiworapongsa T, Mittal P, Hassan S S & Kim C J
(2011) Histopathology   59 , 928–938 Unexplained fetal death has a biological signature of maternal anti‐fetal rejection: chronic chorioamnionitis and alloimmune anti‐human leucocyte antigen antibodies Aims: Chronic chorioamnionitis is a histological manifestation of maternal anti‐fetal cellular rejection. As failure of graft survival is the most catastrophic event in organ transplantation, we hypothesized that fetal death could be a consequence of maternal rejection. The aim of this study was to assess whether there is evidence of cellular and antibody‐mediated rejection in fetal death. Methods and results: Placental histology was reviewed for the presence of chronic chorioamnionitis in unexplained preterm fetal death (n = 30) and preterm live birth (n = 103). Amniotic fluid CXCL10 concentrations were measured with a specific immunoassay. Chronic chorioamnionitis was more frequent in fetal death than in live birth (60.0% versus 37.9%; P < 0.05) and fetal death had a higher median amniotic fluid CXCL10 concentration than live birth (2.0 versus 1.8 ng/ml, P < 0.05), after adjusting for gestational age at amniocentesis. Maternal anti‐human leucocyte antigen class II panel‐reactive seropositivity determined by flow cytometry was higher in fetal death compared to live birth (35.7% versus 10.9%; P < 0.05). Conclusions: Chronic chorioamnionitis is a common pathologic feature in unexplained preterm fetal death. This novel finding suggests that cellular and antibody‐mediated anti‐fetal rejection of the mother is associated with fetal death (graft failure) in human pregnancy.     

Exposure to air pollution during different gestational phases contributes to risks of low birth weight

BACKGROUND: Although there have been growing concerns about the adverse effects of air pollution on birth outcomes, little is known about which specific exposure times of specific pollutants contribute to low birth weight (LBW). METHODS: We evaluated the relationships between LBW and air pollution exposure levels in Seoul, Korea. Using the air pollution data, we estimated the exposure during each trimester and also during each month of pregnancy on the basis of the gestational age and birth date of each newborn. Generalized additive logistic regression analyses were conducted considering infant sex, birth order, maternal age, parental education level, time trend, and gestational age. RESULTS: The monthly analyses suggested that the risks for LBW tended to increase with carbon monoxide (CO) exposure between months 2-5 of pregnancy, with exposure to particles <10 micro m (PM(10)) in months 2 and 4, and for sulphur dioxide (SO(2)) and nitrogen dioxide (NO(2)) exposure between months 3-5. CONCLUSIONS: This study suggests that exposure to CO, PM(10,) SO(2) and NO(2) during early to mid pregnancy contribute to risks for LBW.     

Residential outdoor air pollution and allergen sensitization in schoolchildren in Oslo, Norway

BACKGROUND: Epidemiological studies that have investigated the association between air pollution and atopy have found inconsistent results. Furthermore, often exposure to outdoor air pollution has had limited quality, and more individual exposure is needed. OBJECTIVE: To investigate the relations between early and lifetime exposure to residential outdoor air pollution and allergen sensitization in 9-10-year-old children in Oslo, Norway. METHODS: Sensitization to common allergens was measured by skin prick tests (SPTs), which were performed in 2244 children who had lived in Oslo since birth. Several definitions of positive SPT were used. Information on potential confounding variables was collected by a parental questionnaire. Exposure to outdoor air pollution was assessed by the EPISODE dispersion model, which calculates hourly concentrations of nitrogen dioxide (NO2), particulate matter (PM) with aerodynamic diameter <10 microm (PM10) and <2.5 microm (PM2.5), respectively. RESULTS: We found no associations between long-term air pollution exposure and sensitization to any allergen, any indoor or any pollen allergen. However, lifetime air pollution exposure was associated with sensitization to the house dust mite Dermatophagoides farinae. One interquartile increase of lifetime exposure to NO2, PM10 and PM2.5 was associated with 1.88 (adjusted odds ratio) (1.02, 3.47) [95% confidence interval (CI)], 1.61 (0.96, 2.72) and 1.46 (0.96, 2.22), respectively, for D. farinae. Lifetime exposure was also associated with sensitization to cat in a subpopulation. Both associations diminished after adjusting for a contextual socio-economic factor. CONCLUSION: Long-term exposure to traffic-related pollutants was generally not associated with allergen sensitization in 9-10-year-old Oslo children. However, lifetime exposure was associated with sensitization to D. farinae, and with sensitization to cat in a subpopulation, which may be explained by socio-economic confounding or multiple comparisons. The air pollution levels in Oslo may be too low to reveal associations with sensitization.     

Gene expression profiling in healthy newborns from diverse localities of the Czech Republic

Prenatal exposure to air pollution is associated with intrauterine growth restriction and low birth weight. Gene expression changes in newborns in relation to air pollution have not been sufficiently studied. We analyzed whole genome expression in cord blood leukocytes of 202 newborns from diverse localities of the Czech Republic, differing among other factors in levels of air pollution: the district of Karvina (characterized by higher concentration of air pollutants) and Ceske Budejovice (lower air pollution levels). We aimed to identify differentially expressed genes (DEGs) and pathways in relation to locality and concentration of air pollutants. We applied the linear model to identify the specific DEGs and the correlation analysis, to investigate the relationship between the concentrations of air pollutants and gene expression data. An analysis of biochemical pathways and gene set enrichment was also performed. In general, we observed modest changes of gene expression, mostly attributed to the effect of the locality. The highest number of DEGs was found in samples from the district of Karvina. A pathway analysis revealed a deregulation of processes associated with cell growth, apoptosis or cellular homeostasis, immune response‐related processes or oxidative stress response. The association between concentrations of air pollutants and gene expression changes was weak, particularly for samples collected in Karvina. In summary, as we did not find a direct effect of exposure to air pollutants, we assume that the general differences in the environment, rather than actual concentrations of individual pollutants, represent a key factor affecting gene expression changes at delivery. Environ. Mol. Mutagen. 59:401–415, 2018. © 2018 Wiley Periodicals, Inc.     

Maternal social support predicts birth weight and fetal growth in human pregnancy

OBJECTIVE: Low birth weight is a primary cause of infant mortality and morbidity. Results of previous studies suggest that social support may be related to higher birth weight through fetal growth processes, although the findings have been inconsistent. The purpose of this investigation was to test a model of the association between a latent prenatal social support factor and fetal growth while taking into account relations between sociodemographic and obstetric risk factors and birth weight. METHOD: A prospective study was conducted among 247 women with a singleton, intrauterine pregnancy receiving care in two university-affiliated prenatal clinics. Measures of support included support from family, support from the baby's father, and general functional support. Sociodemographic characteristics were also assessed. Birth outcome and obstetric risk information were abstracted from patients' medical charts after delivery. RESULTS: Structural equation modeling analyses showed that a latent social support factor significantly predicted fetal growth (birth weight adjusted for length of gestation) with infant sex, obstetric risk, and ethnicity in the model. Marital status and education were indirectly related to fetal growth through social support. The final model with social support and other variables accounted for 31% of the variance in fetal growth. CONCLUSIONS: These findings suggest that prenatal social support is associated with infant birth weight through processes involving fetal growth rather than those involving timing of delivery. Biological and behavioral factors may contribute to the association between support and fetal growth, although these mechanisms need to be further explored. These results pave the way for additional research on fetal growth mechanisms and provide a basis for support intervention research.     

Infants thinner at birth exhibit smaller kidneys for their size in late gestation in a sample of fetuses with appropriate growth

Fetal ultrasound measurements were employed to investigate the relationship between weight and ponderal index at birth and kidney size during the second (23 weeks) and third (32 weeks) trimesters of pregnancy in a sample of 25 normally growing fetuses. Kidney volume and kidney volume / fetal weight ratio at 32 weeks are significantly and positively related to both weight and ponderal index at birth, controlling for sex, gestational age at birth, and day of ultrasound measurement. A second‐degree polynomial relationship approximates the predictability of kidney volume fetal weight ratio at 23 weeks to that at 32 weeks, demonstrating shifting growth rates in fetal organ and body growth relationships during midgestation. Sex and parental size are suggested as contributing to these patterns. Females have a surge in renal growth between 23 and 32 weeks to catch up to earlier growing males, and maternal weight significantly predicts incremental growth in kidney volume and the kidney volume / fetal weight ratio at 32 weeks of gestation. The observation that fetuses relatively thin at birth have relatively smaller kidneys for their size in late gestation suggests that the influence of maternal weight on birth outcome may act through organ growth. Am. J. Hum. Biol. 14:398–406, 2002. © 2002 Wiley‐Liss, Inc.