早发型子痫前期-子痫抗凝疗效多中心临床研究

目的探讨丹参、低分子肝素等抗凝药物治疗早发型子痫前期-子痫的有效性和安全性。方法将2008年11月至2010年3月全国21所医院572例早发型子痫前期-子痫患者随机分4组,对照组(1组,仅用硫酸镁)、硫酸镁+丹参组(2组)、硫酸镁+低分子肝素组(3组)、硫酸镁+低分子肝素+丹参组(4组)。收集患者一般情况、治疗及分娩资料,监测并比较治疗前后24h尿蛋白、出凝血指标、血常规、超声及不良反应等指标。结果 (1)接受抗凝治疗患者治疗时间较对照组显著延长(P<0.05)。(2)第3组凝血酶时间(TT)值延长较其他组明显;第3、4组血小板和红细胞压积(HCT)下降显著,但组间差异无统计学意义。(3)第3、4组分别有11例和6例因不良反应而停药。结论单独或联合应用丹参或低分子肝素治疗早发型子痫前期-子痫可延长其孕周,有改善血液浓缩状态趋势,低分子肝素可缓解患者高凝状态,但要注意血小板减少倾向。     

早发型子痫前期4种治疗方案的临床疗效研究

目的:探讨对于早发型子痫前期4种不同治疗方案的临床疗效。方法:随机将我院90例早发型子痫前期患者分为硫酸镁治疗组(硫酸镁组)、硫酸镁+丹参治疗组(硫酸镁+SM组)、硫酸镁+低分子肝素治疗组(硫酸镁+LMWH组)、硫酸镁+丹参+低分子肝素组(硫酸镁+SM+LMWH组),对其分娩等情况及治疗前后的24小时尿蛋白定量(24hPRO)等临床资料进行对比,观察4种临床治疗方案的效果。结果:①硫酸镁+SM组对于自觉症状改善效果较好(96.43%),与硫酸镁组(71.05%)比较,差异有统计学意义(P<0.05)。②治疗3天后实验室指标比较,24hPRO值,硫酸镁组(5.44±0.37g)高于其他3组(P<0.05);延长APTT值,硫酸镁+SM+LMWH组(38.09±3.48秒)高于其他3组(P<0.05)。而其他的实验室指标比较,差异均无统计学意义(P>0.05)。③硫酸镁组延长妊娠平均天数(4.21±2.53天)少于其他3组(P<0.05);硫酸镁组的新生儿存活率(71.05%)最低,与硫酸镁+SM+LMWH组(100.00%)比较,差异有统计学意义(P<0.05)。结论:硫酸镁联合SM、LMWH治疗早发型子痫前期...     

早发型子痫前期解痉抗凝治疗的疗效观察

目的研究对早发型子痫前期孕妇进行解痉抗凝治疗的疗效。方法选取我院2012年5月~2014年5月收治的早发型子痫前期患者70例,将其随机分为对照组和观察组,对照组患者使用硫酸镁进行常规治疗,观察组患者在对照组的基础上增加低分子肝素进行治疗,观察两组患者的疗效。结果治疗后,两组患者的平均动脉压以及24 h尿蛋白都明显下降,差异有统计学意义(P0.05),但两组对比,差异无统计学意义(P0.05);观察组新生儿窒息率明显小于对照组,差异有统计学意义(P0.05)。结论对于早发型子痫前期患者,使用硫酸镁联合低分子肝素进行治疗,能够降低新生儿窒息率,同时安全有效。     

应用低分子肝素对早发型子痫前期患者再次妊娠结局的影响

目的:探讨预防性应用低分子肝素对早发型子痫前期患者再次妊娠结局的影响。方法:选择2010年1月至2015年12月期间,因早发型子痫前期在郑州大学第一附属医院终止妊娠,再次妊娠后在本院定期产检并终止妊娠的患者共99例为研究对象。分为A组:预防性应用低分子肝素57例,B组:未应用低分子肝素42例,两组均为单胎妊娠,比较两组再次妊娠结局。结果:A组延长妊娠时间、新生儿存活率、新生儿出生体质量均多于B组,A组新生儿窒息、胎儿生长受限、早发型子痫前期、子痫前期、严重并发症的发生率均小于B组,差异均有统计学意义(P0.05);A组纤维蛋白原(FIB)、D-二聚体(D-D)水平低于B组,差异有统计学意义(P0.05)。A组本次分娩孕周、新生儿出生体质量、新生儿存活率均大于前次妊娠,严重并发症、胎儿生长受限、新生儿窒息的发生率均小于前次妊娠,差异有统计学意义(P0.05);B组本次分娩孕周、新生儿出生体质量均大于前次妊娠,差异有统计学意义(P0.05);B组两次妊娠严重并发症、新生儿存活、胎儿生长受限、新生儿窒息的发生率比较,差异无统计学意义(P0.05)。结论:早发型子痫前期患者再次妊娠时预防性应用低分子肝素,可降低子痫前期的复发率及严重并发症的发生率,改善围生儿结局,不增加出血事件的风险。     

低分子肝素治疗重度子痫前期患者效果的研究

目的:探讨重度子痫前期患者应用不同剂量低分子肝素的临床效果及安全性。方法:随机将重度子痫前期62例分为3组:A组(大剂量组),在常规治疗的基础上加用低分子肝素5000U/d;B组(小剂量组),加用低分子肝素2500U/d;C组,常规治疗组。通过临床症状、体征及辅助检查的变化判断各治疗组的治疗效果及对母儿的影响。结果:3组患者纳入研究时临床指标无差异(P>0·05);加用低分子肝素组(A、B两组)的临床疗效评分显著高于常规治疗组(C组)(13·43±2·75,11·95±3·46vs9·43±3·81(P<0·05));A组的平均得分高于B组,但统计学分析无显著差异(P>0·05);3组孕妇的肝肾功能、胎儿宫内状况、分娩方式及产后出血量等均无显著差异(P>0·05)。结论:低分子肝素有助于改善重度子痫前期孕妇的治疗效果;低分子肝素对母儿安全。     

早发型重度子痫前期101例临床分析

目的:探讨早发型重度子痫前期的临床特征及对妊娠结局的影响.方法:回顾性分析我院收治的289例重度子痫前期病例(其中早发型组101例,晚发型组188例,围生儿301例)的母婴结局.结果:①早发型组的发病时平均血压、发病孕周、分娩孕周及严重并发症发生率与晚发型组比较,差异有统计学意义(P＜0.05);两组分娩方式比较,差异无统计学意义(P＞0.05);且早发型组胎儿脐血流比值(S/D)、胎儿生长受限(FGR)、早产、胎儿窘迫、新生儿窒息、围生儿死亡的发生率高于晚发型组,差异有统计学意义(P＜0.05);②早发型重度子痫前期按发病孕周分为A组(＜28周)、B组(28 ～31+6周)、C组(32 ～ 33+6周),3组围生儿结局比较,A组病例中胎儿脐动脉S/D≥3、FGR及新生儿窒息的发生率均高于B组及C组(P＜0.05);而A组及B组围生儿死亡率高于C组,差异有统计学意义(P＜0.05);③早发型重度子痫前期病例中脐动脉S/D≥3的病例,FGR、胎儿窘迫、新生儿窒息及围生儿死亡的发生率均高于S/D ＜3的病例(P＜0.05);两者间早产的发生率差异无统计学意义(P＞0.05).结论:早发型重度子痫前期孕妇发病孕周越早,FGR、新生儿窒息、胎儿窘迫及围生儿死亡发生率越高,围生儿结局不佳.基层医院应加强孕期保健,定期行产前检查.     

低分子肝素和丹参抗凝治疗早发型重度子痫前期病例的临床疗效研究

目的:了解丹参、低分子肝素等抗凝药物对早发型重度子痫前期的治疗作用。方法:2006年1月～2010年3月将我院产科病房子痫前期患者65例前瞻性随机分为丹参组23例,低分子肝素组11例,丹参+低分子肝素组15例,对照组16例,收集各组患者的一般情况、分娩情况,对比分析治疗前后的尿蛋白、血常规、出凝血系列、肝肾功能、血脂等指标,了解治疗效果。结果:(1)丹参+低分子肝素组的治疗时间为11.13天,丹参组为9.05天,显著长于(SNK值不同)其他组;(2)新生儿分娩孕周平均为32.45±2.74周,新生儿体重为1533.19±489.71g,围产儿死亡率215.4‰。孕产妇死亡率0%;剖宫产率84.61%,顺产率1.54%,引产率13.85%。各组间分娩孕周、新生儿体重、围产儿和孕产妇死亡率均无显著差异(SNK均为A)。分娩的手术指征以胎儿窘迫、疾病加重为主要因素;(3)各组间治疗前后血常规、肝肾功能、凝血指标中的PT、FIB对比差值无显著差异(SNK均为A),而低分子肝素组TT增加1.35s,APTT增加3.33s,显著长于其他组(SNK值不同)。24h尿蛋白丹参组增加0.6g,增加值少于其他组。结论:应用丹参或丹参+低分子肝素治疗子痫前期患者可延长孕周,丹参缓解尿蛋白明显,低分子肝素缓解高凝状态明显,药物的有效性尚需进一步大样本研究。     

子痫前期孕妇血清中氧化应激产物H_2O_2对sHLA-G表达的影响

目的:探讨子痫前期患者血清中氧化应激产物H2O2对可溶性人类白细胞抗原G(sHLA-G)表达的影响,分析早发型及晚发型子痫前期的病因。方法:选择早发型和晚发型子痫前期孕妇各15例为研究组,以同期正常孕妇15例为对照组。采用比色法及ELISA法分别检测3组研究对象血清中H2O2含量和sHLA-G表达,并进行相关性分析。结果:(1)早发型及晚发型子痫前期组孕妇血清中H2O2呈高水平表达[(58.43±3.56)μmol/L,(29.84±7.67μmol/L)],与正常妊娠组相比[(21.61±4.25)μmol/L],差异均有统计学意义(P均<0.05);早发型子痫前期组孕妇血清中H2O2含量显著高于晚发型子痫前期组(P<0.05)。(2)早发型及晚发型子痫前期组孕妇血清中sHLA-G呈低水平表达[(28.65±9.16)U/ml,(51.84±8.67)U/ml],与正常妊娠组[(98.13±13.26)U/ml]相比,差异有统计学意义(P均<0.05);早发型子痫前期组孕妇血清中sHLA-G表达量显著低于晚发型子痫前期组(P<0.05)。(3)正常妊娠、子痫前期孕妇血清中的H2O2水平与sHLA-G表达呈负相关(r=-0.835,P<0.05)。结论:早发型子痫前期发病早,受氧化应激损伤更严重,血清中sHLA-G表达量更低;氧化应激产物H2O2可能潜在下调sHLA-G表达,与子痫前期发病及病情轻重程度相关。     

早发型重度子痫前期临床处理与母儿结局分析

目的:探讨早发型重度子痫前期的临床处理及对母儿预后的影响.方法:回顾分析我院2007年1月至2010年12月收治的64例早发型重度子痫前期患者的临床资料.按终止孕周分为3组,A组:28周-31+6周16例,B组:32周～33+6周24例,C组:≥34周24例.结果:A、B、C3组并发症的发生率以A组最低,但3组间比较差异无统计学意义(P＞0.05);3组平均期待时间以C组最长,3组之间比较差异均有统计学意义(P＜0.05,P＜0.01);新生儿死亡率A组与C组比较差异有统计学意义(P＜0.05),围生儿死亡率A组与B组、C组比较差异均有统计学意义(P＜0.05).结论:早发型重度子痫前期患者终止妊娠前期待治疗是安全有效的,但需密切监测母胎病情变化,掌握终止妊娠时机极为重要,适当的期待治疗有助于改善母婴结局.     

硫酸镁与山茛菪碱治疗早发型重度子痫前期临床对照研究

目的:对比硫酸镁、山莨菪碱对早发型重度子痫前期的临床治疗效果.方法:对我院产科2005年1月至2008年1月保守治疗的早发型重度子痫前期患者68例随机分为两组.硫酸镁组37例,山莨菪碱组31例,观察两组血压下降、尿蛋白、水肿等情况.结果:硫酸镁组和山莨菪碱组用药24小时、48小时、72小时后,平均动脉压下降明显,与用药前比较差异均有统计学意义(P＜0.05).但两组用药前及用药后24小时、48小时、72小时比较差异无统计学意义(P＞0.05).山莨菪碱组减轻水肿的效果较硫酸镁组更明显(P＜0.05).两组保守治疗时间、终止妊娠孕周、并发症发生情况及围生儿结局相比差异无统计学意义(P＞0.05).两组用药后均无严重药物不良反应发生.结论:山莨菪碱与硫酸镁治疗早发型重度子痫前期疗效相近.     

不同剂量低分子肝素辅助治疗重度子痫前期的临床观察

目的观察不同剂量低分子肝素（LMWH）辅助治疗重度子痫前期的有效性及安全性。方法选取2009年11月至2011年3月在北京友谊医院住院的重度子痫前期患者71例,随机分为常规治疗组（A组20例）、常规疗法＋LMWH25IU／kg·d组（B组17例）、常规疗法＋LMWH50IU／kg·d组（c组16例）、常规疗法＋LMWH75IU／kg·d组（D组18例）,连续治疗7d。观察不同剂量LMWH辅助治疗重度子痫前期在改善临床症状、实验室指标（凝血功能、肝肾功能、血常规、尿蛋白）和围产结局的作用。结果①AT-Ⅲ在A组治疗后有上升,差异无统计学意义（P〉0．05）;应用LMWH的BCD组治疗后均有下降,各组间比较差异均有统计学意义（P〈0．05）;但仅B组治疗后显著低于治疗前,差异有统计学意义（尸=0．020）;D组治疗后24h尿蛋白定量显著低于治疗前（P=0．028）;②不同剂量LMWH组治疗后收缩压均显著低于治疗前（分别为P=0．010、P=0．002、P=0．002、P=0．014）。A组和B组治疗后舒张压显著低于治疗前（P=0．007、P=0．003）。其余各项指标治疗前后比较差异无统计学意义（P〉0．05）。母婴围产结局各组比较差异无统计学意义（P〉0．05）。结论在常规治疗子痫前期的同时加用不同剂量的LMWH对肝肾功能、血常规指标、凝血指标、母婴围产结局未产生明显影响,但大剂量LMWH（75IU／kg·d）在改善24h尿蛋白定量上有一定作用,并是安全的。血压改善的主要作用仍然是常规治疗方法。     

应用硫酸镁治疗胎儿生长迟缓

目的　探讨胎儿生长迟缓 (intrauterinegrowthretardation ,IUGR)孕妇的静脉血与新生儿脐静脉血中镁离子含量的变化及其与新生儿体重的关系。方法　将 39例IUGR孕妇随机分为治疗 1组 14例 ,治疗 2组 14例 ,未治疗组 11例。治疗 1组用 10 %葡萄糖 5 0 0ml 复方丹参液 14ml 低分子右旋糖酐 5 0 0ml静脉滴注 ;治疗 2组除有与治疗 1组相同的处方外 ,再加用 5 %葡萄糖 5 0 0ml 2 5 %硫酸镁 2 0ml静脉滴注 ,并以同期分娩的 12例正常孕妇为对照组。采用全自动生化分析仪 ,测定 4组孕妇的肘静脉血和新生儿脐静脉血中的镁离子含量。结果　治疗 1组孕妇静脉血中镁离子含量[(0 6 9± 0 0 5 )mmol/L]和未治疗组 [(0 6 8± 0 0 2 )mmol/L]比较 ,差异无显著性 (P >0 0 5 ) ,和治疗 2组 [(1 0 6± 0 0 9)mmol/L]比较 ,差异有显著性 (P <0 0 5 ) ,各组新生儿脐血镁离子含量比较 ,差异有极显著性 (P <0 0 1) ,对照组和治疗 2组、未治疗组和治疗 1组比较 ,差异无显著性 (P >0 0 5 ) ,其余各组间比较 ,差异有极显著性 (P <0 0 1) ,各组胎盘重量比较 ,差异有极显著性 (P <0 0 1) ,各组新生儿体重比较 ,差异有显著性 (P <0 0 5 )。结论　镁缺乏是IUGR发生的原因之一 ,中晚期孕妇适量补充镁有预防和治疗IUGR的作用     

Magnesium sulfate in women with mild preeclampsia: a randomized controlled trial

OBJECTIVE: To determine whether magnesium sulfate prevents disease progression in women with mild preeclampsia. METHODS: A total of 222 women with mild preeclampsia were randomized to receive intravenous magnesium sulfate (n = 109) or matched placebo (n = 113). Mild preeclampsia was defined as blood pressure of at least 140/90 mm Hg taken on two occasions in the presence of new-onset proteinuria. Patients with chronic hypertension or severe preeclampsia were excluded. Patients were considered to have disease progression if they developed signs or symptoms of severe preeclampsia, eclampsia, or laboratory abnormalities of full or partial HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. RESULTS: The groups were similar with respect to maternal age, ethnicity, gestational age, parity, and maternal weight at enrollment. Fourteen women (12.8%) in the magnesium group and 19 (16.8%) in the placebo group developed severe preeclampsia after randomization (relative risk = 0.8, 95% confidence interval 0.4, 1.5, P =.41). None in either group developed eclampsia or thrombocytopenia. Women assigned magnesium had similar rates of cesarean delivery (30% versus 25%), chorioamnionitis (3% versus 2.7%), endometritis (5.3% versus 4.3%), and postpartum hemorrhage (1% versus 0.9%), compared to those assigned placebo. Neonates born to women assigned magnesium had similar mean Apgar scores at 1 and 5 minutes as those born to women assigned placebo (7.7 +/- 1.5 versus 7.8 +/- 1.6 and 8.7 +/- 0.7 versus 8.8 +/- 0.6, respectively). CONCLUSION: Magnesium sulfate does not have a major impact on disease progression in women with mild preeclampsia. Magnesium use does not seem to increase rates of cesarean delivery, infectious morbidity, obstetric hemorrhage, or neonatal depression.     

Magnesium sulfate effectively reduces blood pressure in an animal model of preeclampsia.

OBJECTIVE: We tested the ability of magnesium sulfate to reduce hypertension and neonatal growth retardation in an animal model of preeclampsia. STUDY DESIGN: On day 17 of pregnancy, osmotic minipumps were inserted subcutaneously to continuously deliver either vehicle (saline control group), or N-nitro-L-arginine methyl ester (L-NAME) (50 mg/kg/day), or L-NAME (50 mg/kg/day) in combination with magnesium sulfate (60 mg/kg/day). Prior to insertion, blood pressure and heart rate were monitored with a pneumatic tail cuff device. Blood pressure measurements were repeated on days 18, 20, and 21 of pregnancy. Blood was obtained on days 17 and 21, along with urine, to assess magnesium levels and degree of proteinuria. Pups were weighed and measured at 48 hours postpartum. RESULTS: Rats receiving L-NAME developed hypertension within 24 hours of implantation (108 +/- 3.9 vs. 123 +/- 3.4 mmHg, p < 0.05). Magnesium sulfate, given along with L-NAME did not prevent mean blood pressure from increasing, but reduced it by day 21 compared to L-NAME given alone (107 +/- 3.4 vs. 122 +/- 8.7 mmHg, respectively, p < 0.05). Magnesium sulfate reduced neonatal growth retardation by improving the weight of the pups compared to pups from maternal rats given L-NAME alone (6.1 +/- 0.1 vs. 5.2 +/- 0.3 grams, respectively, p < 0.05). CONCLUSION: Maternal magnesium sulfate reduces blood pressure and increases neonatal size compared to L-NAME without magnesium. These findings support a beneficial effect of magnesium in preeclampsia.     

Effects of magnesium sulfate on heart rate,blood pressure variability and baroreflex sensitivity in preeclamptic rats treated with L-NAME

Objective: Magnesium sulfate is used for the treatment of preeclampsia. This study aimed to evaluate effects of magnesium sulfate on heart rate variability (HRV), blood pressure variability (BPV) and baroreflex sensitivity (BRS) in pregnant rats treated with N^G-nitro-.-arginine-methyl ester (L-NAME). Methods: Sprague–Dawley rats were randomly divided into four groups: non-pregnancy and three pregnant groups. From gestational day 2–12, normal pregnancy group (NOR) received sterile water through intravenous injection, LN was injected with L-NAME [25?mg/day] to induce preeclampsia, while LNM group was also treated with magnesium sulfate at 0.3?g/kg at gestational day 13. HRV, BPV and BRS were monitored, and endothelial functions were detected at gestational day 14. Results: Rats with treatment of L-NAME showed significantly increased blood pressure and endothelin-1 concentration and decreased plasma NO concentration; concomitant treatment with magnesium sulfate suppressed blood pressure. Also, rats treated with L-NAME and magnesium sulfate underwent lower heart rate variability (lower absolute and normalized LF) and higher blood pressure variability (lower normalized HF and LF, higher normalized VLF) compared with non-pregnant or normal pregnant rats, whereas normalized LF of HRV in rats co-administered magnesium sulfate returned to normal level. Additionally, rats treated with L-NAME underwent decreased BRS-SP, BRS-NE, BRS LF and HF, and rats with concomitant magnesium sulfate partially reversed the decline (p?>?0.05) and had significantly lower BRS-SP, BRS-NE. Conclusion: Sympathetic and parasympathetic impairment exist in preeclamptic rats treated with L-NAME. Magnesium sulfate may ameliorate alterations in the autonomic nervous system noted in preeclampsia.     

Expectant management of severe preeclampsia and preeclampsia superimposed on chronic hypertension between 24 and 34 weeks' gestation

BACKGROUND: Timing of delivery is difficult to judge in preeclampsia. OBJECTIVE: To compare the differences of maternal and perinatal outcome of patients with severe preeclampsia and essential hypertension with superimposed preeclampsia, with expectant management at 24-34 weeks' gestation. STUDY DESIGN: A retrospective review of a conservative regime using intravenous magnesium sulfate, glucocorticoids and antihypertensive drugs, monitored by serial liver function tests, full blood count, coagulation profile, and renal function tests. Fetal status was assessed by daily non-stress test and ultrasound twice by week. RESULTS: A total number of 100 women had severe preeclampsia and 29 superimposed preeclampsia. The average pregnancy prolongation was 8.4 and 8.5 days, respectively. Oliguria, abruption placentae and HELLP syndrome were frequent complications similar in each group. There were no cases of eclampsia or disseminated coagulopathy in either group. The total neonatal survival rate was 93% in both groups. CONCLUSION: Expectant management is equally safe in both superimposed preeclampsia and severe preeclampsia of early onset.     

Effect of magnesium sulfate on plasma endothelin-1 levels in normal and preeclamptic pregnancies.

OBJECTIVE: We attempted to determine the effects of magnesium sulfate on: (1) endothelin-1 concentration in preeclampsia, preterm labor, and term pregnancy and (2) endothelin-1 release from human umbilical cord endothelial cells. STUDY DESIGN: Plasma samples were prospectively collected from eight women with preeclampsia, six preterm labor patients, and eight term patients undergoing external cephalic version before and 2 hours after magnesium sulfate infusion. Supernatants were collected from human umbilical cord endothelial cells exposed to magnesium sulfate and controls. All samples were assayed with a specific radioimmunoassay for endothelin-1. Paired Student t test and analysis of variance were used for statistical analysis. RESULTS: Magnesium sulfate infusion in preeclampsia lowered endothelin-1 levels compared with preinfusion values (6.6 +/- 3.81 before and 4.75 +/- 2.28 after infusion, p < 0.02). Magnesium sulfate did not have an effect on endothelin-1 concentration in preterm and term pregnancies. Magnesium sulfate did not alter the endothelin-1 release from human umbilical cord endothelial cells. CONCLUSION: A significant reduction of endothelin-1 plasma levels after magnesium sulfate therapy is limited to preeclampsia. In contrast, this lowering effect was not exhibited in women without preeclampsia or in normal endothelial cells.