子痫前期胎盘中代谢相关基因的异常表达

目的:探讨细胞代谢相关基因在子痫前期胎盘组织中的表达谱及其影响机制.方法:使用含12000个与代谢、凋亡、细胞黏附、信号传导、转录因子等有关基因的cDNA表达谱芯片,检测4例妊娠期高血压疾病子痫前期及正常的胎盘组织的基因表达谱差异.并对部分差异表达基因进行了Northern验证.结果:4例子痫前期胎盘中共有44条基因表达发生了变化,其中糖原磷酸化酶(GP-M)基因、瘦素(1eptin)基因、脂蛋白酯酶(LPL)基因及糖代谢相关基因(glucose transporter)表达增强,核苷酸代谢基因(CD73)与能量代谢调节基因(creatine kinase B)表达下降.结论:多种基因表达异常与子痫前期的病理发生有关,细胞代谢相关基因表达异常可能是血管内皮细胞损伤的原因之一.     

子痫前期与代谢组学

<正>子痫前期(preeclampsia,PE)是妊娠期妇女特有的疾病,发病率高达3%,常伴有严重的母婴并发症,是导致孕妇死亡的主要原因[1]。子痫前期是以妊娠中期出现高血压和蛋白尿为特征,分为早发型(34周之前)和晚发型(34周后)子痫前期[2]。子痫前期的发病机制迄今尚未完全阐明,目前认为该病始发于妊娠早期,引起胎盘血管发育障碍,导致胎盘的浅着床、氧化应激及系统性炎症反     

子痫前期和凝血功能异常

子痫前期孕妇表现为病理性高凝状态,凝血功能的监测对妊娠期高血压疾病及其并发症的预防和治疗具有一定的临床意义.随着对子痫前期凝血机制的深入研究,阿司匹林、低分子肝素等抗凝剂在改善子痫前期母胎预后方面的作用受到了更多关注.     

脂代谢异常在子痫前期子痫发病中的作用

妊娠期高血压疾病是妊娠特有的疾病，严重威胁孕妇及胎儿健康与生命，由于病因尚未明了，始终是产科领域的研究热点。本病的基本病理生理变化是全身小血管痉挛及各脏器灌流减少，表现为妊娠期出现高血压、蛋白尿、水肿等症状，分娩结束后大多数患者上述症状可随之消失。重者导致孕妇抽搐、昏迷、颅内出血等严重并发症。本文通过测定子痢前期、子痫患者血脂、脂蛋白和载脂蛋白的变化，探讨其代谢异常在发病中的作用。     

脂代谢和脂肪酸代谢与子痫前期

子痫前期是母体在多因素、多机制和多通路作用下的综合征表现形式。孕前及孕期的脂代谢和脂肪酸代谢异常在某些子痫前期发生发展中发挥了重要作用。认识脂代谢和脂肪酸代谢相关遗传、环境、营养及基础疾病因素与子痫前期的关系,更利于深入理解子痫前期多因素、多机制、多通路的发病机制。     

子痫前期孕妇血清代谢组学分析

目的:比较妊娠子痫前期(PE)患者分娩前后血清代谢轮廓的变化,建立疾病区分模型并筛选出具有潜在临床应用价值的特征代谢物。方法:选取2017年9月-2018年3月天津市第三中心医院收入院的孕妇共45例,其中PE患者(PE组)20例,正常孕妇(对照组)25例,应用超高效液相色谱与质谱联用仪(UPLC-MS)分别检测PE组孕妇分娩前、分娩后以及对照组的血清标本,筛选出差异性特征代谢物并进行分析。结果:构建了妊娠PE组血清代谢轮廓模型,共筛选出溶血磷脂酰胆碱类物质LPC 18:0、LPC 22:6、14-甲基十六烷酸、二十二酸和1,25-二羟基维生素D3-26,23内酯共5种差异性代谢产物,且溶血磷脂酰胆碱类物质LPC 18:0、LPC 22:6和14-甲基十六烷酸3种物质在PE分娩前与分娩后的差异有统计学意义(均P<0.05)。结论:构建代谢轮廓模型具有很强地区分PE患者分娩前后及正常孕妇的能力,筛选出特征代谢物能够反映PE患者代谢水平的变化趋势,为PE的预测、诊治提供参考。     

子痫前期子痫并发止血功能异常的特点与处理

止血功能包括血管壁、血小板、凝血与抗凝血的作用，后者又包括纤维蛋白溶解系统的功能。正常情况下，各部分功能平衡，保证血管内的血液呈流态；血管损伤时血栓形成以止血。正常妊娠中晚期，由于产后止血的需要，大多数凝血因子在肝脏合成增加，同时纤溶活性降低，处于生理性的高凝状态。子痫前期、子痫患者由于血管内皮细胞损伤，血小板活化、抗凝血酶Ⅲ消耗，使机体处于明显的血栓倾向，此种更高水平的高凝状态可导致子痫前期严重并发症的发生，如弥散性血管内凝血（DIC）、胎儿生长受限。     

子痫前期孕妇血清代谢组学分析

目的:比较妊娠子痫前期(PE)患者分娩前后血清代谢轮廓的变化,建立疾病区分模型并筛选出具有潜在临床应用价值的特征代谢物。方法:选取2017年9月—2018年3月天津市第三中心医院收入院的孕妇共45例,其中PE患者(PE组)20例,正常孕妇(对照组)25例,应用超高效液相色谱与质谱联用仪(UPLC-MS)分别检测PE组孕妇分娩前、分娩后以及对照组的血清标本,筛选出差异性特征代谢物并进行分析。结果:构建了妊娠PE组血清代谢轮廓模型,共筛选出溶血磷脂酰胆碱类物质LPC 18:0、LPC 22:6、14-甲基十六烷酸、二十二酸和1,25-二羟基维生素D3-26,23内酯共5种差异性代谢产物,且溶血磷脂酰胆碱类物质LPC 18:0、LPC 22:6和14-甲基十六烷酸3种物质在PE分娩前与分娩后的差异有统计学意义(均P0.05)。结论:构建代谢轮廓模型具有很强地区分PE患者分娩前后及正常孕妇的能力,筛选出特征代谢物能够反映PE患者代谢水平的变化趋势,为PE的预测、诊治提供参考。     

甘油三酯脂肪酶异常与子痫前期的相关性

甘油三酯脂肪酶(ATGL)家族是孕期母体脂质代谢的关键酶,通过水解脂蛋白的甘油三酯和磷脂以释放游离脂肪酸,使母体的脂质转运给胎儿。多项研究表明,子痫前期(PE)孕妇体内多存在脂质代谢紊乱,并与ATGL基因表达异常密切相关。     

子痫前期头颅磁共振异常高危因素分析

目的:探讨子痫前期头颅磁共振异常的高危因素.方法:回顾分析2017年1月至2019年12月在南京大学医学院附属鼓楼医院妇产科分娩的子痫前期及慢性高血压并发子痫前期并接受头颅磁共振检查者,根据影像学检查结果,分为磁共振异常组和正常组.比较两组孕妇的一般临床资料、入院后血压评估、实验室检查结果,通过二元logis-tic回...     

Abnormal 1,25-dihydroxyvitamin D metabolism in preeclampsia.

We previously reported that preeclampsia is associated with hypocalciuria (N Engl J Med 1987; 316:715). The purpose of this study was to determine whether alterations in calcium regulatory hormones are present in preeclampsia and, if so, whether they are responsible for hypocalciuria. Thirty-two pregnant women were studied in the second and third trimesters of pregnancy (11 women with preeclampsia, nine with chronic hypertension, and 12 normotensive women). 1,25-Dihydroxyvitamin D, C-terminal parathyroid hormone, ionized calcium, and urinary calcium excretion were measured. 1,25-Dihydroxyvitamin D was significantly lower in the women with preeclampsia in the third trimester when the disease developed (37.8 +/- 15 pg/ml) than in women with chronic hypertension (75 +/- 15 pg/ml, p less than 0.05) and normal women (65 +/- 10 pg/ml, p less than 0.05). Parathyroid hormone was higher, but not significantly, in those with preeclampsia. Ionized calcium was not significantly different among the three groups. Urinary calcium excretion was abnormally low for pregnancy (less than 50 mg/24 hr) in all but one women with preeclampsia. We conclude that 1,25-dihydroxyvitamin D is reduced in preeclampsia and may lead to hypocalciuria by causing decreased intestinal absorption of calcium, stimulation of parathyroid hormone, and increased distal renal tubular resorption of calcium. The cause of reduced 1,25-dihydroxyvitamin D in preeclampsia is unknown and may be due to either diminished renal or placental production of the hormone.     

子痫前期患者血脂代谢调节的探讨

目的:探讨子痫前期患者脂代谢调节水平及其异常调节情况。方法:采取前瞻性研究方法,随机抽取317例正常孕妇,分别测定不同妊娠周数的血脂和游离脂肪酸(FFA)水平;选取产前规律检查的正常孕妇54例,分别于孕10~14周,20~24周及30~34周测定血脂代谢水平。并随机抽取孕周相同、年龄相同或相近的正常孕妇77例与重度子痫前期77例进行1:1配对研究,比较血脂代谢变化。结果:正常妊娠妇女血清中TG、TCHO和LDL水平随妊娠周数增加而增加,但FFA和HDL水平并未随妊娠的周数的增加而发生明显变化。重度子痫前期TG和FFA水平较对照组明显升高(P<0.05),而HDL水平下降(P<0.05);FFA/HDL和LDL/HDL比值较对照组明显升高(P<0.05),而FFA/TG、FFA/LDL及FFA/TCHO比值无明显变化(P>0.05)。早发型重度子痫前期患者中肝功损害组的TCHO和LDL水平较对照组明显增高(P<0.05)。结论:重度子痫前期患者存在脂质代谢调节异常,具有损伤作用的FFA增加,而具有保护作用的HDL下降,FFA/HDL比值升高,重度子痫前期正常的血脂代谢平衡发生变化,FFA增加可能在重度子痫前期脂质代谢异常调节方面起到一定作用。     

先兆子痫及正常妊娠血脂代谢与凝血-纤溶活性相互影响探讨

目的探讨正常妊娠血脂代谢和凝血-纤溶活性变化规律及其相互影响，探讨血脂代谢和凝血-纤溶活性变化在先兆子痫发病中的作用。方法采用前瞻性研究方法，选取规律产前检查的孕妇114例，分别于孕10～14周、20～24周及30～34周测定血脂水平及凝血相关指标，其中4例发生轻度先兆子痫（晚发型，发病孕周〉34周）。分析比较血脂及凝血相关指标。统计学方法采用t检验、重复测量方差分析及相关性分析方法。结果正常妊娠妇女血清中TG、TCHO和LDL水平随妊娠周数增加而增加（P〈0．01）；血FIB和D—Di—mer水平随妊娠周数的增加而升高、AT-Ⅲ水平下降（P〈0．01）。先兆子痫与正常妊娠相比，TG和TG／HDL比值水平明显升高，HDL、TCHO及LDL水平明显降低，但差异无显著性（P〉O．05）；FIB水平升高，差异无显著性（P〉0．05）。相关性检验显示，血TCHO、TG及LDL水平与血FIB及D—Dimer水平成正相关（P〈0．01），与AT-Ⅲ水平成负相关（P〈0．01）。正常妊娠AT-Ⅲ／TG比值随妊娠周数增加而下降（P〈0．01）。先兆子痫与正常妊娠相比，AT-Ⅲ／TG比值下降，FIB／HDL比值升高，但差异无显著性（P〉0．05）。结论正常妊娠脂质代谢和凝血-纤溶活性变化存在着相关性，先兆子痫患者存在脂质代谢和凝血-纤溶活性异常变化趋势，脂代谢与凝血-纤溶活性对先兆子痫的影响还需要大样本多中心的研究。     

Erythrocyte cation metabolism in preeclampsia

To determine if there are abnormalities in cellular cation regulation in pregnancy-induced hypertension, erythrocyte intracellular levels of calcium, magnesium, sodium, and potassium and circulating parathyroid hormone and "endoxin" were examined in 13 women with pregnancy-induced hypertension and 34 control subjects matched for gestational age (greater than or equal to 35 weeks). Both endoxin and parathyroid hormone levels were higher in patients with pregnancy-induced hypertension than in control subjects (endoxin, 294 +/- 34 vs. 210 +/- 19 pg/ml, p less than 0.05; parathyroid hormone, 0.65 +/- 0.05 vs. 0.60 +/- 0.03 ng/ml); the increase was significant only for endoxin. Intracellular calcium was higher in the patients with pregnancy-induced hypertension (0.033 +/- 0.010 vs. 0.015 +/- 0.001 mEq/L, p less than 0.05, in the patients with pregnancy-induced hypertension and control patients, respectively) but intracellular sodium, potassium, and magnesium levels were not different. This intracellular calcium elevation may be caused directly by the increase in parathyroid hormone or indirectly by the observed elevation in endoxin. Our data indicate that the observed effect is specific because no changes in intracellular sodium, potassium, or magnesium levels were found.     

Abnormal iron parameters in the pregnancy syndrome preeclampsia

OBJECTIVE: Our purpose was to investigate iron status parameters in preeclampsia with a view to exploring their possible contribution to the etiology. STUDY DESIGN: In prepared serum samples from 40 preeclamptic women and matched pregnant control subjects at the John Radcliffe Hospital, Oxford, a number of iron status parameters were measured. Statistical analysis was by the Wilcoxon signed rank test and linear regression. RESULTS: Serum iron concentration, ferritin, and percent saturation of transferrin were significantly higher in the preeclamptic patients than in control subjects, whereas unsaturated iron-binding capacity and apotransferrin levels were significantly lower. No difference was found in hemopexin concentrations in the two groups. Gestational age at the time of sampling was correlated (positively) with only two parameters, total and unsaturated iron-binding capacity, but only in the preeclampsia group. Eighteen percent of preeclamptic subjects had percent transferrin saturation levels in the region associated with iron overload. CONCLUSION: Released iron species in preeclampsia may contribute to the etiology and will exacerbate lipid peroxidation and endothelial cell injury. Given the high prevalence of heterozygosity for hemochromatosis with the associated reduced ability to exclude ingested iron, it would seem inadvisable, in the absence of evidence of iron deficiency, to give iron supplements to pregnant women at high risk for preeclampsia.     

Abnormal hemostasis and coagulopathy in preeclampsia and eclampsia.

Preeclampsia and eclampsia appear to be a state of increased coagulopathy as evidenced by an increase in fibrin formation, activation of the fibrinolytic system, platelet activation and a decrease in platelet count. Routine tests used to assess decompensated disseminated intravascular coagulopathy are of limited value in the preeclamptic and eclamptic population. More sophisticated tests such as determinations of antithrombin III, thrombin-antithrombin III complex, D-dimer, factor VIII antigen/activity ratio, and beta-thromboglobulin, however, show a compensated coagulopathy in the preeclamptic patient. These hemostatic changes, probably the result of endothelial damage, are implicated in the pathogenesis of this disease. A better understanding about the abnormalities of hemostasis and coagulation in the preeclamptic and eclamptic patient may allow the clinician to provide improved management and possibly peripartum therapy.     

Placental glycolysis and energy metabolism in preeclampsia

We examined the possibility that in preeclampsia complicated by fetal growth retardation, placental energy state is low either because of impaired glycolysis or because of ischemia resulting from reduced maternal placental blood flow. Concentrations of pyruvate and lactate, but not of glycogen and glucose, were significantly low in placentas of mothers with severe preeclampsia, supporting previous indirect evidence of inhibited glycolysis. Nevertheless, direct measurements of adenine nucleotide concentrations did not indicate reduced placental energy level in the preeclamptic placentas. This along with a lack of change of the ratio of lactate/pyruvate concentration (an indication of the redox state of cytoplasmic reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide) is also evidence against the hypothesis of general placental ischemia leading to energy deficiency. However, as glycolysis is an important source of precursors, particularly pyruvate, for synthesis of amino acids and lipids, these results suggest that there is a significant metabolic abnormality in placentas of mothers with severe preeclampsia.     

No evidence for lipid peroxidation in severe preeclampsia

OBJECTIVE: This study was undertaken to address the role of oxidative stress in preeclampsia. STUDY DESIGN: We measured urinary 8,12-iso-iPF(2alpha)-VI, a chemically stable, free-radical catalyzed product, in a case control study of severe preeclampsia nested within the trial of Calcium for Preeclampsia Prevention. Cases included 29 women who developed severe preeclampsia and from whom urine had been obtained 10 to 20 weeks before the diagnosis of preeclampsia, 3 to 9 weeks before, and 1 day before through delivery. Controls did not develop hypertension or proteinuria and were matched to cases by center, gestational age at each of 3 corresponding urine collections, and date of enrollment. RESULTS: Urinary 8,12-iso -iPF(2alpha)-VI did not differ significantly between cases and controls before or at diagnosis of preeclampsia, nor did it vary with gestational age. CONCLUSIONS: These results call into question the importance of oxidative stress in the disease and the biochemical rationale for clinical trials of antioxidants to prevent and treat preeclampsia.