妊娠并发脑血管病临床研究

目的 探讨妊娠合并脑血管病的发病时间、病因、危险因素与临床表现,早期诊断,改善母儿预后.方法 对1998年1月～2005年12月我院收治的妊娠合并脑血管病的10例临床病例资料进行回顾性分析.结果 10例妊娠合并脑血管病的病例,确诊脑出血5例,上矢状窦血栓3例,腔隙性脑梗死1例,羊水栓塞致脑栓塞1例.脑出血患者中重度子痫前期(子痫)3例,脑血管畸形1例,血小板减少性紫癜1例.孕妇死亡2例,其余保守治疗好转出院.8例围生儿全部存活.结论 妊娠合并脑血管病好发于重度子痫前期(子痫)、脑血管畸形,血液高凝状态与上矢状窦血栓有关.当出现神经症状及体征时,临床医生应考虑到脑血管病的可能,及时诊治,多数孕产妇可取得较好结局.     

子痫前期患者脐血和胎盘组织中IGF-Ⅱ检测的临床意义

目的:探讨IGF-Ⅱ在子痫前期发病机制中的作用。方法:用免疫组织化学方法检测正常晚孕组和轻度、重度子痫前期患者胎盘组织中IGF-Ⅱ的表达,同时用ELISA方法检测3组研究对象胎儿脐血中IGF-Ⅱ的含量。结果:IGF-Ⅱ在脐血中的含量,重度子痫前期组显著高于轻度子痫前期组(P<0.001),轻度子痫前期组显著高于正常晚孕组(P<0.01);IGF-Ⅱ在胎盘组织中的表达,重度子痫前期组显著低于轻度子痫前期组(P<0.01),轻度子痫前期组显著低于正常晚孕组(P<0.01)。结论:子痫前期时脐血IGF-Ⅱ含量升高可能是子痫前期病理变化的结果,而胎盘组织中IGF-Ⅱ表达减少可能是引发子痫前期的重要因素之一。     

脂源性细胞因子与子痫前期关系的研究

目的:探讨子痫前期(PE)患者血清脂源性细胞因子(脂联素和瘦素)水平的变化及其意义。方法:以53例子痫前期孕妇为研究组(其中轻度子痫前期32例、重度子痫前期21例),20例同期分娩的正常孕妇为对照组。采用ELISA法检测血清脂联素和瘦素水平。同时检测血清甘油三脂(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平。结果:(1)轻度、重度子痫前期患者血清脂联素水平分别为8.88±4.67μg/m l及5.14±2.79μg/m l,明显低于对照组11.61±2.90μg/m l,差异有统计学意义(P<0.01)。而轻度、重度子痫前期患者血清瘦素水平为21.79±15.19ng/m l及27.27±18.38ng/m l,明显高于对照组的12.35±6.51ng/m l,差异有统计学意义(P<0.05,P<0.01),(2)子痫前期患者血清脂联素与TG、TC、LDL-C、HDL-C均显著相关(r分别为-0.658、-0.624、-0.419、0.461),瘦素水平也与上述指标显著相关(r分别为0.534、0.707、0.418、-0.513),(3)子痫前期患者血清脂联素及瘦素水平呈高度负相关(r=-0.760,P<0.01)。结论:脂联素、瘦素等脂源性细胞因子在PE的发病中可能起一定的作用。     

母血中胎儿DNA与子痫前期关系的研究

目的:探讨孕妇外周血中胎儿DNA的浓度水平与子痫前期之间的关系。方法:留取第一次常规产前检查的472例孕妇的外周血并随访。设置阴性对照后,采用实时PCR方法定量检测怀男性单胎并发展为子痫前期的17例孕妇及34例怀男性单胎正常孕妇的血浆胎儿DNA的SRY基因浓度。结果:发展为子痫前期患者的外周血浆胎儿DNA浓度明显高于正常孕妇,中位数分别为165.41copies/ml和48.75copies/ml,有显著的统计学差异(P<0.001)。结论:发展为子痫前期患者外周血中的胎儿DNA明显增高,而浓度水平与子痫前期的严重程度似乎无关。     

RhoA在子痫前期患者胎盘中的表达

目的:检测正常晚期妊娠和子痫前期患者胎盘RhoA的表达,探讨RhoA在子痫前期发病中的作用。方法:用免疫组织化学SP法及RT-PCR检测40例子痫前期和20例正常晚期妊娠胎盘RhoA蛋白及其mRNA的表达。结果:RhoA主要在滋养细胞表达。轻度子痫前期组和重度子痫前期组RhoA蛋白及mRNA均高于正常晚期妊娠组,差异有统计学意义(P<0.05)。结论:子痫前期患者胎盘RhoA的高表达可能与子痫前期的发病有一定的关系。     

子癎前期患者血清胎盘生长因子的变化及意义

目的:探讨胎盘生长因子与子癎前期发病的关系。方法:检测40例子癎前期患者及20例正常晚期妊娠血清胎盘生长因子(PlGF)的水平及胎盘CD34表达,计数微血管密度(MVD)。结果:轻度子癎前期组血清PlGF为201.25±52.33pg/ml,胎盘MVD计数为45.6±4.2,重度子癎前期组分别为165.83±37.54pg/ml,40.2±3.9,两组均低于正常晚期妊娠组315.76±76.98pg/ml,58.2±4.8,差异有显著性意义(P<0.05)。结论:子癎前期患者血清PlGF及胎盘MVD显著降低,可能与子癎前期的发病有一定关系。     

子痫前期患者母胎循环肝细胞生长因子检测及其意义

目的探讨子痫前期母胎循环肝细胞生长因子(HGF)对子痫前期发病的影响。方法采用酶联免疫吸附法测定33例子痫前期孕妇(子痫前期组)和32例正常妊娠孕妇(对照组)外周血、脐静脉血清HGF水平。结果子痫前期组孕妇外周血HGF水平为(142.9±87.64)pg/ml,明显低于对照组的(207.6±110.55)pg/ml(t=2.487,P<0.05);子痫前期组孕妇脐静脉血HGF水平为(13.2±6.28)pg/ml,与正常对照组(16.5±8.22)pg/ml比较差异无统计学意义(t=1.546,P>0.05)。轻度和重度子痫前期孕妇外周血、脐静脉血HGF水平差异均无显著性意义(t=0.382、0.747,均P>0.05)。结论外周血HGF下降可能是子痫前期重要的发病机制之一。     

Acute Pancreatitis and Cholecystitis Associated with Postpartum HELLP Syndrome: A Case and Review

We report a case of preeclampsia associated with hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome and concomitant nonbiliary acute pancreatitis and cholecystitis in the first postpartum day. A thorough investigation ruled out known etiologies of both pancreatitis and cholecystitis. Following conservative treatment, the patient's HELLP syndrome, pancreatitis, and cholecystitis resolved on the third postpartum day. Preeclampsia is associated with microvascular abnormalities that may involve the splanchnic circulation. These abnormalities may cause not only HELLP syndrome but also pancreatitis and cholecystitis. Recognizing that ischemia can damage not only the liver but also the pancreas and gallbladder, could result in improvements in the diagnosis and management of pancreatitis in patients with preeclampsia.     

Pathological Uterine Perfusion in the Second Trimester Is Not Associated with Neutrophil Activation

Objective: Preeclampsia and intrauterine growth retardation (IUGR) are associated with elevated concentrations of myeloperoxidase (MPO) and polymorphonuclear (PMN) elastase, which indicate maternal neutrophil activation. The aim of the study was to measure maternal MPO and PMN elastase plasma concentrations in second trimester pregnancies with pathological uterine perfusion that are a high risk group for preeclampsia and IUGR, and compare them to normal controls. Methods: The study includes 25 pregnancies with normal and 25 pregnancies with pathological uterine perfusion. In both groups, doppler‐sonographic measurement of uterine perfusion was performed in the twenty‐first week of gestation. Maternal plasma concentrations of MPO and PMN elastase were measured using a specific ELISA for both enzymes. Results: The plasma MPO concentration of pregnant women with normal perfusion did not differ significantly from that of the group with pathological perfusion (27.4 ± 3.3 vs. 23.7 ± 2.0 ng/mL). Likewise, the plasma PMN elastase‐concentration also did not show a significant difference between the groups (5.7 ± 0.5 ng/mL normal vs. 8.0 ± 1.0 ng/mL pathological). Patients with pathological perfusion that later developed preeclampsia or IUGR (9/25) showed unchanged MPO and PMN elastase values in the second trimenon compared to those with pathological perfusion and normal outcome. Conclusions: Pathological uterine perfusion in the second trimester was not associated with maternal neutrophil activation. The measurement of the MPO and PMN elastase concentration suggested that neutrophil activation in preeclampsia or IUGR is a secondary effect of the disease rather than a primary pathophysiological factor.     

Angiogenic imbalance and plasma lipid alterations in women with preeclampsia from a developing country

Background: An imbalance between anti-angiogenic factors (e.g. soluble vascular endothelial growth factor receptor-1 (s-FLT1) and soluble endoglin (s-Eng)) and pro-angiogenic factors (e.g. placental growth factor (PlGF)) as well as increased oxidized low-density lipoprotein (ox-LDL) concentrations have been associated with preeclampsia (PE). Risk factors associated with the development of PE, however, are known to be different between developed and developing countries. The aim of the study was to determine the levels of s-FLT1, s-Eng, PIGF, and ox-LDL in women with PE from a developing country. Methods: A multi-center case–control study was conducted. One hundred and forty three women with PE were matched by age and parity with 143 healthy pregnant women without cardiovascular or endocrine diseases. Before delivery, blood samples were taken and serum was stored until analysis. Results: Women with PE had lower concentrations of PIGF (p < 0.0001) and higher concentrations of s-Eng (p = 0.001) than healthy pregnant women. There were no differences between the groups regarding ox-LDL or s-FLT1. Women with early onset PE had higher s-FLT1 concentrations (p = 0.0004) and lower PIGF concentrations (p < 0.0001) than their healthy pregnant controls. Women with late onset PE had higher concentrations of s-Eng (p = 0.005). Women with severe PE had higher concentrations of s-Eng (p = 0.0008) and ox-LDL (p = 0.01), and lower concentrations of PIGF (p < 0.0001). Conclusions: Women with PE from a developing country demonstrated an angiogenic imbalance and an increased rate of LDL oxidation. Findings from this study support the theory that PE is a multifactorial disease, and understanding differences in these subpopulations may provide a better target to approach future therapies.