妊娠期母体甲状腺功能变化及其对胎儿的影响

妊娠期由于其特殊的生理过程甲状腺各项指标的变化很大,妊娠期甲状腺激素的产生、循环、代谢、调节以及甲状腺免疫均会随妊娠的不同阶段而改变。甲状腺激素是胎儿脑神经发育的必需激素,甲状腺激素缺乏严重影响胎儿的脑发育,近年来妊娠期甲状腺功能异常的发病率明显升高,可导致母儿不良妊娠结局。综述近年来关于妊娠期母体及胎儿甲状腺功能变化、相关母体甲状腺疾病发病情况及对胎儿的影响,旨在促进正确诊断妊娠期甲状腺疾病,合理保护妊娠期甲状腺功能,预防妊娠期甲状腺功能异常带来的一系列产科并发症及不良妊娠结局,避免新生儿远期生存质量的影响。     

维生素D缺乏与围生期抑郁症的相关性

维生素D（Vitamin D,VD）作为孕产期所必需的营养素之一,其不仅与骨代谢有关,而且具有影响脑内神经免疫调节、神经营养因子和神经传递在内的多重神经活性。近年研究发现,VD对抑郁症的发生有不同程度的影响。而产前和产后抑郁症作为抑郁症的分支,其与VD的关系也备受关注。VD缺乏不仅可能导致复发性流产、妊娠期糖尿病和子痫前期等,还与妊娠期和产后的抑郁症状有关。有文献报道VD缺乏可能是围生期抑郁症的重要危险因素之一。围生期合理补充VD对抑郁症有一定的防治作用,但对于VD补充的时机和剂量还需要更多的研究证实。结合近年发表的国内外文献,探讨VD缺乏与围生期抑郁症之间的相关性,以期为疾病的早期预防、早期诊断和及时治疗提供理论依据,并为后期的研究提供新思路。     

代谢组学在母胎医学中的研究进展

代谢组学是以定量描述生物体受刺激或基因修饰后代谢物变化为目标的新兴组学,其研究对象是细胞、组织、器官的小分子化合物。妊娠期母体代谢机制是宫内环境和胎儿结局的重要决定因素,这些代谢机制发生变化可引起妊娠相关疾病,从而对妊娠结局造成影响。目前尚缺乏妊娠相关疾病的早期临床诊断方法及特异染色体疾病(如21-三体综合征)和胎儿畸形的最佳诊断方法。将代谢组学的方法应用于产科各种生理病理状态研究,有望实现妊娠相关疾病的预测及发病机制的阐释,对妊娠相关疾病的防治和母婴预后有重要意义。综述代谢组学在妊娠相关疾病中的应用及发展潜力。     

妊娠合并急性白血病一例临床分析

目的：探讨妊娠合并急性白血病的临床特点,以提高对该疾病的诊治水平,改善母婴不良结局。方法：回顾性分析南方医科大学深圳医院收治的1 例妊娠晚期合并急性髓系白血病患者的诊治过程,并结合相关文献对该疾病进行分析。结果：本例患者于妊娠晚期发现急性髓系白血病,给予纠正贫血、促胎肺成熟、保护脑神经细胞等对症处理,于妊娠32＋1周行子宫下段剖宫产术娩出一活女婴。术后行白血病常规化疗。文献显示妊娠早期发现白血病应立即终止妊娠后进行常规白血病治疗;妊娠中晚期暴露于化疗药物会增加胎儿生长受限和早产的风险,但并不增加胎儿畸形的风险,可根据孕周大小制定治疗方案。结论：妊娠合并白血病的治疗应兼顾疾病本身、母体、胎儿及患者意愿等多方面因素,需要多学科团队合作,选择最佳的治疗方案以降低孕产妇不良妊娠结局的发生风险。     

细胞因子信号传导抑制因子3与妊娠的研究进展

细胞因子信号转导抑制因子3（SOCS3）通过调节细胞因子信号传导通路对多种细胞及细胞因子具有调节作用,是炎症和细胞凋亡的关键调节物。妊娠时母-胎单位局部微环境存在大量细胞因子,细胞因子参与妊娠期胚胎植入、胎盘形成、胎儿生长和分娩等过程,细胞因子受多方面因素精密调控,使之处于稳定状态有助于正常妊娠。SOCS3作为细胞因子信号传导调节因子参与妊娠及分娩过程,研究表明SOCS3表达异常与流产、早产、妊娠期高血压疾病和妊娠期糖尿病等妊娠疾病的发生发展有关,深入研究SOCS3在妊娠疾病中的作用,可以为妊娠相关疾病的诊断和治疗等方面提供理论依据。     

妊娠合并急性白血病一例临床分析

目的:探讨妊娠合并急性白血病的临床特点,以提高对该疾病的诊治水平,改善母婴不良结局。方法:回顾性分析南方医科大学深圳医院收治的1例妊娠晚期合并急性髓系白血病患者的诊治过程,并结合相关文献对该疾病进行分析。结果:本例患者于妊娠晚期发现急性髓系白血病,给予纠正贫血、促胎肺成熟、保护脑神经细胞等对症处理,于妊娠32~(+1)周行子宫下段剖宫产术娩出一活女婴。术后行白血病常规化疗。文献显示妊娠早期发现白血病应立即终止妊娠后进行常规白血病治疗;妊娠中晚期暴露于化疗药物会增加胎儿生长受限和早产的风险,但并不增加胎儿畸形的风险,可根据孕周大小制定治疗方案。结论:妊娠合并白血病的治疗应兼顾疾病本身、母体、胎儿及患者意愿等多方面因素,需要多学科团队合作,选择最佳的治疗方案以降低孕产妇不良妊娠结局的发生风险。     

胎儿及新生儿免疫溶血性疾病研究进展

胎儿及新生儿免疫溶血性疾病是由母体IgG型同种免疫性红细胞抗体进入胎儿体内,作用于表达抗体对应抗原的胎儿红细胞,以胎儿及新生儿溶血为主要病理过程,以贫血和新生儿黄疸为主要临床表现的围产期常见疾病。本文综述了国内外近年来在胎儿及新生儿免疫溶血性疾病的病理生理、红细胞同种免疫性抗体与胎儿及新生儿免疫溶血性疾病的临床相关性、妊娠同种免疫的实验室检测,以及胎儿及新生儿免疫溶血性疾病高危病例的临床评估、治疗和预防方面的研究进展。     

胎儿肺成熟和最佳分娩时期

现已证明母体患各种合并症及异常妊娠时,胎儿肺成熟或延迟或被促进。因此,根据母体疾病的不同,当确定终止妊娠时期时,掌握胎儿肺成熟度常有利于对胎儿的处理。现就正常妊娠与母体患各种疾病时胎儿肺成熟的关系对照说明如下。一、正常妊娠:在正常妊娠过程中,几乎无需测定羊水中肺表面活性物质,但在异常妊娠或伴有合并症时,胎儿肺成熟度却不相同。作者由羊水分离肺表面活性质后,用的是蔗糖密度梯度超离心组分法,可从羊水中分离出与肺表面活性物质极相似的物质。所采取的羊水除因早产住院者外,全部是妊娠经过及所生新生儿均完全正常的羊水。用此     

妊娠合并宫颈癌一例

妊娠合并宫颈癌较为罕见,早期临床表现并不典型。由于缺乏妇科肿瘤筛查意识,易与胎膜早破、先兆早产等疾病相混淆,导致治疗延误。妊娠合并宫颈癌的治疗尚无成熟且规范的方案,尤其是妊娠中期宫颈癌的治疗存在很大争议,需要根据病理检查、分期、胎儿发育情况及孕妇的妊娠期望等制定个体化综合治疗方案。回顾性分析1例以阴道流血流液入院,经保守治疗失败后,行剖宫产术终止妊娠的中期妊娠合并宫颈癌的诊治经过,并对相关文献进行复习,以期为疾病的诊治提供经验。     

重度子痫前期母体和胎盘维生素D代谢紊乱

目的:探究重度子痫前期(sPE)母体及胎盘中维生素D(VD)代谢情况。方法:选取2016年8月至2017年3月于武汉市第四医院建卡的妊娠妇女101例,按孕妇情况将其分为sPE组(n=43)及对照组(n=58)。采集各受试者母体血、脐带血及胎盘组织,记录胎儿胎龄,测量新生儿体质量及身长;采用酶联免疫吸附法检测血清及胎盘组织中VD代谢物水平;采用RT-PCR法检测胎盘组织中1α-羟化酶、24-羟化酶及维生素D受体(VDR)mRNA水平。分析胎盘VDR mRNA水平与母体、脐带血清中25(OH)VD水平的关系,以及胎盘VDR mRNA水平与新生儿体质量、身长的关系。结果:sPE组孕妇母体血清中25(OH)VD、1,25(OH)_2VD浓度明显低于对照组(P0.05);sPE组孕妇母体血清中24,25(OH)_2VD、3-epi-25(OH)VD浓度明显高于对照组(P0.05);sPE组胎盘组织中25(OH)VD浓度明显低于对照组(P0.05);sPE组胎盘组织中24,25(OH)_2VD、3-epi-25(OH)VD浓度明显高于对照组(P0.05);sPE组孕妇胎盘中1α-羟化酶与24-羟化酶mRNA水平明显低于对照组(P0.05);VDR mRNA水平明显高于对照组(P0.05);sPE组新生儿体质量与身长明显小于对照组(P0.05);胎盘VDR mRNA水平与脐带血清中25(OH)VD水平呈负相关(P0.05);胎盘VDR mRNA水平与新生儿体质量及身长呈负相关(P0.05)。结论:sPE孕妇母体及胎盘均存在VD代谢紊乱;sPE可导致胎儿发育不良;VD代谢紊乱与sPE胎盘及胎儿发育有关。     

微量元素对妊娠和胚胎发育的影响

微量元素参与人体许多生理过程,对妇女妊娠和胚胎发育至关重要,其缺乏或过量均可增加妊娠并发症的发病风险,并影响胚胎正常发育。如铁缺乏常引起缺铁性贫血,增加孕产妇感染概率并影响胎儿大脑发育;孕妇血清锌浓度降低与妊娠期糖尿病和子痫前期的发病风险增加有关,另外,锌缺乏还可导致胎儿体型发育和神经系统发育受损;母体锰暴露会损害胎儿神经系统发育;孕妇血清铜浓度过低与多种不良妊娠结局有关,包括自然流产、胎儿生长受限、胎膜早破等;硒缺乏同样与妊娠期糖尿病和子痫前期的发病风险增加密切关联,但过量摄入硒会导致脐带血脂质水平升高。综述微量元素对妊娠和胚胎发育的影响可规避妊娠风险,并对促进胚胎的正常发育具有重要的临床意义。     

Fetal microchimerism: self and non-self, finally who are we?

For a long time, the conventional view was that the fetus and maternal vascular system are kept separate. In fact there is a two-way traffic of immune cells through the placenta and the transplacental passage of cells is in fact the norm. The fetal cells can persist in a wide range of woman's tissue following a pregnancy or an abortion and she becomes a chimera. Fetal cells have been found in the maternal circulation and they were shown to persist for almost three decades in humans, thus demonstrating long-term engraftment and survival capabilities. Microchimerism is a subject of much interest for a number of reasons. Studies of fetal microchimerism during pregnancy may offer explanations for complications of pregnancy, such as preeclampsia, as well as insights into the pathogenesis of autoimmune disease which usually ameliorates during pregnancy. The impact that the persistence of allogenic cells of fetal origin and the maternal immunological response to them has on the mother's health and whether it is detrimental or beneficial to the mother is still not clear. Although microchimerism has been implicated in some autoimmune diseases, fetal microchimerism is common in healthy individuals. On the beneficial side, it has been proposed that genetically disparate fetal microchimerism provides protection against some cancers, that fetal microchimerism can afford the mother new alleles of protection to some diseases she has not, that fetal microchimerism can enlarge the immunological repertoire of the mother improving her defense against aggressor. Fetal cells are often present at sites of maternal injury and may have an active role in the repair of maternal tissues.     

The influence of iodine deficiency during pregnancy of fetal and neonatal development

The iodine is fundamental substrate for thyroid hormones synthesis. Thyroxine and triiodothyronine play a crucial role in human brain development and maturation. It is well known, that not only fetal, but also maternal thyroid hormones are essential for normal prenatal central nervous system development. During pregnancy complex changes of maternal thyroid function occur and they are influenced by the maternal iodine supply. With decreasing iodine intake, maternal goiter and hypothyroxinemia as well as fetal and neonatal hypothyroidism become more prevalent. The severity of iodine deficiency and hypothyroidism in the mother during early and midgestation is related to the severity of the neural damage in the fetus. In severe iodine deficiency, central nervous system damage is already irreversible at birth and can only be prevented by correction of the maternal iodine deficiency early in pregnancy. Therefore iodine supplementation during pregnancy is now strongly recommended.     

Fetal genotypes and pregnancy outcomes in 35 families with mitochondrial trifunctional protein mutations

OBJECTIVE: The purpose of this study was to evaluate the effects of fetal genotype on maternal and fetal outcomes in families with mitochondrial trifunctional protein mutations in the United States. Trifunctional protein has 3 enzymatic activities that include long-chain 3-hydroxyacyl-CoA dehydrogenase, which catalyzes long-chain fatty acid beta-oxidation. STUDY DESIGN: We analyzed pregnancy history and offspring genotypes in 35 families with heterogeneous mutations. The fetal genotype was determined in utero in 11 pregnancies and after birth in 50 pregnancies. RESULTS: Forty-nine percent of the women who carried affected fetuses had acute fatty liver of pregnancy. Another 11% of the women had the syndrome of hemolysis, elevated liver enzymes, and low platelets, or preeclampsia. All women who had the maternal illness carried fetuses with isolated long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency. Sixty-eight percent and 43% of the affected pregnancies also were associated with premature delivery and intrauterine growth retardation, respectively. No maternal or fetal complications were associated with heterozygous or wild-type fetal genotypes. CONCLUSION: Fetal mitochondrial trifunctional protein defects should be considered a cause for maternal liver disease, preterm labor, and intrauterine growth retardation.     

Fetal microchimerism: benevolence or malevolence for the mother?

For a long time, the conventional view was that the fetus and maternal vascular system are kept separate. In fact there is a two way traffic of cells through the placenta and the transplacental passage of cells is in fact the norm. The fetal cells can persist in a wide range of woman's tissues following a pregnancy or an abortion and she becomes a chimera. Fetal cells have been found in the maternal circulation and they were shown to persist for the entire life in humans, thus demonstrating long-term engraftment and survival capabilities. Microchimerism is a subject of much interest for a number of reasons. Studies of fetal microchimerism during pregnancy may offer explanations for complications of pregnancy, such as preeclampsia, as well as insights into the pathogenesis of autoimmune diseases which usually ameliorate during pregnancy. The impact of the persistence of allogenic cells of fetal origin and of the maternal immunological response to them on the mother's health is still not clear. On the beneficial side, it has been proposed that genetically disparate fetal microchimerism provides protection against some cancers, that fetal microchimerism can afford the mother new mechanisms of protection to some diseases, that fetal microchimerism can enlarge the immunological repertoire of the mother improving her defense against aggressor. Fetal cells are often present at sites of maternal injury and may have an active role in the repair of maternal tissues.     

Fetale Thrombophilie

Recent findings suggest that inherited or acquired maternal thrombophilic disorders lead to recurrent fetal loss, preeclampsia, intrauterine growth restriction and placental abruption. On the fetal side, there is a growing body of evidence that fetal thrombophilia is closely related to catastrophic perinatal events, such as stroke (resulting in cerebral palsy) or limb ischemia via arterial thrombosis, cerebral sinus venosus thrombosis or renal vein thrombosis. Furthermore, an association between fetal thrombophilia and adverse pregnancy outcome has been reported. Fetal thrombotic vasculopathy has been assumed to be a plausible underlying cause for placental lesions and neonatal sequelae. This review aims to tabulate and discuss the findings regarding the weight of fetal thrombophilic factors and the potential association with obstetric and neonatal complications derived from the current literature.     

The term breech presentation. A retrospective study with regard to the planned mode of delivery

BACKGROUND: To analyze retrospectively a large group of term breech and vertex deliveries, with regard to the influence of the mode of delivery on the frequency of fetal and maternal complications. METHODS: All singleton breech deliveries after completed 36 weeks of pregnancy, with a live fetus, delivered at Rogaland Central Hospital, from September 1 1996 to the May 10 2001 were included (n = 575). Correspondingly as a control group, 582 cases in vertex presentation were analyzed. RESULTS: Planned vaginal delivery (VD) for the fetus in breech presentation (n = 448) in comparison with elective caesarean section (CS) (n = 127) increased early neonatal morbidity (3.6% vs. 0%). The frequency of Apgar scores < 7 at 5 min also increased (4.2% vs. 0.8%), as well as umbilical artery pH < 7.0 (4.4% vs. 0%), and referrals to the neonatal intensive care unit (NICU) (15.8% vs. 6.3%). Corresponding figures for planned VD of the fetus in vertex presentation were: 0.5% neonatal morbidity, 0.2% Apgar scores < 7 at 5 min, 8.1% admissions to NICU and 1.5% pH < 7.0 in umbilical arteries. Results comparing maternal morbidity in the different breech groups were inconclusive, but there were more maternal complications in the breech group planned for VD than in the corresponding vertex group (5.1% vs. 1.9%). CONCLUSIONS: Elective CS for breech presentation will significantly decrease the risks for the fetus in comparison with planned VD.     

Excessive maternal weight and pregnancy outcome.

OBJECTIVES: This study was undertaken to determine the influences of increased maternal prepregnancy weight and increased gestational weight gain on pregnancy outcome. STUDY DESIGN: This was a longitudinal retrospective study of 7407 term pregnancies delivered from 1987 through 1989. After excluding cases with multiple fetuses, stillbirths, fetal anomalies, no prenatal care, selected medical and surgical complications, and those with incomplete medical records, 3191 cases remained for analyses by determination of odds ratios for obstetric outcomes, by chi 2 tests for significant differences and by adjustment for risk factors with stepwise logistic regression. RESULTS: Both increased maternal prepregnancy weight (body mass index) and increased maternal gestational weight gain were associated with increased risks of fetal macrosomia (p less than 0.0001), labor abnormalities (p less than 0.0001), postdatism (p = 0.002), meconium staining (p less than 0.001), and unscheduled cesarean sections (p less than 0.0001). They were also associated with decreased frequencies of low birth weight (p less than 0.001). The magnitude of the last was less than that of the other outcomes. CONCLUSIONS: Increased maternal weight gain in pregnancy results in higher frequencies of fetal macrosomia, which in turn lead to increased rates of cesarean section and other major maternal and fetal complications. Because these costs of increased maternal weight gain appear to outweigh benefits, weight gain recommendations for pregnancy warrant careful review.     

Inherited thrombophilia and poor pregnancy outcome

Gestational vascular complications are a major cause of maternal and fetal morbidity.A growing body of evidence suggests a significant role for inherited thrombophilia in the development of gestational vascular complications. While the majority of women with thrombophilia will have an uneventful gestation, case-control studies demonstrated that thrombophilia is more prevalent in cohorts of women with pregnancy loss and early-onset pre-eclampsia. Placental abruption and severe intrauterine growth restriction (IUGR) may also be associated with thrombophilia. Placental pathological findings in women with thrombophilia are hallmarked by thrombosis and fibrin deposition potentially to a greater degree than in normal pregnancy. Preliminary non-randomized studies suggest a benefit for prophylaxis with unfractionated and low-molecular-weight heparin (LMWH), and prospective randomized trials are in progress to define whether LMWH is effective in preventing pregnancy loss and other gestational vascular complications in women with thrombophilia and previous fetal wastage.