Noninvasive Fetal Lung Maturity Prediction Based on Amniotic Fluid Turbidity Using Ultrasonic Histogram Measurement Function

Background: Amniotic fluid turbidity increases with fetal lung maturation due to vernix and lung surfactant micelles suspended in the amniotic fluid. This study focused on this phenomenon and evaluated the presence or absence of respiratory distress syndrome (RDS)/transient tachypnea of the newborn (TTN) by quantitatively assessing the brightness of the amniotic fluid turbidity using a noninvasive ultrasound histogram measurement function. Methods: We included cases of singleton pregnancies managed at the Niigata University Medical and Dental Hospital between November 2020 and March 2022. Histograms of amniotic fluid turbidity were measured at the center of the amniotic fluid depth, avoiding the fetus, placenta, and umbilical cord, with the gain setting set to 0, and the average value was obtained after three measurements. Histograms of fetal urine in the bladder were measured similarly. The value obtained by subtracting the fetal bladder brightness value from the amniotic brightness value based on histogram measurements was used as the final amniotic fluid brightness value. Results: We included 118 cases (16 of RDS/TTN and 102 of control). The gestational age of delivery weeks was correlated with amniotic fluid brightness (Spearman’s rank correlation coefficient was 0.344;p = 0.00014). Amniotic fluid brightness values were significantly lower in the RDS/TTN group than in the control group (RDS/TTN: 16.2 ± 13.5, control: 26.3 ± 16.3;p = 0.020). The optimal cutoff value of amniotic fluid brightness to predict RDS/TTN was 20.3. For predicting RDS/TTN, the sensitivity, specificity, positive predictive value, and negative predictive value were 91.7%, 69.6%, 26.2%, and 94.1%, respectively. Conclusions: The quantitative value of the amniotic fluid brightness by histogram measurements may provide an easy and objective index for evaluating the presence or absence of RDS/TTN.

Lamellar Bodies Count (LBC) as a Predictor of Fetal Lung Maturity in Preterm Premature Rupture of Membranes Compared to Neonatal Assessment

Background: Respiratory distress syndrome (RDS) is a major cause of neonatal morbidity and mortality, affecting approximately 1% of all live births and 10% of all preterm infants. Lamellar bodies represent a storage form of pulmonary surfactant within Type II pneumocytes, secretion of which increases with advancing gestational age, thus enabling prediction of the degree of FLM. Preterm premature rupture of membranes (PPROM) complicates approximately 1/3 of all preterm births. Birth within 1 week is the most likely outcome for any patient with PPROM in the absence of adjunctive treatments. Respiratory distress has been reported to be the most common complication of preterm birth. Sepsis, intraventricular haemorrhage, and necrotizing enterocolitis also are associated with prematurity, but these are less common near to term. Objective: To assess the efficacy of the amniotic fluid lamellar body counting from a vaginal pool in predicting fetal lung maturity in women with preterm premature rupture of membranes. Methods: This study was conducted at Ain Shams University Maternity Hospital in the emergency ward from January 2019 to September 2019. It included 106 women with singleton pregnancies, gestational age from 28 - 36 weeks with preterm premature rupture of membranes. This study is designed to assess the efficacy of the amniotic fluid lamellar body counting (LBC) from a vaginal pool in predicting fetal lung maturity in women with preterm premature rupture of membranes. Results: The current study revealed a highly significant increase in the lamellar body count in cases giving birth to neonates without RDS compared to that cases giving birth to neonates with RDS. Also, no statistically significant difference between LBC and age, parity and number of previous miscarriages in the mother was found. Gestational age at delivery was significantly lower among cases with respiratory distress. Steroid administration was significantly less frequent among cases with respiratory distress. However, lamellar bodies had high diagnostic performance in the prediction of respiratory distress. Conclusion: Lamellar body count (LBC) is an effective, safe, easy, and cost-effective method to assess fetal lung maturity (FLM). It does not need a highly equipped laboratory or specially trained personnel, it just needs the conventional blood count analyzer. Measurement of LBC is now replacing the conventional Lecithin/Sphyngomyelin L/S ratio. LBC cut-off value of ≤42.5 × 103/μL can be used safely to decide fetal lung maturity with sensitivity of 95.7% and specificity of 97.6%.

Expression of Lung Surfactant Proteins SP-B and SP-C and Their Modulating Factors in Fetal Lung of FGR Rats

This study investigated the expression of lung surfactant proteins SP-B and SP-C, and their modulating factors TTF-1 and PLAGL2 in the fetal lung of rats with fetal growth restriction（FGR）. The rat FGR model was established by prenatal hypoxia in the first stage of pregnancy, 180 rats for experiment served as hypoxia group, and 197 healthy rats served as normal control group. The FGR incidence in hypoxia was compared with that in normal control group. The histological changes in the fetal lung were observed under the light microscope and electronic microscope in two groups. The SP-B, SP-C, TTF-1 and PLAGL2 proteins were determined in the fetal lung of two groups immunohistochemically. The expression levels of SP-B, SP-C, TTF-1 and PLAGL2 protein and m RNA in the fetal lung of two groups were detected by using Western blotting and RT-PCR respectively. The FGR rat model was successfully established by using hypoxia. Pathologically the fetal lung developed slowly, and the expression levels of SP-B, SP-C, TTF-1 and PLAGL2 protein and mR NA in the fetal lung were significantly reduced in hypoxia group as compared with those in normal control group. It was suggested that maternal hypoxia in the first stage of pregnancy could induce FGR, and reduce the expression of SP-B and SP-C, resulting in the disorder of fetal lung development and maturation.

Expression of Lung Surfactant Proteins SP-B and SP-C and Their Regulatory Factors in Fetal Lung of GDM Rats

This study investigated the expression of lung surfactant proteins (SP-B and SP-C),and regulatory factors [forkhead box A2(FOXA2)and nitrolyogenic FOXA2 (N-FOXA2)]in the fetal lung of rats with gestational diabetes mellitus (GDM)in order to study the mechanism of pulmonary dysplasia.The rat GDM model was established by using streptozotocin intraperitoneally in the first stage of pregnancy.There were 10 rats in the GDM group,and 10 healthy rats in normal control group without any treatment.Fetal lungs of two groups were taken at day 21 of pregnancy.Blood glucose levels of maternal rats and fetal rats were measured by Roche blood glucose meter.The histological changes in the fetal lung were observed under the light microscope in both groups.The SP-B,SP-C and FOXA2were determined in the fetal lung of two groups immunohistochemically. The expression levels of SP-B,SP-C,total FOXA2,FOXA2 in nucleus (n-FOXA2), N-FOXA2 proteins were detected by Western blotting,and the relative expression levels of SP-B,SP-C,FOXA2 mRNA in the fetal lung of two groups were detected by RT-PCR.The results showed that blood glucose levels of maternal rats and fetal rats in GDM group were higher than those in control group.The light microscope revealed fetal lung development retardation in GDM group.The expression of SP-B and SP-C in GDM group was significantly reduced as compared with control group (P<0.05).As compared with control group,the n-FOXA2 expression was significantly decreased in the fetal lung tissue,and N-FOXA2 was significantly increased in control group (P<0.05),but there was no significant changes in the total FOXA2(P>0.05).It was concluded that GDM can cause fetal lung development and maturation disorders,and FOXA2 in fetal lung tissue decreases while nitrocellulose FOXA2 increases.

Prenatal assessment of normal fetal pulmonary grey-scale and lung volume by three-dimensional ultrasonography

Objective To quantitatively analyze the fetal lung echo and right lung volume in the third trimester by real-time three-dimensional ultrasound(3-D US)and evaluate the feasibility of fetal lung maturity.Methods A total of 732 women with normal singleton pregnancies between 28 and 42 weeks of gestation underwent ultrasound examination.The 3-D US equipment with a 3.5-5 MHz transabdominal transducer was used for the fetal biometric measurement.The echogenicity ratio between fetal lung and liver was compared.The fetal lung volume was calculated by the rotational multiplanar technique for volume measurement(VOCAL).Results The right fetal lung volume increased with the increase of gestational age with a linear positive correlation(r=0.884,P<0.01).After 34 weeks,the echogenicity ratio of fetal lung to liver was more than 1.1.Conclusion The echogenicity of lung/liver and fetal lung volume could be used as normal fetal predictable indicators for fetal lung maturity.

Ultrasonographic Segmentation of Fetal Lung with Deep Learning

The morbidity and mortality of the fetus is related closely with the neonatal respiratory morbidity, which was caused by the immaturity of the fetal lung primarily. The amniocentesis has been used in clinics to evaluate the maturity of the fetal lung, which is invasive, expensive and time-consuming. Ultrasonography has been developed to examine the fetal lung quantitatively in the past decades as a non-invasive method. However, the contour of the fetal lung required by existing studies was delineated in manual. An automated segmentation approach could not only improve the objectiveness of those studies, but also offer a quantitative way to monitor the development of the fetal lung in terms of morphological parameters based on the segmentation. In view of this, we proposed a deep learning model for automated fetal lung segmentation and measurement. The model was constructed based on the U-Net. It was trained by 3500 data sets augmented from 250 ultrasound images with both the fetal lung and heart manually delineated, and then tested on 50 ultrasound data sets. With the proposed method, the fetal lung and cardiac area were automatically segmented with the accuracy, average IoU, sensitivity and precision being 0.98, 0.79, 0.881 and 0.886, respectively.

Evaluation of thalamus echogenicity by ultrasound as a marker of fetal lung maturity

The present study evaluated fetal thalamic echogenicity by ultrasound as a possible marker of fetal lung maturity in comparison with other ultrasound makers. A prospective longitudinal study performed in Al-Elwiya Maternity Teaching Hospital in Baghdad, Iraq during the period from April 2010 to March 2011. One hundred and forty two pregnant women (36 to 42 weeks of gestation) who were admitted for elective cesarean section and referred for an obstetric ultrasound scan at the same day of their elective cesarean section were included. Scanning with linear ultrasound with convex transducer frequency of 3.5 MHz was utilized to measure the biparietal diameter and the state of echogenicity was recorded as echogenic or echolucent, in addition to amniotic fluid vernix and the placental changes. The presence of echogenic thalamus as a sign of fetal lung maturity had a specificity of 86.53% which is higher than the three other signs of lung maturity;the positive predictive value was (89.6%) which is also higher than the three other signs, but the sensitivity was 63.33% and negative predictive value was 57.69% which is lower than the presence of vernix in the amniotic fluid, 86.66 and 67.56 respectively. In conclusion, evaluation of echogenic thalamus is beneficial, and can be considered as a new marker of fetal lung maturity;however, further studies are required to strengthen such idea.

<i>Stachybotrys chartarum</i>(<i>atra</i>) spore extract alters surfactant protein expression and surfactant function in isolated fetal rat lung epithelial cells, fibroblasts and human A549 cells

Moulds, notably Stachybotrys chartarum (atra), are constant contributors to air pollution particularly to air quality in buildings. The spores themselves or their volatile organic products are present in variable amounts in almost all environments, particularly in buildings affected by flooding. These moulds and products can account for the sick building syndrome and have been tied to such occurrences as the outbreak of pulmonary hemosiderosis and hemorrhage in infants in Cleveland, Ohio. The present study was designed to investigate the effects of S. chartarum extracts on surfactant protein expression, surfactant quality and cell survival in the developing lung. S. chartarum extracts were incubated with cultures of several cell types;isolated fetal lung type II cells and fetal lung fibroblasts, and human lung A549 cells, a continuously growing cell line derived from surfactant producing type II alveolar cells. MTT formazan assays were employed to test cell viability. The synthesis and release of the predominant surfactant protein A (SP-A), which is involved in the regulation of surfactant turnover and metabolism, and surfactant protein B (SP-B) involved in shuttling phospholipids between surfactant subcompartments was also assessed. Antibodies to these proteins and western blotting results were used to assess the quantity of protein produced by the various cell types. A novel approach utilizing captive bubble surfactometry was employed to investigate the quality of surfactant in terms of surface tension and bubble volume measurements. Electron microscopy was used to examine changes in cellular structure of control and S. chartarum-treated cells. Results of the study showed that exposure to the S. chartarum extracts had deleterious effects on fetal lung epithelial cell viability and their ability to produce pulmonary surfactant. S. chartarum extracts also induced deleterious changes to the developing fetal lung cells in terms of expression of SP-A and SP-B as well as to the surface tension reducing abilities of the pulmonary surfactant. Ultrastructurally, spore toxin associated changes were apparent in the isolated lung cells most notably in the lamellar bodies of fetal rat lung alveolar type II and human A549 cells. This study has demonstrated the potential damage to surfactant production and function which may be induced by inhaling S. chartarum toxins.

Investigating the correlation of Fgf signaling and Wnt signaling pathway with interuterine hyperglycemia-induced fetal lung heteroplasia

Pregnancy with diabetes mellitus(PGDM)has been known to affect the em br yonic development of various systems.No doubt that it has a negative impact on the respiratory system,but the specific pathogenesis is not clear.In this study,firstly we demonstrated that the fetuses had immature lung development in PGDM,including pulmonary epithelial cell decreased and fibrous tissue increased.Secondly,we show Fgf signaling and Wnt signal would be activated in PGDM.For further study,we used in vitro experiments showed that the transcription factor GATA6,lung epithelial related-factors gene was down-regulated in high glucose groups,and the expression of Wnt signal-related and Fgf signal-related gene were up-regulated in high glucose groups;Treated with high glucose and used the inhibitor of Wnt and Fgf signal,the expression of GATA6 and epithelial related-factors gene were up-regulated,while the expression of fibrosis-related genes was down-regulated.

Cigarette Smoke Induces Apoptosis by Activation of Caspase-3 in Isolated Fetal Rat Lung Type II Alveolar Ep-ithelial Cells <i>in Vitro</i>

Smoking during pregnancy is a major source of fetal exposure to numerous harmful agents present in tobacco smoke. Lung development involves complex biochemical processes resulting in dramatic changes which continue even after birth. In addition to type I cells which form the blood-air barrier, type II alveolar epithelial (AE) cells have important and diverse functions related to immunological protection and stabilization of the alveolus through synthesis and secretion of the pulmonary surfactant. Apoptosis or programmed cells death is an important physiological process during lung embryogenesis and for the proper maintenance of homeostasis. Caspases are proteases that play important roles in regulating apoptosis. Caspase-3 is the key executioner caspase in the cascade of events leading to cell death by apoptosis. We explored the hypothesis that cigarette smoke extract (CSE) induces apoptosis in fetal rat lung type II AE cells by activation of caspase-3. To analyze these factors, isolated fetal rat lung type II AE cells were used. The cells were exposed to different concentrations of CSE (5%, 10% or 15%) (v/v) for 60 min. The results of the present study showed that CSE induced apoptosis in fetal rat lung type II AE cells with a significant increase (p 0.05) in caspase-3 activity and decrease in cell proliferation at CSE concentrations of 10% and 15% (v/v). These observations indicate that cigarette smoke extract induces apoptosis by activation of caspase-3 in fetal rat lung type II AE cells in a dose-dependent manner and may potentially alter the regulated development of the lung and the appearance of the surfactant-producing type II alveolar cells which are critical for the establishment of adequate gas exchange at birth.

高级别胎儿型肺腺癌并头皮转移1例

胎儿型肺腺癌(fetal adenocarcinoma of the lung,FLAC)是一种罕见的肺部肿瘤。FLAC分为低级别FLAC(low-grade FLAC,L-FLAC)和高级别FLAC(high-grade FLAC,H-FLAC),两者在临床病理特征、生物学行为和临床结局方面有所不同。大多数H-FLAC患者是重度吸烟的中年人。本研究描述了1例罕见的非吸烟年轻男性患者,其最初表现为头顶肿块,最终被诊断为H-FLAC。本文旨在增进对FLAC的了解和认识,提高对该疾病的重视,以防止该疾病漏诊与误诊,加强早期识别、精准诊断,从而推进后续的有效治疗、改善预后。

主肺动脉收缩期加速时间/射血时间比值评估重度子痫前期胎儿肺成熟度

目的探讨胎儿主肺动脉收缩期加速时间(AT)/射血时间(ET)比值对重度子痫前期胎儿肺成熟度的预测价值。方法选取2021年1月至2022年12月因重度子痫前期在我院住院并自愿接受超声检查的孕妇65例,根据孕周分为早发型(孕20~33^(+6)周)重度子痫前期组(A组,n=30)和晚发型(孕34~40周)重度子痫前期组(B组,n=35)。选取超声检查孕周与A、B组相匹配的正常孕妇作为各自对照组(分别为30例、35例)。超声多普勒测量胎儿主肺动脉血流参数,包括AT、ET、AT/ET、收缩期峰值流速(PSV)。于分娩即刻采集羊水(约15 mL),检测羊水卵磷脂/鞘磷脂(L/S)值。比较A、B组胎儿主肺动脉血流参数及其与对照组有无差异,分析血流参数与羊水L/S的相关性。结果A组、B组胎儿主肺动脉AT、ET、AT/ET、PSV比较差异有统计学意义(P<0.05),且均小于各自对照组(均P<0.05)。A组、B组胎儿主肺动脉AT/ET比值与羊水L/S均呈正相关(r分别为0.821、0.383,均P<0.05)。受试者操作特征曲线分析显示AT/ET诊断早发型及晚发型子痫前期的曲线下面积分别为0.839、0.833,当假阳性率为5%时,灵敏度分别为0.853、0.912,特异度分别为0.583、0.611,截断值分别为0.185、0.255。结论胎儿主肺动脉AT/ET比值能对重度子痫前期做出初步诊断,并可定量评估胎儿肺成熟度,可为临床提供一种新的简单、无创、可重复的评估方法。

早发型重度子痫前期孕妇胎儿主肺动脉多普勒流速曲线参数的变化及意义

目的探讨早发型重度子痫前期孕妇胎儿主肺动脉多普勒流速曲线参数的变化及其对胎儿肺成熟度的预测价值。方法选取30例早发型重度子痫前期孕妇设为研究组,并根据新生儿结局的不同将其进一步分为呼吸窘迫综合征(RDS)组17例和非RDS组13例,另选取同期产检的80名正常妊娠孕妇设为正常对照组。比较各组孕妇胎儿主肺动脉多普勒流速曲线参数,并分析各参数对新生儿RDS的预测价值。结果研究组孕妇胎儿收缩期加速时间(AT)、收缩期射血时间(ET)短于对照组,收缩期加速时间与射血时间比值(AT/ET)低于对照组,差异有统计学意义(P<0.05);RDS组孕妇胎儿AT、ET短于非RDS组,差异有统计学意义(P<0.05),但2组AT/ET差异无统计学意义(P>0.05)。二元Logistic回归分析结果显示,三者联合预测新生儿RDS的方程为logit(P)=AT+(-0.560/1.048)×ET+(-2.464/1.048)×AT/ET。受试者工作特征曲线分析结果显示,AT、ET、AT/ET单独及联合预测新生儿RDS的曲线下面积分别为0.837、0.877、0.712及0.929,敏感度分别为94.1%、94.1%、47.1%及94.1%,特异度分别为58.1%、75.3%、84.9%及78.5%。结论早发型重度子痫前期孕妇胎儿主肺动脉多普勒流速曲线参数AT、ET、AT/ET数值均降低,应用多普勒超声监测胎儿的主肺动脉流速曲线能够有效评估其肺成熟度。

SD大鼠胚胎-胎仔发育毒性试验背景数据的建立

目的总结国家药物安全评价监测中心2013-2022年SD大鼠胚胎-胎仔发育毒性试验各指标的正常值范围,建立SD大鼠胚胎-胎仔发育毒性试验各指标的背景数据库,为药物胚胎-胎仔发育毒性评价提供参考。方法对本中心2013-2022年11项SD大鼠胚胎-胎仔发育毒性试验中对照组共计205只孕鼠和3037只胎鼠各项胚胎发育和胎仔生长发育指标进行统计分析,计算其平均数、标准差、变异系数和95%置信区间。指标包括孕鼠妊娠期体重和体重增长幅度、孕鼠摄食量、妊娠结局(妊娠率、平均黄体数、平均着床数、平均活胎数、活胎率、吸收胎率、死胎率)、胎仔生长发育情况(胎仔重、胎盘重、性别比)、胎仔外观异常率、内脏异常率和骨骼异常率。结果孕鼠妊娠期体重呈增长趋势,妊娠后期体重增长幅度明显增大。孕鼠摄食量随着妊娠时间的增加呈增长趋势。妊娠第20天进行剖腹产,妊娠率为93.2%,平均黄体数、着床数和活胎数分别为18.0±3.2,15.9±2.8和14.8±3.0,活胎率为93.4%,死胎率为6.6%;胎仔雄/雌性别比为0.94,平均体重为(3.6±0.3)g,胎盘平均重量为(0.6±0.3)g。胎仔外观异常发生率约为0.2%,内脏异常率约为0.8%。骨骼异常率约为1.2%,未骨化和骨化不全的发生率较高,主要发生于胸骨和舌骨等,胎仔的掌骨骨化数、跖骨骨化数和骶尾椎骨化数分别为7.0±0.7,8.0±0.1和7.4±0.5,第Ⅰ~Ⅳ胸骨骨化率较高,平均为98.6%~99.9%,第Ⅴ胸骨骨化率为(68.0±28.4)%,第Ⅵ胸骨骨化率为(82.8±23.9)%。结论初步建立了本GLP实验室SD大鼠胚胎-胎仔发育毒性试验中各指标背景数据库,为生殖毒性研究提供参考。

氟诺哌齐对新西兰家兔胚胎-胎仔发育毒性及毒代动力学

目的研究氟诺哌齐(fronopezil)对新西兰家兔胚胎-胎仔发育的影响及其伴随毒代动力学,为临床用药提供参考。方法按妊娠顺序将孕兔分为溶媒(1%羟丙基甲基纤维素+1.5%聚乙二醇400水溶液)对照组、环磷酰胺(18 mg·kg^(-1),阳性对照)组及氟诺哌齐3.6,9.0和22.5 mg·kg^(-1)组。溶媒对照组和氟诺哌齐组于妊娠第6~18天(GD6-18)ig给药,环磷酰胺组于GD6-20 ig给药。GD_(28)处死孕兔,检测胚胎-胎仔发育,ELISA检测GD5,GD_(18)和GD_(28)孕兔血清中性激素水平,首末次给药前后采血进行伴随毒代动力学研究,采用高效液相色谱串联质谱法检测血浆、胎仔、胎盘和羊水中的药物浓度。结果氟诺哌齐3.6,9.0和22.5 mg·kg^(-1)对孕兔的体重、增重、摄食量和妊娠结局及胎仔的外观、内脏、骨骼和体格生长发育均未见明显影响;仅在GD_(18)或GD_(28)各剂量组卵泡刺激素、雌二醇和孕酮水平有一定程度波动。伴随毒代动力学研究结果表明,氟诺哌齐可通过胎盘屏障,但在孕兔和胎仔体内无明显蓄积;环磷酰胺组胎仔体重、顶臀长和连胎子宫重均低于溶媒对照组(P<0.01),外观和骨骼均出现畸形。结论氟诺哌齐对新西兰家兔胚胎-胎仔发育毒性的未见有害作用剂量为22.5 mg·kg^(-1),为药效起效剂量的125倍,该剂量下GD_(18)血药峰浓度为1093μg·L^(-1),药时曲线下面积为6650μg·h·L^(-1)。

母胎界面免疫代谢微环境调节胚胎着床的研究进展

胚胎着床诱导母胎界面发生适应性的代谢重编程,形成低氧、低度炎症和弱酸性的微环境,这种微环境通过调节免疫细胞的募集、激活、代谢和极化,有助于子宫内膜容受态建立、蜕膜化、滋养细胞侵袭和母胎免疫耐受。胚胎成功着床需要免疫炎性反应和以糖酵解为主导的代谢重编程适时、适度的启动和结束。由病理因素介导的免疫代谢失调会导致胚胎着床失败或着床后流产等不良妊娠结局。巨噬细胞是种植窗口期子宫内膜数量最多的抗原提呈细胞,凭借极强的免疫可塑性和代谢灵活性,在母胎免疫代谢微环境的调节中发挥关键作用。综述母胎界面微环境中的免疫代谢调控机制,为制定临床干预策略以改善自然妊娠和辅助生殖助孕结局提供参考。

妊娠34 周前胎膜早破的治疗进展

未足月胎膜早破(preterm premature rupture of the membranes,PPROM)特别是孕龄<34周的胎膜早破是临床上处理比较困难的问题,期待治疗增加了母体感染、产后出血等并发症的发生风险;胎儿也可能存在宫内感染,胎膜早破所致羊水过少;期待时间过长可导致胎儿骨骼发育异常、胎儿肢体粘连、胎肺发育不全等不良后果。在无继续妊娠禁忌证情况下,期待治疗能明显降低新生儿发病率和病死率。因此,在制订诊疗方案时需结合多方面因素进行考虑,得出最佳治疗方案,以期减少母儿并发症发生。本文通过对PPROM的治疗进展进行综述,为临床工作者提供帮助。

反复胚胎种植失败行PGT-A妇女的临床特点分析

目的分析反复胚胎种植失败妇女行植入前遗传学筛查(PGT-A)技术的临床特点。方法选取498例体外受精-胚胎移植治疗的不孕症妇女,其中反复种植失败(RIF)行PGT-A妇女79例(RIF组),对照组419例。根据是否获得整倍体胚胎将79例RIF患者分为获得整倍体胚胎组51例(RIF-S)和未获得组28例(RIF-F)。观察其临床特点。结果RIF组年龄大于对照组,基础卵泡刺激素(FSH)、促黄体生成素(LH)、雌二醇(E_(2))水平均高于对照组,基础窦卵泡计数(AFC)少于对照组,外源性促性腺激素(Gn)用量、人绒毛膜促性腺激素(HCG)日E2水平、获卵数、MII卵数、2PN数均低于对照组(P<0.05)。RIF-S组年龄小于RIF-F组,活检胚胎数、D3优胚数、囊胚数、优囊数均多于RIF-F组(P<0.05)。结论高龄及卵巢储备功能差的女性容易发生RIF。

产前糖皮质激素促胎肺成熟的药物利用评价

目的探讨糖皮质激素在产前促胎肺成熟中应用的合理性。方法2019年至2021年每年按住院号顺序,从电子病历系统中提取前100例应用糖皮质激素促胎肺成熟的患者的用药相关信息,从用药指征、用药时机、使用方法、重复疗程指征、治疗疗程数、各疗程间隔时间等方面评价药物应用的合理性。结果58例患者无指征用药,占所有患者的19.3%;4例患者无指征重复疗程用药,占所有患者的1.3%;168例妊娠24~36^(+6)周者在给药7 d后分娩,占相应孕龄患者的64.1%,132例妊娠24~36^(+6)周者足月分娩,占相应孕龄患者的50.4%;重复疗程中有12例在给药7 d后分娩,占重复疗程者的85.7%。结论该院产前糖皮质激素在促胎肺成熟方面存在过度用药现象,临床应严格用药指征、优化治疗方案,合理应用糖皮质激素以保障用药的有效性和安全性。

兔胚胎-胎仔发育毒性实验阳性模型的建立

目的探讨兔胚胎-胎仔发育毒性实验中,经口灌胃环磷酰胺建立兔致畸实验模型的方法,为致畸实验研究提供实验室背景数据。方法取健康受孕的普通级新西兰兔66只,按动物体质量采用随机数字法分为溶酶对照组(0.5%羧甲基纤维素钠)和环磷酰胺染毒组(20 mg/kg),交配成功后于孕兔GD 6~GD 18按2 mL/kg进行灌胃染毒。染毒期间观察临床表现,统计孕兔的体质量、成功受孕率、黄体数、活胎数、死胎数和吸收胎数等指标,记录胎仔的体质量、身长、外观畸形、内脏畸形和骨骼畸形等指标。结果环磷酰胺组孕兔的体质量和溶酶对照组相比,差异无统计学意义(P>0.05);环磷酰胺组孕兔黄体数、活胎数和着床数与溶酶对照组相比均降低,差异均有统计学意义(P<0.05);环磷酰胺组胎仔的重量、身长和胎盘重量与溶酶对照组相比均降低,差异均有统计学意义(P<0.05);环磷酰胺组胎仔的外观、内脏和骨骼的异常发生率明显升高,与溶酶对照组相比,差异有统计学意义(P<0.01或P<0.05)。结论环磷酰胺经口灌胃染毒,在20 mg/kg的灌胃剂量下,给药周期短,胎仔的畸形率高,畸形种类多,不引起母体毒性,可建立较好的兔胚胎-胎仔发育毒性实验模型。