血清可溶性Fas与胎盘组织胎盘生长因子的表达在早发型重度子痫前期发病中的作用

目的:探讨血清可溶性Fas与胎盘组织胎盘生长因子在早发型重度子痫前期发病中的作用。方法:采用ELISA和免疫组化法分别检测20例早发重度子痫前期患者、35例晚发重度子痫前期患者和40例正常晚期妊娠患者血清可溶性Fas(Soluble Fas,sFas)和胎盘组织胎盘生长因子(placental growth factor,PlGF)的表达。结果:正常妊娠组、早发重度组、晚发重度组血清sFas水平分别为(1.17±0.53)、(6.68±0.97)和(3.17±0.74)mg/L,早发重度组、晚发重度组均显著高于正常对照组,差异有显著性(P<0.05)。早发重度组又明显高于晚发重度组,差异有显著性。正常妊娠组胎盘组织PlGF表达的平均灰度值显著高于早发型及晚发型重度子痫前期组,其中早发型子痫前期重度组表达最低。早发重度组中血清sFas与PlGF呈负相关,相关系数-0.748。结论:重度子痫前期患者血清sFas表达升高,且早发重度组表达显著高于晚发重度组,并与PlGF呈负相关,说明其异常表达可能是早发重度子痫前期发病的主要原因。     

胎盘早剥23例临床研究

目的：通过对23例胎盘早剥的临床分析,探讨胎盘早剥早期诊断和积极处理的重要性。方法：将23例胎盘早剥按发病诱因、症状、体征、超声结果、母婴结局进行探讨。结果：胎盘早剥发生率为0．488％,其中妊娠期高血压5例,外伤、咳嗽及性生活引起4例,原因不明12例,围产儿死亡率为0．17％,腹痛及阴道流血为主要症状。结论：胎盘早剥对母儿生命威胁很大,早期诊断非常重要。并发症主要有产后出血、子宫胎盘卒中等,一旦确诊,必须立即终止妊娠。     

中期妊娠并发胎盘早剥及弥漫性血管内凝血1 例报告

1临床资料患者36岁,孕2产1,因“停经22周,胎动消失2 d,牙龈出血7 h”于2008年11月13日4:55急诊入院。患者末次月经2008年5月27日,未产检,入院前2 d开始未觉胎动,未重视,入院前1 d夜间无明显诱因出现牙龈出血,后来我院急诊就诊,超声示:无胎心搏动,胎盘位于右前壁,胎盘内低至无回声区。血常规:WBC 15.11×109/L,Hb 100 g/L,PLT 92×109/L。凝血功能:PT＞180 s,APTT＞109 s。拟诊“死胎、胎盘早剥、弥漫性血管内凝血（DIC）？”,即收住入院。患者曾于1996年平产1胎,有“肾结石”病史2年,平素口服中药治疗,否认高血压病史。入院体格检查:体温36.7℃,脉搏80次/min,呼吸20次/min,血压125/83 mmHg(1 mmHg=0.133 kPa),宫底脐上4指,轻压痛,腹肌略紧张,宫缩规律（30 s/2 min）,强度中弱。入院后复查血常规:WBC 16.74×109/L、Hb 92 g/L、PLT 75×109/L。凝血功能:PT＞120 s、APTT＞180 s、FDP＞129 μg/ml。超声示:无胎心,双顶径6.1 cm,胎盘上方见11.6 cm×6.9 cm回声不均区。诊断:死胎、胎盘早剥、DIC。立即报病危,予吸氧,补充血容量,完善备血、血小板、冷沉淀等术前准备,急诊行全麻下剖宫取胎术,术中见子宫增大如孕5个半月大小,两侧宫角处呈紫蓝色,切开子宫下段,宫腔内大量不凝血涌出,迅速徒手取出胎儿及胎盘组织,检查胎盘80%面积见凝血块压迹。术中见胎盘剥离面及子宫切口广泛渗血,宫缩尚可,术中以试管法取静脉血5 ml,轻叩管壁,15 min后仍不凝,术中复查血常规:WBC 14.34×109/L、Hb 75 g/L、PLT 48×109/L。交替输注纤维蛋白原2 g,冷沉淀20 U,血小板10 U,红细胞悬液及血浆1 200 ml,并按摩子宫、应用促宫缩药物及缝扎止血,组织渗血情况好转,宫缩好,腹腔留置引流管1根后关腹。宫腔内积血及术中出血共约800 ml,术后转ICU监护2 d,抗生素预防感染,输血及冷沉淀改善凝血功能,低分子肝素改善循环功能,呋塞米利尿及对症治疗,术后2 d各项指标基本恢复正常。术后第8天,患者恢复良好出院,出院前复查血常规Hb 131 g/L、PLT 202×109/L,凝血功能:PT 25.6 s、APTT 28.9 s、FDP 11.63 μg/ml。出院诊断:孕22周,G2P1,死胎;胎盘早剥（重度）;DIC。     

胎盘早剥51例临床分析

目的：探讨胎盘早剥的病因、早期诊断及处理方法。方法：回顾性分析我院2005年1月～2006年12月收治的51例胎盘早剥患者的临床资料,分析胎盘早剥的发病诱因、新生儿预后及胎盘的位置对胎盘早剥产前诊断的影响。结果：2年内分娩总数6586例,胎盘早剥发生率为O．77％,发病诱因以胎膜早破（43．1％）为首位,其次为重度子痫前期（13．7％）和妊娠期糖尿病（11．8％）,外伤、疤痕子宫、脐带过短以及其他因素分别占9．8％、9．8％、3．9％和7．8％。孕产妇并发DIC及凝血功能障碍2例,无死亡。新生儿轻度窒息13例,重度窒息7例,围产儿死亡2例（3．9％）。胎盘位于子宫前壁者产前诊断20例（71．4％）,产后诊断9例（39．1％）;位于子宫后壁者产前诊断8例（28．6％）,产后诊断14例（60．9％）。结论：阴道流出血性羊水或流血及腹痛为典型临床表现,后壁胎盘发生胎盘早剥产前不易诊断,少部分无典型症状仅在顺产后发现轻度胎盘早剥。重视诱因及临床表现,结合B超等辅助检查有助于胎盘早剥的早期诊断,及时正确处理可以降低孕产妇和围产儿的死亡率。     

纤维蛋白原定量测定在胎盘早剥早期诊断中的意义

目的通过对孕妇血浆纤维蛋白原（Fbg）定量测定、及对纤维蛋白原动态观察,结合临床症状、体征及B超等检查,对胎盘早剥早期做出诊断。方法对本院产科2001年1月至2009年1月96例确诊为胎盘早剥的患者进行回顾性分析。结果96例胎盘早剥的患者中,纤维蛋白原低于3.5g/L的71例,占73.96%。结论纤维蛋白原定量测定可作为胎盘早剥早期诊断的诊断依据。     

胎盘生长因子对培养的人脐静脉内皮细胞分泌炎性因子的影响

目的 观察胎盘生长因子(placental growth factor, PlGF)对血管内皮细胞分泌炎性因子的影响.方法 体外培养人脐静脉内皮细胞(human umibilical vein endotheial cells, HUVEC),并采用ELISA技术来观察0～50 ng/mL的重组人PlGF(rhPlGF)作用不同时间(4～48 h)对HUVEC分泌单核细胞趋化因子-1(monocyte chemotactic protein-1, MCP-1)、可溶性血管细胞黏附分子-1(soluble vascular-cell adhesion molecule-1, sVCAM-1)及P-选择素(P-Selectin)功能的变化.结果 rhPlGF对HUVEC分泌MCP-1的刺激作用具有一定的时间及剂量依赖关系,以50 ng/mL的PlGF作用48 h的作用最为明显(P<0.05).与对照组相比,作用于HUVEC 4 h,5～50 ng/mL的PlGF均能明显增加P-Selectin的分泌.但是,不同浓度的rhPlGF处理不同时间,HUVEC分泌sVCAM-1的量与相应时间对照组比较,差异均无统计学意义.结论 PlGF对HUVEC分泌MCP-1及P-Selectin等有明显的促进作用.提示PlGF对内皮细胞分泌炎性因子功能的影响可能很复杂.     

胎盘早剥合并弥漫性血管内凝血急诊处理

胎盘早剥是妊娠中晚期的严重并发症,合并弥漫性血管内凝血(DIC)时,可导致孕产妇和围产儿的发病率及死亡率明显增加,早期诊断和急诊处理是改善围产结局的关键。急诊处理胎盘早剥合并DIC的主要措施在于维持血容量,补充凝血因子,并及时终止妊娠。胎儿存活者应剖宫产终止妊娠,胎儿已死亡者可考虑经阴道分娩。     

胎盘植入的MRI表现1例报道

患者,女,39岁.药物流产后2月余,阴道流血半月余,自述未见绒毛组织排出.患者婚后先后顺产、剖腹产生育2女.妇科检查:子宫如3个月孕大,形态不规则,活动可,无压痛;余阴性.实验室检查:B-HCG:195.73 ng/ml,术后B-HCG:4.6 mg/ml.     

Seasonal variation in placental abruption

Objective: To characterize seasonal patterns of placental abruption among Jewish and Bedouin parturients in the Southern part of Israel. Methods: A retrospective population-based study comparing all singleton pregnancies of patients with and without placental abruption was conducted. Deliveries occurred between the years 1988 and 2010. A ‘classical’ model of time series was used, allowing to assess trend and periodic patterns of placental abruption. Results: During the study period, 241,408 deliveries took place, of which 1685 (0.7%) were complicated with placental abruption. Placental abruption was significantly more common among Bedouin parturients: 0.77% (n = 948) vs. 0.623% (n = 737), p < 0.001. A non-linear negative correlation was noted in the incidence of placental abruption (coefficient = ?0.002) during the entire study period. Time series analysis demonstrated annual cycle frequency, seasonal cycle and weekly cycle of placental abruption. The seasonal incidence of placental abruption was higher during spring (B = 7.15) and lower during summer (reference) for both populations (Jewish and Bedouins). Weekly cycle showed significantly higher incidence on Saturday (B = 3.4) and lowest on Tuesday (B = ?4.66) for both groups. The daily differences were accentuated in the Bedouin population (B = 3.7 vs. B = 2.93 in the Jewish population). Conclusion: Placental abruption was significantly more common in the Bedouin population. Both populations demonstrated the same annual and seasonal patterns, with higher incidence in spring and autumn.     

Thrombin receptor on the placental syncytiotrophoblastic plasma membrane

Summary Purified placental syncytiotrophoblastic membrane has been used in a radioreceptor assay to study the binding of tritium radiolabeled human thrombin. Binding was found to be saturable at higher membrane concentrations when using a fixed amount of ligand and showed a hyperbola analogous to enzyme-substrate binding. A Scatchard plot was linear and revealed homogeneous binding sites with a high-affinity constant K_a=3×10¹⁰ M⁻¹ and capacity of 3.05×10¹¹ sites/mg of membrane protein. This high-affinity compares well with chick and embryo cell thrombin receptor which has homogeneous sites and high-affinity in contrast to platelet thrombin receptor which exhibits multiple binding sites and cooperative effects as previously noted. A thrombin receptor on the placenta might serve to mobilize thrombin into placental tissue leading to conversion of fibrinogen into fibrin, fibrinoid necrosis being so common in certain placentae. A receptor-mediated transplacental passage of thrombin into the fetal circulation is also proposed.