Rozprawy doktorskie: „Preeclampsia”

1

Tsiakkas, Andreas. "Screening for preeclampsia". Thesis, Manchester Metropolitan University, 2016. http://e-space.mmu.ac.uk/617510/.

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Background: Preeclampsia (PE) affects 2-3% of all pregnancies and is a major cause of maternal and perinatal morbidity and mortality. It is thought to occur due to abnormal placentation characterised by poor trophoblastic invasion resulting in oxidative stress and release of factors that promote endothelial dysfunction and inflammation. The current approach of screening for PE is to identify risk factors from maternal demographic characteristics and medical history. In the United Kingdom, the National Institute for Health and Clinical Excellence (NICE) has issued guidelines recommending that women should be considered to be at high risk of developing PE if they have any 1 high-risk factor or any 2 moderate-risk factors. With this approach, defined by NICE, at a screen positive rate of 11%, the detection rate (DR) for total PE is 35%. Such a screening approach has two main limitations. Firstly, it does not provide individualised, patient specific results and secondly, it does not allow the integration of biomarkers for improving the performance of the screening test. However, the integration of such biomarkers is essential in achieving an effective screening strategy for PE. Objectives: The aims of the papers included in this thesis are firstly, to identify and quantify the effects of variables from maternal characteristics and medical history on specific biochemical markers, secondly to present a model for standardising biochemical marker measurements in all three trimesters of pregnancy into multiples of the normal median (MoM) values, thirdly to summarize the distribution of MoM values in pregnancies with normal outcomes and those that subsequently develop PE and fourthly, to examine the potential improvement in performance of screening for PE at 30-34 weeks’ gestation by maternal factors alone with the addition of biophysical and biochemical markers. Methods: The data for this thesis were derived from prospective screening of women with singleton pregnancies attending for three routine hospital visits at 12, 22 and 32 or 36 weeks’ gestation. We have recorded a series of maternal characteristics and history, measured the maternal weight and height as well as the uterine artery pulsatility index (UTPI), mean arterial pressure (MAP), serum concentration of placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFLIT-1). The pregnancy outcomes were obtained from the hospital maternity records or the general medical practitioners of the women. Bayes theorem was used to combine the a priori risk from maternal factors with various combinations of biomarker MoM values. The potential value of biophysical and biochemical markers in improving the performance in screening for PE were evaluated. Results: Firstly, in pregnancies that developed PE, serum PlGF is decreased, while sFLIT-1, MAP and UTPI were increased, secondly, the separation in MoM values from normal is greater with earlier than later gestational age at which delivery for PE is necessary and thirdly, the slope of the regression lines of PlGF MoM with gestational age at delivery in pregnancies that develop PE increases with gestational age at screening. Combined screening at 30-34 weeks’ gestation by maternal factors, MAP, UTPI, PlGF, and sFLIT-1 predicted 98% (95% confidence interval, 88- 100%) of preterm PE and 49% (95% confidence interval, 42-57%) of term PE, at a false positive rate of 5%. Conclusions: This thesis has demonstrated that biophysical and biochemical markers increase significantly the performance of screening for PE and as a result the timing and content of clinical visits can be defined by the patient-specific risk of developing the disease. The vast majority of women would be screened low risk and these can follow the routine antenatal care, whereas those few who are high risk could be directed to a more specialized pathway, where early therapeutic interventions prophylactically may lead to the prevention of the disease and close follow-up will reduce the adverse consequences of PE.

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2

Sandgren, Jeremy Anton. "Vasopressin in preeclampsia". Diss., University of Iowa, 2019. https://ir.uiowa.edu/etd/6849.

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Preeclampsia is a devastating disorder of pregnancy characterized by high blood pressure, proteinuria, headache, renal glomerular endotheliosis, multi-organ system failure, and fetal and maternal demise. As reviewed in Chapter I, not much is known about the pathogenesis of preeclampsia, contributing to a lack of biomarkers and treatments for the disease. In Chapter II, we review arginine vasopressin, a circulating neuropeptide hormone with important fluid balance and cardiovascular actions. Vasopressin binds to numerous receptors throughout the body to elicit its effects and is associated with various disease states. In Chapter III, we discuss evidence for vasopressin as an etiology of preeclampsia. Specifically, that vasopressin secretion is elevated very early in pregnancies affected by preeclampsia and infusion of vasopressin into pregnant C57BL/6J mice causes physiological features similar to those seen in preeclampsia. In Chapter IV, we show that vasopressin administration during mouse pregnancy models specific subtypes of preeclampsia through time- and receptor-specific mechanisms. The role of angiotensin 1a receptors on vasopressin-producing cells in fluid homeostasis is shown in Chapter V and their role in metabolism is depicted in Chapter VI. Overall, we conclude that vasopressin is an important mediator of features of preeclampsia and that angiotensin 1a receptors on vasopressin-producing cells are important for normal fluid homeostasis.

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3

Abu-alkheir, Wijdan Yahya. "Novel factors in preeclampsia". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10047860/.

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Preeclampsia (PE) is a hypertensive disorder of human pregnancy that is characterised by widespread vascular endothelial cell activation, inflammation, and oxidative stress. The regulation of chemokines and adhesion molecules in these cells is important in inflammatory responses. This thesis explores the hypothesis that the levels of soluble Fractalkine (sFkn), a marker of inflammation, are increased in PE, and that over-expression of the protective enzyme, heme oxygenase-1 (HO- 1), reduces sFkn. We found that sFkn release was not increased in plasma and placenta lysates in patients with PE compared to normal pregnancy. However, it was induced by the pro-inflammatory cytokines, tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ), in human umbilical endothelial cells (HUVECs). Honokiol, an antioxidant agent, significantly reduced sFkn release. Collectively, these studies indicate that cytoprotective HO-1 pathway and Honokiol may offer partial protection against PE, by down-regulating sFkn and reducing the impact of pro-inflammatory factors in PE. Affymetrix Gene array profile of human placenta identified high expression of two new factors involved in the pathogenesis of PE, Noggin, and Leucine rich and immunoglobulin like domains protein 1 (Lrig1). This led us to investigate whether the expression level of Noggin and Lrig1 changes in preeclamptic placentas. Quantitative polymerase chain reaction (qPCR) revealed no significant differences in expression of Noggin at the messenger RNA (mRNA) level between normal and IV preeclamptic placenta. Western blot (WB) analysis of Noggin demonstrated an increase in the expression levels throughout gestation. In contrast, the expression of Lrig1, both at mRNA and at the protein level, was significantly higher in the PE placenta compared to the normal placenta. Immunohistochemical staining showed that Noggin and Lrig1 are expressed and localised in the cytotrophoblast and syncytiotrophoblast. These data suggest that Noggin and Lrig1 are found in human placenta and their expression is altered in PE. Further studies are needed to validate the significance of these early studies.

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4

Akolekar, Ranjit. "Early prediction of preeclampsia". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25473.

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Preeclampsia (PE) is a major cause of perinatal and maternal morbidity and mortality. In the United Kingdom, the National Institute for Clinical Excellence (NICE) has issued guidelines on routine antenatal care recommending that at the booking visit a woman’s level of risk for PE should be determined and the subsequent intensity of antenatal care should be based on this risk assessment. This method relies on a risk scoring system derived from maternal characteristics and medical history; the performance of screening by this method is poor with detection of less than 50% of cases of preterm-PE and term-PE. The objective of this thesis is to develop a method for the estimation of the patient-specific risk for PE by combining the a priori risk based on maternal characteristics and medical history with the results of biophysical and biochemical markers obtained at 11-13 weeks’ gestation. Such early identification of high-risk pregnancies could lead to the use of pharmacological interventions, such as low-dose aspirin, which could prevent the development of the disease. The data for the thesis were derived from two types of studies: First, prospective screening in 65,771 singleton pregnancies, which provided data for maternal factors and serum pregnancy associated plasma protein-A (PAPP-A). In an unselected sequential process we also measured uterine artery pulsatility index (PI) in 45,885 of these pregnancies, mean arterial pressure (MAP) in 35,215 cases and placental growth factor (PLGF) in 14,252 cases. Second, cases-control studies for evaluating the ten most promising biochemical markers identified from search of the literature; for these studies we used stored serum or plasma samples obtained during screening and measured PLGF, Activin-A, Inhibin-A, placental protein-13 (PP13), P-selectin, Pentraxin-3 (PTX-3), soluble Endoglin (sEng), Plasminogen activator inhibitor-2 (PAI-2), Angiopoietin-2 (Ang-2) and soluble fms-like tyrosine kinase-1 (s-Flt-1). A competing risk model was developed which is based on Bayes theorem and combines the prior risk from maternal factors with the distribution of biomarkers to derive patient-specific risk for PE at different stages in pregnancy. The prior risk was derived by multiple regression analysis of maternal factors in the screening study. The distribution of biophysical and biochemical markers was derived from both the screening study and the case-control studies. The prior risk increased with advancing maternal age, increasing weight, was higher in women of Afro-Caribbean and South-Asian racial origin, those with a previous pregnancy with PE, conception by in vitro fertilization and medical history of chronic hypertension, type 1 diabetes mellitus and systemic lupus erythematosus (SLE) or antiphospholipid syndrome (APS). The estimated detection rate (DR) of PE requiring delivery at < 34, < 37 weeks’ gestation and all PE, at false positive rate (FPR) of 10%, in screening by maternal factors were 51, 43 and 40%, respectively. The addition of biochemical markers to maternal factors, including maternal serum PLGF and PAPPA, improved the performance of screening with respective DRs of 74, 56 and 41%. Similarly, addition of biophysical markers to maternal factors, including uterine artery PI and MAP, improved the performance of screening with respective DRs of 90, 72 and 57%. The combination of maternal factors with all the above biophysical and biochemical markers improved the respective DRs to 96, 77 and 54%. The findings of these studies demonstrate that a combination of maternal factors, biophysical and biochemical markers can effectively identify women at high-risk of developing PE.

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5

Tahir, Hassaan. "Familial Aggregation of Severe Preeclampsia". Thesis, Linköpings universitet, Statistik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-73266.

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It has been proved from several studies that the genetic influence has been the most significant factor for having preeclampsia (PE). Still there are many uncertainties about origin and magnitude of the genetic effects as no specific inheritance patterns have been established. In this study, heritage risk of PE is in both the woman’s family and her partner’s family to her risk of PE is examined, along women and men own history with same and different partners. Moreover it is also examined whether timing of onset of PE is also has any impact on familial clustering of PE. Here, we used the population based Danish birth and multi generation registers to identify a cohort of women who have given birth during 1978 to 2008; which consisted of 1,79,69,28 singleton deliveries. This information is linked with pedigree information from the Danish Family Relation Database to define both maternal and paternal relationships. Risk ratios were estimated comparing women with and without various PE histories. It is found that the recurrence risk of a woman suffering from PE is 12.4 with 95% confidence limits (11.9, 12.8). Woman's recurrence risk diminishes only slightly when she changes partner means that particularly maternal genetic factors play the largest role, compared to male partner whose recurrence risk almost diminishes if he changes his female partner. Women and men from families with PE contribute to risk of PE in pregnancies they are involved in. The woman’s family history is still more important compared to man family history of PE; except for increased rick in pregnancies fathered by men who were born to preeclamptic mothers. The recurrence risk of a women suffering from PE, if she already has suffered from this condition before 34 weeks is found to be very high (RR=25.4 with 95% confidence limits (21.8, 29.1)) with same male partner. It is found that early-onset PE and later-onset varieties have a clear genetic component but the intensity of early onset is stronger than late onset varieties. There are both maternal and paternal genetic contributions to early-onset PE, with the maternal ones seeming to be stronger.

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6

Vanderlelie, Jessica, i n/a. "Placental Oxidative Stress in Preeclampsia". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060918.161726.

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Affecting 6-8% of all pregnancies, preeclampsia is the leading cause of maternal morbidity in the western world and is charactensed by hypertension, proteinuria, edema and platelet aggregation. Despite its prevalence and severity, no comprehensive theory or single factor has been suggested to explain the pathophysiology of this multi system disorder of pregnancy, with the only therapies being bed rest, pharmacological symptom management and if necessary early delivery. Oxidative stress plays an important role in the pathophysiology of preeclampsia, resulting from defective trophoblast invasion, reductions in placental perfusion and placental hypoxia/reoxygenation. The inability of endogenous antioxidant systems up regulated in normal pregnancy, to control increased levels of oxidative stress, is suggested as a possible factor in the feed forward generation of reactive oxygen species and placental oxidative stress. That in turn may stimulate increased syncytiotrophoblast apoptosis, endothelial cell activation and the maternal hyper immune response characteristic of preeclampsia. Analysis of the research literature revealed that previous evaluations of placental oxidation and antioxidant enzyme activity in preeclampsia were by no means comprehensive, and exhibited significant inter-study variations. It was the aim of this thesis to clarify the placental oxidative state and the endogenous antioxidant activity of glutathione peroxidase, thioredoxin reductase, thioredoxin and superoxide dismutase in human placentae in an attempt to determine if variations in antioxidant function were due to changes in gene expression or protein oxidation. The findings reported in this thesis indicate the presence of increased levels of oxidative stress in the preeclamptic placenta, associated with significant reductions in antioxidant enzyme capacity. Quantitative real-time PCR analysis of placental samples revealed that deceases in antioxidant capacity in the placenta are more likely to be related to the significant oxidative burden within the tissue rather than reductions in gene expression. A number of animal models exist to investigate components of preeclampsia pathophysiology, however the ability of these models to mimic the oxidative and antioxidant features of preeclampsia remains unclear. The exposure of pregnant rats to N(G)-nitro-L-arginine methyl ester is a widely used model of endothelial cell dysfunction during preeclampsia. It was the aim of this thesis to determine the biochemical characteristics of this model in an attempt to assess its effectiveness in mimicking oxidative changes in the preeclamptic placenta. Although this model is capable of producing a syndiome in rats similar to the disorder in terms of physiology, this is not manifest in terms of placental biochemistry. The importance of selenium in the synthesis of selenobased antioxidants such as glutathione peroxidase and thioredoxin reductase is well documented. Increasing demand for selenium by the developing fetus may be linked to reductions in selenium status during pregnancy. Considering preeclampsia is associated with significant reductions in selenium status it may be hypothesised that reductions in antioxidant function may be linked to selenium inadequacy. The modulation of dietary selenium in pregnant rats was used to determine the importance of selenium during pregnancy and its effect on antioxidant function and placental oxidative stress. The results of this analysis revealed that selenium deficiency causes a pregnancy specific condition similar to preeclampsia. This condition was found to be associated with increased placental oxidative stress and significant reductions in the systemic activity of selenobased antioxidants that could be modified through selenium supplementation. In summary, data obtained in this thesis indicate that placental oxidative stress and reduced antioxidant enzyme activity play a significant role in the pathogenesis of preeclampsia. These studies support the hypothesis that antioxidant sufficiency is crucial in the maintenance of oxidative balance and that antioxidant dysfunction may result in damage to the placenta and the progression of the disease. These novel data further our understanding of the pathophysiology of preeclampsia and provide new insight into the pathogenesis of clinical complications exhibited in this condition, suggesting antioxidant therapy as a possible means for improving the health outcomes of both mother and baby.

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7

Lai, J. "Third-trimester prediction of preeclampsia". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1561522/.

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Preeclampsia (PE) is a common complication of pregnancy affecting upto 10% of the population. Screening in the UK has centred on identifying risk factors early in pregnancy, in order to determine the need for aspirin administration for risk prevention. Whilst screening late on, has no role in treatment or prevention of disease, it does serve a vital role in the stratification of a timely delivery. Recent studies have highlighted the importance of such an approach in improving maternal and fetal morbidity and mortality. In the cohort-control study, stored plasma from 50 cases that developed PE at or after 34 weeks were matched with 250 unaffected controls. At 11-13 weeks in the PE group compaired to controls, serum PAPP-A and PlGF were lower (0.748 and 0.824 vs 1.0 MoM), but free b-hCG, sEng and activin-A were not significantly different. At 30-33 weeks, in the PE group, there was a decrease in PlGF (0.356 MoM), increase in free β-hCG (1.750 MoM), sEng (1.390 MoM) and activin-A (1.47 MoM), but PAPP-A was not significantly different from controls. The uterine artery PI, MAP, sBP and dBP were assessed in a screening population of 4,294 with detections rate of upto 70% of intermediate PE. A survival time model for the time of delivery for PE by combination of maternal characteristics and history with PlGF and sFlt-1 multiple of the median (MoM) values was devised. Screening by the biochemical test detected 100%, 76%, and 62% of PE with delivery within four, six and eight weeks of the visit, at a fixed false positive rate of 5%. In conclusion, although both biochemical and biophysical tests are useful in the detection of PE, using the angiogenic markers alone at 30-33 weeks can effectively identify all women who require delivery due to PE in the subseqeunt 4 weeks from testing.

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8

Vanderlelie, Jessica. "Placental Oxidative Stress in Preeclampsia". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365679.

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Affecting 6-8% of all pregnancies, preeclampsia is the leading cause of maternal morbidity in the western world and is charactensed by hypertension, proteinuria, edema and platelet aggregation. Despite its prevalence and severity, no comprehensive theory or single factor has been suggested to explain the pathophysiology of this multi system disorder of pregnancy, with the only therapies being bed rest, pharmacological symptom management and if necessary early delivery. Oxidative stress plays an important role in the pathophysiology of preeclampsia, resulting from defective trophoblast invasion, reductions in placental perfusion and placental hypoxia/reoxygenation. The inability of endogenous antioxidant systems up regulated in normal pregnancy, to control increased levels of oxidative stress, is suggested as a possible factor in the feed forward generation of reactive oxygen species and placental oxidative stress. That in turn may stimulate increased syncytiotrophoblast apoptosis, endothelial cell activation and the maternal hyper immune response characteristic of preeclampsia. Analysis of the research literature revealed that previous evaluations of placental oxidation and antioxidant enzyme activity in preeclampsia were by no means comprehensive, and exhibited significant inter-study variations. It was the aim of this thesis to clarify the placental oxidative state and the endogenous antioxidant activity of glutathione peroxidase, thioredoxin reductase, thioredoxin and superoxide dismutase in human placentae in an attempt to determine if variations in antioxidant function were due to changes in gene expression or protein oxidation. The findings reported in this thesis indicate the presence of increased levels of oxidative stress in the preeclamptic placenta, associated with significant reductions in antioxidant enzyme capacity. Quantitative real-time PCR analysis of placental samples revealed that deceases in antioxidant capacity in the placenta are more likely to be related to the significant oxidative burden within the tissue rather than reductions in gene expression. A number of animal models exist to investigate components of preeclampsia pathophysiology, however the ability of these models to mimic the oxidative and antioxidant features of preeclampsia remains unclear. The exposure of pregnant rats to N(G)-nitro-L-arginine methyl ester is a widely used model of endothelial cell dysfunction during preeclampsia. It was the aim of this thesis to determine the biochemical characteristics of this model in an attempt to assess its effectiveness in mimicking oxidative changes in the preeclamptic placenta. Although this model is capable of producing a syndiome in rats similar to the disorder in terms of physiology, this is not manifest in terms of placental biochemistry. The importance of selenium in the synthesis of selenobased antioxidants such as glutathione peroxidase and thioredoxin reductase is well documented. Increasing demand for selenium by the developing fetus may be linked to reductions in selenium status during pregnancy. Considering preeclampsia is associated with significant reductions in selenium status it may be hypothesised that reductions in antioxidant function may be linked to selenium inadequacy. The modulation of dietaty selenium in pregnant rats was used to determine the importance of selenium during pregnancy and its effect on antioxidant function and placental oxidative stress. The results of this analysis revealed that selenium deficiency causes a pregnancy specific condition similar to preeclampsia. This condition was found to be associated with increased placental oxidative stress and significant reductions in the systemic activity of selenobased antioxidants that could be modified through selenium supplementation. In summary, data obtained in this thesis indicate that placental oxidative stress and reduced antioxidant enzyme activity play a significant role in the pathogenesis of preeclampsia. These studies support the hypothesis that antioxidant sufficiency is crucial in the maintenance of oxidative balance and that antioxidant dysfunction may result in damage to the placenta and the progression of the disease. These novel data further our understanding of the pathophysiology of preeclampsia and provide new insight into the pathogenesis of clinical complications exhibited in this condition, suggesting antioxidant therapy as a possible means for improving the health outcomes of both mother and baby.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
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9

Bergman, Lina. "Cerebral biomarkers in women with preeclampsia". Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-322780.

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Preeclampsia and eclampsia are among the most common causes of maternal and fetal mortality and morbidity worldwide. There are no reliable means to predict eclampsia or cerebral edema in women with preeclampsia and knowledge of the brain involvement in preeclampsia is still limited. S100B and neuron specific enolase (NSE) are two cerebral biomarkers of glial- and neuronal origin respectively. They are used as predictors for neurological outcome after traumatic brain injuries and cardiac arrest but have not yet been investigated in preeclampsia. This thesis is based on one longitudinal cohort study of pregnant women (n=469, Paper I and III), one cross sectional study of women with preeclampsia and women with normal pregnancies (n=53 and 58 respectively, Paper II and IV) and one experimental animal study of eclampsia (Paper V). In Paper I and III, plasma concentrations of S100B and NSE were investigated throughout pregnancy in women developing preeclampsia (n=16) and in women with normal pregnancies (n=36) in a nested case control study. Plasma concentrations were increased in women developing preeclampsia in gestational week 33 and 37 for S100B and in gestational week 37 for NSE compared to women with normal pregnancies. In Paper II and IV, increased plasma concentrations of S100B and NSE were confirmed among women with preeclampsia compared to women with normal pregnancies. Furthermore, increased plasma concentrations of S100B correlated to visual disturbances among women with preeclampsia (Paper II) and plasma concentrations of S100B and NSE remained increased among women with preeclampsia one year after delivery (Paper IV). In Paper V, an experimental rat model of preeclampsia and eclampsia demonstrated increased serum concentrations of S100B after seizures in normal pregnancy (n=5) and a tendency towards increased plasma concentrations of S100B in preeclampsia (n=5) compared to normal pregnancy (n=5) without seizures. Furthermore, after seizures, animals with magnesium sulphate treatment demonstrated increased serum concentrations of S100B and NSE compared to no treatment. In conclusion; plasma concentrations of S100B and NSE are increased in preeclampsia during late pregnancy and postpartum and S100B correlates to visual disturbances in women with preeclampsia. The findings are partly confirmed in an animal model of eclampsia.

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10

Luque, Suma Marta. "Factores nutricionales asociados a la preeclampsia". Master's thesis, Universidad Nacional Mayor de San Marcos, 2017. https://hdl.handle.net/20.500.12672/8029.

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Determina los factores nutricionales asociados a la preeclampsia en las gestantes que acuden al Instituto Nacional Materno Perinatal durante el periodo enero - marzo 2016. Se selecciona a 47 pacientes con diagnóstico de preeclampsia y 48 pacientes sin dicho diagnóstico. La selección de los controles se realiza considerando el apareamiento por edad de las gestantes. Los resultados revelan que la edad promedio de las gestantes con preeclampsia es de 29.7 ±7 años y de las gestantes sin preeclampsia es 29.3±6.5 años, muchas (46.8%) procedentes de Lima Este y amas de casa (72.3%). En el análisis de los factores nutricionales dietarios se observa que el consumo de omega 3<3.7 g/d (p=0.007; OR= 3.273; IC=1.4-7.9), calcio<800 mg/d (p<0.001; OR=6.3; IC=2.4-16.2), Zinc< 9.5 mg/d (p<0,001; OR=4.8; IC=1.9-11.7), magnesio< 290 mg/d (p=0.033; OR= 4.05; IC= 1.0-15.8) y potasio<4700 mg/d (p=0,003; OR=4.1; IC=1.6-10.7) son factores de riesgo asociados al diagnóstico de preeclampsia. Sin embargo, no se encuentra asociación significativa entre el consumo de carbohidratos mayor a 312 g/d (p=0.864) ni a mayor a 451 g/d (p=0.210) con la preeclampsia.
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11

Michel, Michelle Estella. "Prediction, prevention and management of preeclampsia". Thesis, Boston University, 2013. https://hdl.handle.net/2144/12161.

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Thesis (M.A.)--Boston University
Background: Pregnancy-related health complications can pose imminent threats to the health of both mother and fetus. Gestational hypertension accompanied by proteinuria after 20 weeks’ gestation characterize the condition known as preeclampsia, which puts mothers and their fetuses at risk for a number of adverse outcomes. Significance: From 1987 to 2004, the incidence of preeclampsia rose by 25%. Adverse outcomes in the mother-to-be include preterm delivery, acute renal failure and maternal death. As a result of preeclampsia, the fetus can suffer intrauterine growth restriction, preterm birth and low birth weight. Aim: Researchers have explored a number of strategies to predict, prevent and manage preeclampsia. This work will explore the various strategies employed and documented in the literature. Conclusion: Treatments that may be beneficial for the mother (delivering the infant), may not necessarily be beneficial for the fetus (may have a young gestational age) and vice versa. Therefore, determining the appropriate method of handling each case of preeclampsia is critical to the work of the obstetrician, and should be decided from evidence-based treatments and management.

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Reep, Daniel T. "Placental Eicosanoids and Sphingolipids in Preeclampsia". VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5553.

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Placental dysfunction is implicated in the pathogenesis of preeclampsia. Chemical signals between the placenta and maternal circulation are a suspect cause of endothelial dysfunction and maternal hypertension. This study examined select lipid mediators of inflammation produced by the placenta. Patients were recruited from Virginia Commonwealth University’s pregnancy clinics and placentas were collected at delivery. Forty-eight-hour explant cultures of villous placental tissue were used to model lipid production. Electrospray ionization mass spectrometry was used to quantify concentrations of free lipids in the culture media. Bicinchoninic acid assays were performed to quantify protein in each culture for normalization of lipid data. After analysis, it was found that severity of preeclampsia was correlated with a unique lipid profile. Pro-inflammatory hydroxyeicosatetraenoic acids and sphingolipids were elevated. Aspirin usage in patients who developed preeclampsia was found to attenuate accumulation of isoprostane oxidative stress markers and thromboxane production while preserving omega-3-fatty acid and increasing prostacyclin levels.

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13

Kawasaki, Kaoru. "Metabolomic Profiles of Placenta in Preeclampsia: Antioxidant Effect of Magnesium Sulfate on Trophoblasts in Early-Onset Preeclampsia". Kyoto University, 2019. http://hdl.handle.net/2433/243298.

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14

Blazquez, Ventura Anna. "Donation of Gametes and Risk of Preeclampsia". Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/664115.

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Preeclampsia (PE) complicates between 2 and 8 % of all pregnancies, and it could be classified in two subgroups: Pre-term PE (delivery < 37 weeks of gestation) and term PE (delivery > 37 weeks). The first is believed to be due to an immune maladaptation of the mother to fetal antigens, taking place in the placenta, so there is an intrinsic placental dysfunction. This subtype is more severe, with prematurity, intrauterine growth restriction and adverse consequences for also the mother. The origin of the second is hypothesized to be in a hidden cardiovascular dysfunction of the mother that, due to the increase in hemodynamic demands secondary to the pregnancy, leads to an hypoperfusion of a primary functional placenta and finally to PE. It has been largely described the association between gamete donation and PE, but the cause of this relationship is still on debate: the risk factors of patients undergoing oocyte donation (OD), the high multiple pregnancy rate, the ovarian failure, the infertility or the reproductive treatment could justify it. Additionally, many studies show that there is a decrease in PE after repeated exposure to partner’s sperm and an increase after oocyte or sperm donation, leading to the assumption that the the lack of recognition of embryo antigens after gamete donation have a role in the pathogenesis of PE. Finally, the freezing of the embryos has been related to an increase of PE, always in in vitro fertilization pregnancies with own oocytes (IVF). The explanation could be in an effect of cryopreservants or the freezing/thawing process of those embryos, or also in the different endometrial hormonal milieu that fresh embryo transfer (freshET) and frozen-thawing embryo transfer (FET) IVF patients have. This thesis consists in 4 projects that try to study the relationship between gamete donation and PE: The first is a metaanalysis comparing the incidence of PE between OD pregnancies and IVF, to avoid the bias of compare OD with spontaneous conception pregnancies. The OR of PE in OD compared to IVF is 3.12 (2.56-3.85), and even after adjustment for maternal age and multiple pregnancy the difference remains statistically significative. This data suggest that in OD, the origin of PE is related to an immune maladaptation of the mother to fetal agents. The second project is a retrospective cohort study of patients pregnant by OD that compares the incidence of PE between freshET and FET (with the same hormonal preparation). There is no difference in the incidence of preterm PE or term PE between groups, even after adjusting for confounding factors. With the same hormonal environment there is no difference in PE incidence, inferring that hormonal milieu has a role in the pathogenesis of PE, and that PE origin is more related to the mother or the placenta than to the embryo. The third is a descriptive study of double-donation (DD) (donation of both sperm and oocyte) treatment. These patients have multiple risk factors (advanced maternal age, nuliparity, multiple pregnancy and gamete donation) for developing PE. The last is a retrospective cohort study that compares the incidence of PE between OD pregnancies and DD pregnancies. DD cases compared to OD have an OR of 2.68 [95%CI 1.02, 7.04, p=0.038] for preterm PE, but no difference in term PE. After adjustment for confounding factors, the rate of preterm PE is still increased on DD with significance. These results support the immunological theory of PE origin, as in DD pregnancies, the embryo is completely allogenic to the mother, thus increasing only preterm PE comparing to OD. In assisted reproduction, the more the donated gametes a recipient receive, the more the risk for developing PE. Preterm PE is more severe, but an early diagnose could lead to preventing measures, as giving aspirin. OD and DD patients should be aware of their high risk for developing PE, as well as their physicians.
La preeclampsia (PE) se clasifica en PE pretérmino (parto < 37 semanas) y PE a término (parto > 37 semanas). La primera se debe a una mala adaptación inmunológica de la madre al feto que tiene lugar en la placenta, dando lugar a una disfunción placentaria intrínseca, y es la más severa. La segunda se debe a un defecto cardiovascular materno que, secundario al incremento en las demandas hemodinámicas por la gestación, lleva a una hipoperfusión de una placenta inicialmente funcional, y finalmente a la PE. La relación entre PE y donación de gametos se ha descrito en múltiples ocasiones, pero la causa de dicha asociación sigue siendo debatida. También se ha descrito un incremento de PE en gestaciones obtenidas tras transferencia de embriones vitrificados (FET) comparado con embriones en fresco (freshET), siempre en pacientes que realizaron ciclos de fecundación in vitro con óvulos propios (FIV), teniendo ambos grupos diferente ambiente hormonal endometrial. Esta tesis consiste en 4 proyectos que estudian la relación entre donación de gametos y PE: El primero en un meta análisis que compara PE en donación de óvulos (OD) y FIV, evitando el sesgo de comparar OD con gestaciones espontaneas. La OD confiere el triple de riesgo de PE que la FIV, sugiriendo que en OD, el origen de la PE está relacionada con una mala adaptación inmunitaria de la madre a antígenos embrionarios. El segundo es un estudio retrospectivo de cohortes que compara, en gestantes tras OD, la incidencia de PE en freshET con FET. Con la misma preparación endometrial, no hay diferencia en PE pretémino ni a término entre grupos. El origen de la PE se relaciona más con factores maternos o placentarios que embrionarios. El tercero es un estudio descriptivo de tratamientos de doble donación (DD) (recepción de tanto óvulos como semen de donantes), que revela que se trata de pacientes con múltiples factores de riesgo para desarrollar PE. El cuarto es un estudio de cohortes retrospectivo que compara PE en DD con OD. La DD incrementa la PE pretérmino comparado con OD, pero no a término, apoyando la teoría inmunológica de la PE, ya que en DD el embrión es completamente alogénico a la madre.

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15

Ødegård, Rønnaug A. "Preeclampsia - maternal risk factors and fetal growth". Doctoral thesis, Norwegian University of Science and Technology, Department of Cancer Research and Molecular Medicine, 2002. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-484.

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Preeclampsia is a complex and variable maternal disturbance that ranges from a dramatic onset at early gestation to slowly developing symptoms towards term. Hypertension and renal involvement with proteinuria are cardinal signs, which are often accompanied by fluid retention, blood-clotting dysfunction, and reduced organ perfusion. HELLP (haemolysis, elevated liver enzymes, and low platelet count) syndrome is regarded as a variant of preeclampsia, and the fulminante disease, eclampsia, includes convulsions. Preeclampsia is the main cause of maternal and fetal morbidity and mortality in western countries (1, 2), and in Nordic countries, 17 percent of maternal deaths have been ascribed to preeclampsia (2). Antenatal care in Norway includes on average 12 doctor/midwife consultations per pregnancy (3), and since blood pressure monitoring and urinary testing are main aims of the consultations, preeclampsia is a pregnancy complication that also generates substantial societal costs.

Paper II, III, IV and V reproduced with permission of Elsevier, sciencedirect.com

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16

Xie, Fang. "Infection and immunity in pregnancy and preeclampsia". Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/30063.

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Preeclampsia is a hypertensive disorder of pregnancy, which shares similar risk factors with atherosclerosis. There is increasing evidence to suggest that Chlamydia pneumoniae (C. pneumoniae) and cytomegalovirus (CMV) are linked with atherosclerosis and may trigger inflammation during pregnancy. However, the roles of these two microbes and the underlying immune mechanism remain unclear. Case control studies were preformed to examine the evidence of C. pneumoniae and CMV infection, immune response and Toll like receptor (TLR) gene variations in women with preeclampsia compared with normotensive intrauterine growth restriction (nIUGR), and normal pregnancy and non-pregnancy controls. At each stage, a systematic review and data synthesis methodology are applied to place our findings within the context of published studies in the area of C. pneumoniae and CMV infection and TLR gene variations in preeclampsia to clarify apparent discrepancies in these studies. In the first paper, an increase of C. pneumoniae genomic DNA loads was detected in preeclampsia when compared with normal pregnancy and non-pregnancy controls. Data synthesis indicated C. pneumoniae IgG seropositivity was more prevalent in preeclampsia patients. The second paper detected that preeclampsia had higher CMV IgG antibody level than normal pregnancies. Further, anti-CMV IgG seropositivity was more prevalent in women with preeclampsia than nIUGR and normal pregnancy controls. The third paper discussed up-regulated neutrophil TLR2 and TLR4 protein as well as mRNA expression in preeclampsia where the difference was more markedly in an early-onset preeclampsia condition. Early-onset preeclampsia was associated with elevated mRNA expression of cryopyrin, NF-kappaBp50, NF-kappaBp65 and IL-1β, as well as increased pro- versus anti-inflammatory cytokine ratios (TNF-α/IL-10 and IL-6/IL-10). Finally, in the fourth paper, data synthesis has suggested that gene variations in TLR2 or TLR4 were associated with early-onset preeclampsia. In summary, our findings indicated that infection with C. pneumoniae and CMV may trigger the maternal inflammation crossing the threshold development of preeclampsia. A better understanding of immunology and genetic basis of preeclampsia may reveal therapeutic opportunities for treatment of this disorder and lead to improved health for both mother and fetus.

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17

Turner, Elizabeth. "NMR Studies Towards a Biomarker of Preeclampsia". Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534444.

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Norman, Justine. "The nature of glomerular dysfunction in preeclampsia". Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29500.

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Normal pregnancy was compared to preeclamptic (PE) pregnancy with respect to glomerular ultrafiltration nitric oxide (NO) activity, derived from the metabolism of L-arginine (L-arg) to citrulline. Two biomathematical models, the "isoporous plus shunt" (mean pore size ro, shunt component wo) and "lognormal" (mean pore size U, standard deviation S), together with fractional dextran clearance (betaD) enabled estimation of glomerular ultrafiltration parameters (Kf~ ultrafiltration coefficient, DP-transglomerular pressure). NO activity was assed from plasma and 24hr urinary NOx (nitrate and nitrite), second messenger cyclic GMP (cGMP) and NO synthase inhibitor asymmetric-D-methyl-arginine 9ADMA). Late pregnant (LP) and post partum (PP) data are presented. As NO might mediate gestational renal vasodilatation, the effects of infused L-arginine (NO precursor) compared to glycine, on ultrafiltration were examined, testing the hypothesis that NO deficiency is important in renal vasoconstriction and hypofiltration of PE.;Normal pregnancy is associated with increased GFR, ERPF, wo and S (p<0.05). PE pregnancy is associated with reduced Kf but increased ro, wo U and S. PE values PP approach controls. From the indices that were utilised, there was no evidence of significant NO deficiency in Preeclampsia and even if there was a relative deficiency the infusion of the NO precursor L-arginine failed to augment the decreased renal haemodynamics of Preeclampsia. In PE the hypofiltration therefore has both a haemodynamic and a structural basis, it recovers PP and L-arg has no ameliorating effect in LP, or PP.

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19

Hill, Lori. "Racial Differences in the Genetics of Preeclampsia". VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2643.

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Preeclampsia (PE), characterized by hypertension and proteinuria after 20 weeks of gestation, affects 5-8% of pregnancies worldwide. Although preeclampsia is a significant cause of maternal and perinatal mortality and morbidity, its etiology remains to be elucidated. Racial differences have been observed for preeclampsia, with U.S. Blacks having higher rates and more severe disease, compared to U.S. Whites and Hispanics. One potential source of racial differences in preeclampsia is genetic variation between populations. Genetic susceptibility to preeclampsia is well established, but the specific contributions of maternal vs. fetal genes, and how these vary among racial groups is poorly understood. This dissertation addressed racial differences in the genetics of preeclampsia in Chileans, U.S. Blacks, and U.S. Whites through candidate gene studies and variance components modeling. First, we determined whether three genes, which are relevant to the pathophysiology of preeclampsia, Catechol-O-methyltransferase (COMT), Methylenetetrahydrofolate reductase (MTHFR), and Endoplasmic reticulum aminopeptidase 2 (ERAP2), were associated with the risk for preeclampsia in Chilean and U.S. Black mothers and fetuses. We found that the maternal COMT and an interaction between the fetal COMT and MTHFR were associated with the risk for preeclampsia in Chileans. We also found that the fetal ERAP2 was associated with the risk for preeclampsia in U.S. Blacks. We next used structural equation modeling of a unique Children of Twins (COT), supplemented with full and half-siblings, study design to investigate the fetal genetic, maternal genetic, shared environmental, and unique environmental contributions to preeclampsia in U.S. Whites and Blacks. Through this modeling we uncovered a unique source of racial differences in preeclampsia. We found that U.S. Whites and Blacks showed a similar prevalence of preeclampsia in first births, but across the next three births, the prevalence in Whites declined to a greater degree than in Blacks. In conclusion we have identified specific maternal and fetal genes that contribute to the risk for preeclampsia. Furthermore, we have identified sources of racial differences in preeclampsia, which include differences in associations between COMT, MTHFR, and ERAP2 and the risk for preeclampsia among populations and differences in the prevalence of preeclampsia across subsequent births between U.S. Whites and U.S. Blacks.

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20

Johnson, Abbie Chapman. "Mechanisms of Seizure during Pregnancy and Preeclampsia". ScholarWorks @ UVM, 2015. http://scholarworks.uvm.edu/graddis/336.

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Eclampsia is defined as de novo seizure in a woman with the hypertensive complication of pregnancy known as preeclampsia (PE), and is a leading cause of maternal and fetal morbidity and mortality worldwide. The pathogenesis of eclamptic seizure remains unknown, but is considered a form of hypertensive encephalopathy where an acute rise in blood pressure causes loss of cerebral blood flow (CBF) autoregulation and hyperperfusion of the brain that results in vasogenic edema formation and subsequent seizure. However, eclamptic seizure can occur during seemingly uncomplicated pregnancies, in the absence of hypertension and PE, suggesting that normal pregnancy may predispose the brain to hypertensive encephalopathy or seizure, independently of PE. The overall goal of this dissertation was to investigate the effect of pregnancy and PE on the cerebrovasculature and neurophysiological properties that may promote brain injury and eclamptic seizure. For this dissertation project, a rat model of PE was established that combined placental ischemia, induced by restricting blood flow to the uteroplacental unit, and maternal endothelial dysfunction that was induced by a prolonged high cholesterol diet. Rats with PE developed several PE-like symptoms, including elevated blood pressure, fetal growth restriction, placental dysfunction, and were in a state of oxidative stress and endothelial dysfunction. We found that pregnancy had an overall protective effect on the maintenance of CBF that was potentially due to a nitric-oxide dependent enhancement of the vasodilation of cerebral arteries to decreased intravascular pressure. Further, maintenance of CBF during acute hypertension was similar in pregnancy and PE. Thus, it does not appear that pregnancy and PE are states during which CBF autoregulation is compromised in a manner that would promote the development of hypertensive encephalopathy. However, the brain was found to be in a hyperexcitable state during normal pregnancy that was augmented in PE, and could contribute to onset of eclamptic seizure. Under chloral hydrate anesthesia, generalized seizure was induced by timed infusion of the convulsant pentylenetetrazole (PTZ), with simultaneous electroencephalography that was stopped at the first onset of spikewave discharge indicative of electrical seizure. Seizure threshold was determined as the amount of PTZ required to elicit seizure. Compared to the nonpregnant state, seizure threshold was ~44% lower in pregnant rats and ~80% lower in rats with PE. Further, pregnant rats were more susceptible to seizure-induced vasogenic edema formation than the nonpregnant state. Mechanisms by which pregnancy and PE lowered seizure threshold appeared to be through pregnancy-associated decreases in cortical gamma-aminobutyric acid type A receptor (GABAAR) subunits and PE-induced disruption of the blood-brain barrier (BBB) and microglial activation, indicative of neuroinflammation. Magnesium sulfate (MgSO4), the leading treatment for seizure prophylaxis in women with PE, restored seizure threshold to control levels by reversing neuroinflammation in PE rats, without affecting BBB permeability. Overall, this dissertation provides evidence that pregnancy increases susceptibility of the brain to seizure and vasogenic edema formation that likely contribute to the onset of eclampsia during seemingly uncomplicated pregnancies. Further, the pathogenesis of eclampsia during PE likely involves breakdown of the BBB and subsequent neuroinflammation, resulting in a state of greater seizure susceptibility that is ameliorated by MgSO4 treatment.

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21

Chau, Katrina. "Modulating placentation in the prevention of preeclampsia". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/18799.

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The basis of preeclampsia is an abnormally functioning placenta and modulating placentation may mitigate the clinical syndrome of preeclampsia. This thesis explores the role of placental growth factor (PlGF) in placentation in an in vitro model of early placental development and in vivo model of experimental preeclampsia. The mechanism of action of aspirin, known to reduce the rate of early preeclampsia, was also explored in an animal model Firstly, co-cultures of human uterine microvascular endothelial cells and a first trimester trophoblast cell line were treated with PlGF to observe the effect upon cell integration. Secondly, a mouse model was used to study the effect of early PlGF treatment prior to the induction of experimental preeclampsia with a continuous infusion of TNF-α. Finally, the same mouse model was used to study the mechanism of action of aspirin. Co-cultures were treated with recombinant human PlGF (rhPlGF) at increasing concentrations under two oxygen tensions (2% and 21% O2). Co-cultures treated with tumour necrosis factor-α (TNF-α) were then treated with rhPlGF. Placental growth factor had no effect on endothelial and trophoblast cell interactions regardless of dose or oxygen tension and did not rescue the adverse effects of TNF-α. Pregnant mice were treated with daily intraperitoneal injections of either vehicle or recombinant mouse PlGF-2 (rmPlGF-2) from gestational day (gd) 10. At gd 13 TNF-α was administered continuously via subcutaneous osmotic pump. Blood pressure was recorded continuously by intra-arterial radiotelemeter (n = 5 per group) and placental perfusion was measured using magnetic resonance imaging (n = 3 per group). A similar study was done with the oral administration of low dose aspirin in place of rmPlGF-2. Although both rmPlGF-2 and aspirin increased the placenta mRNA expression of PlGF, this did not attenuate the clinical features of experimental preeclampsia. These studies demonstrate that although PlGF is shown to be decreased in early pregnancy of preeclamptic women, administration of PlGF does not alter placentation in an in vivo or in vitro model. Increased expression of PlGF induced by low-dose aspirin similarly had no effect on clinical outcomes. Clinically, this supports the use of PlGF as a marker of placentation rather than an avenue for therapeutic intervention.

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22

Jonsson, Yvonne. "Cytokines and immune balance in preeclampsia : a survey of some immunological variables and methods in the study of preeclampsia". Doctoral thesis, Linköping : Linköpings universitet, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med924s.pdf.

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Stolk, Megan. "Characterisation of novel TAC3 a d TACR3 gene variants and polymorphisms in patients with pre-eclampsia /". Thesis, Stellenbosch : University of Stellenbosch, 2007. http://hdl.handle.net/10019.1/1748.

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Thesis (MSc (Genetics))—University of Stellenbosch, 2007.
In South Africa, pre-eclampsia is the second highest cause of maternal deaths. The incidence of this disease in the Western Cape alone is 6.8% and places a large burden of health care facilities. The placenta and implantation thereof is thought to play the most significant role in the onset of this disease. Among the many theories for its aetiology, is the acknowledged two - stage theory. This is based on evidence that pre-eclamptic placentas demonstrate altered remodelling and invasion into the uterine endometrium and myometrium. The sub-optimal endometrium invasion leads to less oxygenation of the placental environment causing transient hypoxia. Consequently, the placenta is thought to release unknown factors into the maternal circulation which then culminates in clinical features associated with pre-eclampsia. Neurokinin B is thought to be one of these placental factors and subsequently binds to the NKB receptor in the maternal system. Endothelium-derived nitric oxide synthase has recently been shown to activate this receptor. The aim of this study was to investigate the role of neurokinin B (TAC3) and the neurokinin B receptor (TACR3) genes in the predisposition of pre-eclampsia and their interaction with eNOS in the South African coloured population together with a matched control cohort.

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González, Sepúlveda Roberto Hernán. "Evaluación de la disfunción endotelial y el estrés oxidativo a través de la concentración de la dimetilarginina asimétrica y el malondialdehido como marcadores tempranos de preeclampsia". Tesis, Universidad de Chile, 2009. http://repositorio.uchile.cl/handle/2250/131028.

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Memoria para optar al Título Profesional de Médico Veterinario
La preclampsia es un síndrome del embarazo que se caracteriza por presentar hipertensión arterial, proteinuria y edema. Este síndrome tiene involucrado en su fisiopatología mecanismos como son el estrés oxidativo, una deficiente angiogenesis y disfunción endotelial. El objetivo de este estudio es evaluar un marcador de disfunción endotelial como es la dimetilarginina asimétrica y un marcador de estrés oxidativo como es el malondialdehido en mujeres preeclampticas como predictores de esta patología. Se realizó un estudio de cohorte retrospectivo seleccionando mujeres embarazadas chilenas controladas en el Departamento de Obstetricia y Ginecología, Hospital Clínico de la Universidad de Chile. A un grupo de mujeres con PE (casos) y a un grupo de mujeres con embarazos normales (controles) se les tomó muestras de plasma para determinar estos marcadores a las 12 y 22 semanas de gestación. El análisis de varianza no arrojó diferencias significativas entre mujeres preeclampticas y mujeres con embarazazos normales. Pero al analizar las mujeres que presentaron restricción de crecimiento fetal (RCF) a las 22 semanas se registró una diferencia significativa en los promedios de la dimetilarginina asimétrica entre casos y controles. Esto nos hace concluir que la dimetilarginina asimétrica tendría una importante relevancia fisiopatológica en las mujeres que cursan con restricción de crecimiento fetal.

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25

Hultin, Hella. "Calciumhomeostasis and Vitamin D in Obesity and Preeclampsia". Doctoral thesis, Uppsala universitet, Endokrinkirurgi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-145209.

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Normal physiological functioning is highly dependent of calcium and the concentration range is very narrow. Normal calcium levels are so crucial to survival that the body will de-mineralize bone if the levels are insufficient. A prerequisite for normal calcium uptake is a normal Vitamin D level. Insufficient levels of Vitamin D are associated to several diseases. The aims of this thesis were to study the relationship between pregnancies and hyperparathyroidism (pHPT) (I), between pHPT and pregnancy with preeclampsia (II) and also to determine if disturbances in calcium homeostasis with vitamin D deficiency are apparent in preeclamptic women (III). The aim was also to study calciumhomeostasis in obese patients before and after bariatric surgery (IV and V) with emphasis on vitamin D status, parathyroid secretion and bone mineral density (BMD). A correlation was found between a history of pHPT and pregnancy with preeclampsia, with an odds ratio of 6,89 ( 95% CI 2.30, 20.58). Parathyroid hormone was significantly raised in preeclamptic pregnancies but vitamin D deficiency was present both in preeclamptic and healthy pregnancies. A certain polymorphism of the Vitamin D receptor (baT haplotype), overrepresented in pHPT, was not over expressed in preeclampsia. Hypovitaminosis D was present in more than 70% of bariatric patients preoperatively, which did not change after surgery, despite great weight loss and start of Vitamin D supplementation. BMD was significantly lower in bariatric patients with a negative correlation to the time elapsed since surgery. A small increase in BMD could be noted 10-13 years after bariatric surgery, possibly due to gradual weight gain. CiCa-clamping in obese patients demonstrated a disturbed calcium homeostasis with a left-shifted calcium-PTH relationship and a lower set-point of calcium. This disturbance persisted one year postoperatively. In conclusion, derangements in calcium homeostasis with decreased levels of Vitamin D are present in preeclampsia and obesity. A history of pHPT should be viewed as a risk factor for preeclampsia. Life long follow-up is necessary after bariatric surgery, and an individually adjusted high dose Vitamin D substitute is probably needed to avoid a development of osteoporosis.

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26

Aardenburg, Robert. "Low plasma volume in the pathophysiology of preeclampsia". Maastricht : Maastricht : Universiteit Maastricht ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=9379.

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Blair, John. "DNA methylation studies of preeclampsia and related conditions". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44801.

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Preeclampsia is a leading cause of maternal and fetal death throughout the world. It is caused by placental dysfunction and clinically characterized by hypertension and other adverse outcomes. Early-onset preeclampsia (EOPET) is a severe form of the disorder. Despite much investigation, the underlying biology of EOPET is unclear. It is known that disrupted oxygen delivery and altered cellular differentiation are characteristics of preeclampsia placentas, and that this likely has an effect on the placental molecular profile. This thesis primarily investigates DNA methylation, a key component in regulating gene expression, in placentas and cellular states related to EOPET. Investigating placental cells exposed to hypoxia, we found 147 CpG sites in cytotrophoblast whose DNA methylation was significantly altered by exposure to hypoxia for 24 hours. Many of these sites overlapped with the 223 CpG sites that were altered between normoxic cytotrophoblast and syncitiotrophoblast, however the change was in the opposite direction (hypomethylated vs. hypermethylated), implying hypoxia can molecularly prevent differentiation in trophoblast cells. Expanding on these findings to look at DNA methylation in placental tissue from preeclampsia pregnancies, we found significant differences at 282 CpG sites. Several of these differences occurred in genes that have functional relevance for the development of EOPET. Many of the candidate genes also showed differential gene expression in preeclampsia placentas. To investigate the utility of these candidate CpGs as 1st trimester EOPET biomarkers, placentas with increased susceptibility to preeclampsia (trisomy 16) were investigated across gestational ages. There were many DNA methylation differences in 3rd trimester trisomy 16 placentas that were shared with chromosomally normal 3rd trimester EOPET placentas, suggesting a common molecular profile of preeclampsia prone placentas, regardless of etiology. Comparing 1st trimester trisomy 16 against 3rd trimester trisomy 16, we found 77 CpG sites differentially methylated in both conditions, and further found 3 changes in first trimester trisomy 16 shared with 3rd trimester EOPET. Overall, these studies have identified several molecular changes in EOPET and related conditions that provide insight into the biology of the disorder while also providing novel candidates to investigate further in a clinical setting.

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Dayan, Natalie. "Obesity and preeclampsia in in-vitro fertilization pregnancies". Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121135.

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Background: Obese and overweight women are frequent users of in-vitro fertilization (IVF) owing to the association between increased body mass index (BMI) and infertility. Policies that impose BMI restrictions for access to IVF exist in some countries, based on limited evidence suggesting that obese women experience reduced IVF success rates. However, there is a paucity of data on the frequency and risk of preeclampsia in the obese IVF population. More data would help inform such policies. Objectives: (i) To evaluate the respective effects of an elevated BMI (> 25 kg/m2) and the use of IVF on the risk of preeclampsia; (ii) to assess whether the risk of preeclampsia associated with an elevated BMI is different between twins and singletons; and (iii) to assess whether the effect of elevated BMI is modified by IVF treatment. Methods: The study population originated from a cohort of births delivered at the Royal Victoria Hospital in Montreal, Canada recorded between 2001 and 2008 in the McGill Obstetric and Neonatal Database (MOND). Associations were investigated with descriptive statistics, univariate and multivariate logistic regressions. We assessed effect modification by comparing observed to expected combined effects of a raised BMI and IVF treatment on preeclampsia. Results: Preeclampsia complicated 4.4% of pregnancies. There was an increased risk of preeclampsia among overweight and obese mothers (adjusted OR 3.1, 95% CI 2.5, 3.7). IVF treatment did not confer a heightened risk of preeclampsia in multivariate analyses (adjusted OR 1.0, 95% CI 0.7, 1.5). There was heterogeneity of the effect of BMI in singletons vs. multiples. There was evidence for synergism between IVF and obesity among singletons. Conclusions: Our study confirms the strong association between high BMI and preeclampsia. Despite a null effect of IVF on its own, obese women with singleton pregnancies who use IVF have a higher relative and absolute risk of preeclampsia than spontaneous singleton pregnancies. Given that preeclampsia is a serious complication of pregnancy, its risk should be considered in policy decisions about access to IVF treatment in the overweight and obese population.
Contexte: Les femmes en surpoids sont des utilisateurs fréquents de fécondation in-vitro (FIV) en raison de l'association entre l'augmentation de l'indice de masse corporelle (IMC) et l'infertilité. Les politiques qui imposent des restrictions IMC pour l'accès à la FIV existent dans certains pays, basé sur des données limitées suggérant que les femmes obèses ont des taux de succès de FIV réduits. Cependant, il y a un manque de données sur la fréquence et le risque de prééclampsie chez la population de FIV obèses. Plus de données aideraient à informer ces politiques. Objectifs: (i) dévaluer les effets respectifs d'un IMC élevé (> 25 kg/m2) et l'utilisation de la FIV sur le risque de pré-éclampsie, (ii) évaluer si le risque de pré-éclampsie associé à un IMC élevé est différent entre jumeaux et singletons, et (iii) évaluer si l'effet de l'IMC élevé est modifié par un traitement de FIV. Méthodes: Notre cohorte comprend les naissances de l'Hôpital Royal Victoria, à Montréal, Canada enregistrées entre 2001 et 2008 dans la base de données obstétriques McGill et néonatale (MOND). Les associations ont été étudiées avec les statistiques descriptives, univariées et des régressions logistiques multivariées. Nous avons évalué la modification de l'effet observé en comparant les effets combinés attendus d'un IMC élevé et un traitement de FIV sur la pré-éclampsie. Résultats: La prééclampsie complique 4,4% des grossesses. Il y avait un risque accru de pré-éclampsie chez les mères en surpoids et obèses (OR ajusté 3,1, IC 95% 2.5, 3.7). FIV ne conférait pas un risque accru de pré-éclampsie dans les analyses multivariées (OR 1,0, IC 95% de 0,7, 1,5). Il y avait hétérogénéité de l'effet de l'IMC dans les grossesses de singletons vs multiples. Il y avait en évidence d'une synergie entre FIV et un IMC élevé chez les singletons. Conclusions: Notre étude confirme la forte association entre un IMC élevé et la pré-éclampsie. Les femmes en surpoids avec des grossesses uniques qui utilisent la FIV ont un risque plus élevé relative et absolue de la pré-éclampsie que pendant les grossesses spontanées. Étant donné que la pré-éclampsie est une complication grave de la grossesse, le risque doit être pris en compte dans les décisions politiques concernant l'accès à un traitement par FIV dans la population en surpoids et obèses.

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Cockell, Anna Patricia. "Material vascular function in normal pregnancy and preeclampsia". Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265331.

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Rolnik, Daniel Lorber. "Prediction of preeclampsia and its prevention with aspirin". Thesis, Manchester Metropolitan University, 2018. http://e-space.mmu.ac.uk/621256/.

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Background: Preeclampsia (PE) affects 2-3% of all pregnancies and is a major cause of maternal and perinatal morbidity and mortality. The current approach to screening for PE is based on the identification of risk factors from maternal characteristics and medical history. This approach, however, fails to identify a high proportion of cases of PE and does not provide individualised, patient-specific results. An alternative approach is to combine maternal factors with biophysical and biochemical markers to estimate the individual probability of developing PE with higher detection rates. To date, no intervention is proven to reduce the risk of the disease, and several studies evaluating the use of aspirin for prevention of PE led to inconclusive results. Objectives: The aims of the studies included in this thesis are, first, to prospectively validate in a large European population a first-trimester algorithm for prediction of PE that combines maternal demographic characteristics and medical history with biophysical and biochemical markers; second, to compare this method of screening to the performance of currently used guidelines; third, to evaluate a possible beneficial effect of aspirin initiated at 11 to 14 weeks of gestation and at a dose of 150 mg in the prevention of PE in a multicentre, double-blind, placebo-controlled randomised trial; and fourth, to analyse a potential role of cell-free DNA testing in the prediction of PE. Methods: Combined screening for PE was applied in the first or second trimester, and women found to be at high-risk in the first trimester were offered participation in a double-blind trial of aspirin against placebo in six European countries. We have recorded maternal characteristics and history, measured the uterine artery pulsatility index (UtPI) on ultrasound, the mean arterial pressure (MAP), serum concentration of pregnancy-associated plasma protein A (PAPP-A) and placental growth factor (PLGF). Pregnancy outcomes were obtained from the hospital maternity records. Bayes theorem was used to combine the a priori risk from maternal factors with the results of biomarker measurements and estimate individual probabilities. In the randomised trial, the analysis was performed in an intention-to-treat basis and the treatment effect on the primary outcome (the development of PE with delivery before 37 weeks of gestation) was reported with 95% confidence interval (CI), and on secondary outcomes with 99% CI. Cell-free DNA fetal fraction was compared with other first trimester markers for PE and in a case-control study. Results: Detection rates of combined screening, for a false-positive rate (FPR) of 10%, were 89% (95% CI 79-96%), 75% (95% CI 70-80%) and 47% (95% CI 44- 51%) for PE < 32 weeks, preterm PE and term disease, respectively. The performance of combined screening was superior to methods based on risk factors alone, both in the first and second trimesters. The use of aspirin by high-risk women reduced the incidence of preterm PE by 62% (adjusted odds ratio 0.38, 95% CI 0.20- 0.74). Secondary analyses have shown that the effect of aspirin was influenced by the level of compliance to treatment and was consistent in different subgroups according to maternal characteristics and obstetric history, but there was no evidence of beneficial effect of aspirin in women with chronic hypertension. Aspirin reduces the length of stay in NICU and costs through a reduction in premature births before 32 weeks due to PE. Fetal fraction on cell-free DNA testing correlates with other first trimester markers, but its role in screening for PE is uncertain. Conclusions: This thesis has demonstrated that combined screening for PE is superior to current guidelines based on maternal characteristics and history alone, and that aspirin, at a daily dose of 150 mg and given to high-risk patients from 11 to 14 weeks until 36 weeks of gestation, reduces the incidence preterm PE and the length of stay in NICU. The effect of the medication depends on good adherence to treatment and is questionable in patients with chronic hypertension.

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Lazdam, Merzaka. "Cardiovascular impact of preeclampsia on mother and offspring". Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:2914ce9e-5619-4d46-94cd-b1d8a2122dcb.

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Preeclampsia is one of the leading causes of maternal and fetal mortality and morbidity. Furthermore, women who have had preeclampsia have an increased risk of cardiovascular events over the next 10-15 years. Indeed, preeclampsia is associated with a four-fold increase in the risk of hypertension and double the risk of fatal and non fatal ischaemic heart disease and stroke. In addition, offspring born to preeclampsia are more likely to have higher blood pressure from childhood and stroke in later life. The risk to mother and offspring is greatest when preeclampsia is diagnosed at an earlier gestation, suggesting a more severe form of preeclampsia. As the long term cardiovascular risk to both mother and child is known from delivery, the main interest of my research was to identify key phenotypic variations in mothers and children during the years between the episode of preeclampsia and emergence of established cardiovascular disease, which might explain the link between the two conditions. This information could then be used to devise ways to identify subjects at greatest risk of later cardiovascular disease and to establish intermediate endpoints for future preventative interventions. Therefore, in a case control study, women diagnosed with preeclampsia between 1998 and 2003 and their offspring were recruited and underwent comprehensive cardiovascular and metabolic phenotyping. Furthermore, young adults born preterm to hypertensive pregnancy were also investigated in their twenties. The research demonstrates that early-onset preeclampsia, diagnosed before 34 weeks gestation, is associated with blood pressure patterns in mothers 6-13 years after pregnancy that are distinct from those seen following later-onset disease. Furthermore, there is evidence of distinct differences in cardiac, vascular and metabolic profiles in these individuals with women having evidence of increased arterial stiffness, changes in cardiac function and reduced capillary density. Preterm offspring of hypertensive pregnancies similarly have higher blood pressure than seen in those born following late-onset disease and, in young adult life, have reduced endothelial function and changes in cardiac size proportional to this dysfunction. This research demonstrates adverse cardiac and vascular remodelling after preeclampsia in mothers and offspring that are evident before the development of clinical cardiovascular disease. The identified differences in cardiac and vascular function may be useful as surrogate endpoints in future preventive trials.

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Boij, Roland. "Aspects of inflammation, angiogenesis and coagulation in preeclampsia". Doctoral thesis, Linköpings universitet, Avdelningen för neuro- och inflammationsvetenskap, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-132446.

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Preeclampsia is a major challenge to obstetricians, due to its impact on maternal and fetal morbidity and mortality and the lack of preventive and treatment strategies. The overall aim of this thesis is to increase the knowledge of the pathogenesis of preeclampsia including the role of inflammation, angiogenesis and coagulation, both locally at the fetomaternal interface and in the maternal circulation. Uncompensated maternal endothelial inflammatory responses to factors from stressed trophoblasts seem to be a major contributor to the syndrome, together with an imbalance in angiogenesis and an activated coagulation system. An increasing amount of data indicates an involvement of the immune system with defect tolerance to the conceptus as an integral part of the pathogenesis, at least in early-onset preeclampsia (EOP). We showed that a single administration of human preeclampsia serum in pregnant IL-10−/− mice induced the full spectrum of preeclampsia-like symptoms including hypoxic injury in uteroplacental tissues and endotheliosis in maternal kidneys. Importantly, preeclampsia serum, as early as 12 to 14 weeks of gestation, disrupted cross talk between trophoblasts and endothelial cells in an in vitro model of endovascular activity (Tube formation test). These results indicate that preeclamptic sera can be used to better understand the pathophysiology and to predict the disorder. Preeclampsia has been associated with increased inflammation, aberrant angiogenesis and activated coagulation, but their correlation and relative contribution are unknown. We found that markers for all these mechanisms were independently associated with preeclampsia. Cytokines, chemokines, and complement factors seem all to be part of a Th1-associated inflammatory reaction in preeclampsia, more pronounced in EOP than in late-onset preeclampsia (LOP), in line with a more homogeneous pathogenesis in EOP as based on placental pathology. In women with intrauterine growth restriction (IUGR), with an anticipated pathologic placentation, only differences in levels for sFlt-1 and PlGF were found in comparison with mothers without IUGR. Thus, sFlt-1 and PlGF seem to be indicators of placental pathology, while other biomarkers might also reflect maternal endothelial pathology. Chemokines, in contrast to cytokines, may prove to be useful markers in preeclampsia. A deficiency in regulatory T (Treg) cells causing reduced immune regulatory capacity has been proposed in preeclampsia. Utilizing recent advances in flow cytometry phenotyping, we found no major alterations in circulating Treg numbers in preeclamptic women compared with normal pregnant and non-pregnant women. However, preeclampsia was associated with increased fractions of CTLA-4+ and CCR4+ cells within Treg subpopulations, which is in line with a migratory defect of Treg cells, and potentially associated with a reduced number of suppressive Treg cells at the fetomaternal interface. As we found that corticosteroid treatment affected the results, it should be accounted for in studies of EOP. Chemokines are supposed to be part of the immune adaptation in pregnancy. We found a decreased expression of CCL18 (Th2/Tregassociated), in trophoblasts from preeclamptic compared to normal pregnant women, indicating a local regulatory defect in preeclampsia, in line with our finding of a possible migratory defect of circulating Treg cells. Due to increased expression of CCL20 (Th17) and CCL22 (Th2) in first trimester placenta and increased circulating levels of CXCL10 (Th1) and CCL20 (Th17) in third trimester preeclamptic women, we suggest that CCL20 and CCL22 may be important for implantation and early placentation while in third trimester of a preeclamptic pregnancy CXCL10 and CCL20 mainly mirror maternal increased endothelial inflammation and aberrant angiogenesis. In summary, we found that preeclampsia is associated with increased inflammation, aberrant angiogenesis and activated coagulation, caused by placental factors in maternal peripheral circulation, more pronounced in the early-onset form of preeclampsia. It also appears that there is a defective modulation of the immune system in preeclamptic pregnancies. The results provide a better understanding of the pathogenesis of preeclampsia and have given suggestions to predictive markers for preeclampsia in the future.

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Gunnarsdóttir, Jóhanna. "Epidemiological Studies of Preeclampsia : Maternal & Offspring Perspectives". Doctoral thesis, Uppsala universitet, Obstetrik & gynekologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-320138.

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Preeclampsia is a placental-related disorder characterized by generalized endothelial activation. Vascular predisposition is associated with the occurrence of preeclampsia and the recurrence risk is substantial. Onset of preeclampsia is preceded by placental hypo-perfusion, and placental over-production of vasoconstrictive agents might explain symptoms such as hypertension and proteinuria. Preeclampsia is associated with the birth of small-for-gestational-age (SGA) infants. The trajectory of postnatal growth in SGA-born children is described as catch-up, but it is unclear whether prenatal preeclampsia is independently associated with postnatal growth. The objectives were: firstly, to study the association between partner change and prior miscarriages on the occurrence of preeclampsia and SGA; secondly, to study postnatal growth in children prenatally exposed to preeclampsia; and thirdly, to address the association between blood pressure (BP) changes during pregnancy and risks of preeclampsia and SGA. Population-based cohort studies were performed with information from the following registers: Swedish Medical Birth Register, Uppsala Mother and Child Database and Stockholm-Gotland Obstetric Database. Associations were estimated with logistic and linear regression analyses, with adjustments for maternal characteristics, including body mass index, pre-gestational diseases and socioeconomic factors. The results were, firstly, that partner change was associated with preeclampsia and SGA birth in the second pregnancy but depended on the outcome of the first pregnancy, and that a history of recurrent miscarriages was associated with increased risks of preeclampsia and SGA. Secondly, prenatal exposure to preeclampsia was associated with increased offspring growth in height during the first five years. This association was also seen in children born with normal birth weight for gestational age. Thirdly, pre-hypertension in late gestation and elevated diastolic BP from early to mid-gestation were both associated with SGA birth. Further, women with pre-hypertension in early gestation without lowered diastolic BP until mid-gestation seemed to represent a risk group for preeclampsia. To conclude, the importance of previous pregnancy outcomes in the antenatal risk evaluation was highlighted. Secondly, the results imply that postnatal growth trajectory is related to maternal preeclampsia, in addition to SGA. Thirdly, the association between BP changes within a normal range and SGA may challenge the clinical cut-off for hypertension in pregnancy.

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Morano, Danila <1973&gt. "Marker sierici per la predizione precoce della preeclampsia". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/700/1/Tesi_Morano_Danila.pdf.

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Morano, Danila <1973&gt. "Marker sierici per la predizione precoce della preeclampsia". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/700/.

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MOHAMED, Nahid. "Comparison of Fetal Thymus Size in Normal and Preeclamptic Pregnancies: Is Thymus Size Smaller in Fetuses of Women with Preeclampsia?" Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10003.

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Objective To determine whether the thymus is smaller in the fetuses of preeclamptic mothers than in those of normal controls. Methods This was a cross-sectional, prospective, comparative study of sonographically-determined fetal thymus measurements in 39 pregnancies with preeclampsia and 70 healthy pregnancies. Results Both the diameter and the perimeter of the fetal thymus were significantly smaller in pregnancies with preeclampsia than in healthy controls. The means of the thymus diameter were 28.6 ± 5.9 and 32.9 ± 4.5 mm and of the thymus perimeters 80.9 ± 16.5 and 93.1 ± 16.6 mm for preeclamptic and healthy pregnancies, respectively (P < 0.001). General linear models showed that smaller fetal thymuses in preeclamptic pregnancies were independent of gestational age, estimated fetal weight, small-for-gestational age status and antenatal steroid use. Conclusions Thymic involution appears to be a fetal response to preeclampsia, strengthening the evidence for the involvement of the immune system in the disease. Preeclampsia is associated with smaller fetal thymuses.

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Porras, Poma Rayda. "Manejo expectante de preeclampsia severa en el embarazo pretérmino en el Hospital Nacional Docente Madre Niño "San Bartolomé" del 01 de enero 2002 al 31 de diciembre 2006". Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2007. https://hdl.handle.net/20.500.12672/2527.

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Objetivo: El objetivo del estudio fue determinar los resultados del manejo expectante de la preeclampsia severa en embarazos menores de 34 semanas. Material y métodos: Se realizó un estudio descriptivo, observacional, retrospectivo de corte transversal con 79 gestantes preeclámpticas severas entre las 23 – 34 semanas que recibieron manejo expectante durante el período comprendido entre el 01 de enero del 2002 y el 31 de diciembre de 2006,llevado a cabo en el Hospital Nacional Docente Madre Niño “San Bartolomé”,el análisis estadístico se realizó con el programa 14.0. Resultados: El antecedente personal más frecuente fue la preeclampsia (22,8%), mientras que el antecedente familiar más importante fue la hipertensión arterial (58,2%). Las complicaciones maternas más frecuentes en fueron la falla renal aguda (16,5%) y el síndrome HELLP (13,9%). La restricción de crecimiento intrauterino (81%) y la muerte intraparto (6,3%) fueron las principales complicaciones fetales, mientras que la asfixia neonatal (7,6%) fue la complicación neonatal más frecuente. Las indicación más frecuente para terminar el embarazo fue la preeclampsia refractaria al tratamiento (26,6%). En el 57% de casos el tiempo de prolongación del embarazo con el manejo expectante fue de 1 – 3 días. La vía del parto en el 89,9% fue por cesárea y el peso promedio de los recién nacidos estuvo comprendido entre los 1000 – 1499 gramos en el 31,6% de casos y en el 30,4% entre los 1500 – 1999 gramos.Resultados: Se concluyó que el manejo expectante de la preeclampsia severa entre las 23 – 34 semanas de gestación fue factible, debiendo realizarse en forma selectiva y en instituciones que garanticen una estricta vigilancia materno – fetal. Palabras Clave: Preeclampsia severa, manejo expectante, embarazo pretérmino.
Tesis de segunda especialidad

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Quispe, Salas Cris Leydi. "Relación de ciertos factores asociados y el desarrollo de preeclampsia en gestantes atendidas en el IEMP durante el período agosto-noviembre del 2003". Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2004. https://hdl.handle.net/20.500.12672/360.

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Se trata de un estudio caso control, el cual tuvo como objetivo el determinar la relación que pudiera existir entre la infección urinaria ,el broncoespasmo y el intervalo intergenésico con el desarrollo de preeclampsia .Este estudio se realizó en el Instituto Especializado Materno Perinatal, entre los meses de agosto y noviembre del 2003, en donde se comparó 75 puérperas que tuvieron preeclampsia con 75 puérperas que no tuvieron la enfermedad, pareadas con respecto a la edad materna. Se analizó los factores potenciales asociados a preeclampsia usando la prueba de asociación Odd Ratio (OR), pruebas de diferencias de proporciones Chi cuadrada y pruebas de diferencia de medias “t student”. Resultados: La preeclampsia estuvo asociada a infección urinaria durante el embarazo con un OR : 5.4 (IC 95% 1.7 – 17.4) , constituyendo el principal factor asociado. La infección vaginal mostró también asociación a preeclampsia : OR: 4.6 (IC 95 % 1.3-14.0) . El intergenésico largo (>48 meses) estuvo asociado a preeclampsia con un OR: 4.6 (IC 95 % 1.4-15.3). Conclusiones: El intervalo intergenésico largo y las infecciones (urinaria y vaginal) constituyen factores de riesgo para el desarrollo de preeclampsia. Las mujeres que tienen alguno de estos factores poseen un riesgo incrementado para que su embarazo sea complicado con preeclampsia.
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Cowan, Joyce. "Women's experience of severe early onset preeclampsia a hermeneutic analysis : this thesis is submitted to Auckland University of Technology in partial fulfillment of the degree of Master of Health Science (Midwifery), 2005". Full thesis. Abstract, 2005.

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Ruiz, Santacruz Javier Sebastian. "Maternal Mortality and Morbidity Related to Hypertensive Disorders During Pregnancy : A Socio-Demographic view in Colombia". Thesis, Stockholms universitet, Sociologiska institutionen, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-78664.

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Reducing maternal mortality is number five in the United Nations Millennium Development Goals. Preeclampsia is a particular form of hypertension during the pregnancy period that can cause maternal deaths. In Colombia, is the first cause of morbidity and maternal mortality (Serrano-Díaz & Díaz-Martinez 2005). This study attempts to determine how the socio-demographic causes that are involved in the development in order to contribute to the description of the environmental causes, more specifically to determine if socio-demographic factors influence the development of the disease. This study is based on data from two sources especially, one from the National Department of Statistics (DANE) or Statistics Colombia to give a better contextualization about the rates and tendencies of the Maternal Mortality Ratio (MMR) on ICD-10 codes related with obstetric risks. The other called GenPE project (Genetics and Preeclampsia), which has been developed in Colombia and it has had a great impact on the genetic factors but contains socio-demographic information. For this purpose some statistical robustness checks as chi-square tests, logistic regression and multilevel models to determine which is the way to conceptualize the problem. The findings stress on more prenatal care early in the pregnancy (p<0.01) as well as the intensity or number of controls (p<0.01) to decrease the risk of preeclampsia. Besides, familiar background regarding hypertensive disorders is still important in the development of the disease (p<0.01), which gives information as an environmental and genetic contribution.
GenPE proyect in genetics and preeclampsia

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Lopez, Vargas Victor. "Prevalencia de trastornos hipertensivos en gestantes hospitalizadas en El Hospital Nacional Hipolito Unanue en el periodo enero- diciembre del 2015". Bachelor's thesis, Universidad Ricardo Palma, 2016. http://cybertesis.urp.edu.pe/handle/urp/545.

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Objetivó: Determinar la prevalencia de los diferentes tipos de trastornos hipertensivos en gestantes hospitalizadas en el Hospital Nacional Hipolito Unanue en el periodo enero – diciembre del 2015 Método: La población es de 224 casos con el diagnostico de ingresos de hipertensión gestación – pre eclampsia, obteniéndose una muestra de 142 pacientes, el diseño de estudio es observacional, retrospectivo, transversal. El dato obtenido fue mediante la revisión detallada de las historias clínicas de los pacientes hospitalizados en el Hospital Nacional Hipólito Unanue Resultado: el trastorno hipertensivo con mayor prevalencia con el 53. 03% es hipertensión gestacional, el 42.42% es pre eclampsia. El intervalo de edad de 20 – 35 años fue el más frecuente con El 65.15%. Respecto a la gestación se puede observar que se presenta el 62.12% en paciente multigesta,y el 37.88% en primigestas. También se observa que el 57.58% son gestantes de 37- 40 semanas de gestación y el 3.03% son puérperas inmediatas. La cefalea persistente fue el síntoma más común con el 38.25%.En cuanto a los exámenes auxiliares se encontró, la más prevalente a la proteinuria con el 35.9%, y la menos prevalente es la creatinina con el 2.56%. Los controles prenatales se encontró una prevalencia del 63.64% con igual o más de 6 controles, el 30.3% con menos de 6 controles y el 6.06% sin controles prenatales. Conclusión: Se concluye que la hipertensión gestación es el trastorno hipertensivo más frecuente.

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Aufdenblatten, Myriam. "Prematurity is related to high placental cortisol in preeclampsia /". [S.l.] : [s.n.], 2009. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Rudra, Carole B. "Periconceptional ambient air pollutant exposure and subsequent preeclampsia risk /". Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/10914.

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Herraiz, Raya Sonia. "Efecto del sildenafilo sobre un modelo de preeclampsia animal". Doctoral thesis, Universitat de València, 2010. http://hdl.handle.net/10803/77723.

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La preeclampsia (PE) es una patología especifica del embarazo que afecta a un 5-10% de estos. Aunque se la considera una enfermedad de las fases iniciales de la gestación, se manifiesta clínicamente a partir de la semana 20. Caracterizada por hipertensión, proteinuria y edema maternos, aumenta la morbimortalidad perinatal porque los fetos sufren retraso del crecimiento intrauterino y prematuridad. Aunque el cuadro clínico está ampliamente caracterizado, la etiología de la enfermedad es desconocida, están involucrados factores genéticos, inflamatorios, inmunológicos y ambientales que provocan una serie de alteraciones que conducen a una disfunción endotelial, un desequilibrio vasomotor y un desarrollo placentario deficiente. La placenta es un elemento clave en el desarrollo de la PE ya que puede aparecer en embarazos sin feto presente (embarazo molar) y una vez se ha instaurado, la única cura posible, es la finalización del embarazo. Durante la gestación normal, el trofoblasto invade los vasos uterinos y los remodela, transformándolos en tubos laxos de alto flujo y baja resistencia que aseguran un aporte sanguíneo adecuado a la placenta y el feto. El mantenimiento de la vasodilatación en estos vasos es fundamental para su remodelación. En PE, esta invasión es muy superficial y la remodelación falla, por ello no caen las resistencias ni se modifican los vasos, dando lugar a un aporte sanguíneo muy deficiente al feto. La vasodilatación tiene lugar mediante la liberación local de oxido nítrico (ON) que a través de su segundo mensajero, el GMP cíclico, evita la contracción de las fibras musculares que rodean el vaso, manteniéndolo por tanto dilatado. En PE, se ha detectado una disminución del cGMP y los nitritos en orina por lo que se sabe que existe vasoconstricción por falta de factores vasomotores (ON-cGMP). Una terapia para mantener la vasodilatación es administrar sildenafilo (SC), inhibidor selectivo de la fosfodiesterasa 5, enzima encargado de degradar al cGMP, así produce vasodilatación porque mantiene su concentración intracelular. SC ha sido testado en numerosos estudios animales donde ha demostrado ser un potente vasodilatador y no tener efectos nocivos sobre los fetos. Material y métodos. En un modelo animal de PE desarrollado en rata, mediante inhibición crónica de la síntesis de ON, con L-NAME, probamos la eficacia del tratamiento con SC. Lo administramos a baja dosis y desde el inicio de la gestación, para que actúe en el proceso de invasión y formación de la placenta. Evaluamos la tensión arterial, la evolución del peso y la mortalidad pre- y post-natal de la descendencia y su desarrollo neurológico, función hemodinámica materna y fetal mediante ecografía Doppler. Resultados. La administración de SC desde el inicio de la gestación a baja dosis, corrige el cuadro materno de la PE, ya que normaliza la tensión arterial y la proteinuria. En cuanto a la hemodinámica materna, normaliza los índices de resistencia de las arterias uterinas gracias a la vasodilatación que provoca su administración. En la descendencia, al administrarlo en el modelo de PE, mejora el retraso del crecimiento fetal aunque no lo corrige por completo, elimina la mortalidad intra-útero y mejora la supervivencia hasta la edad adulta. En cuanto a la perfusión al feto, el modelo de PE reduce la cantidad de sangre que llega al corazón fetal y al administrar SC bajan las resistencias en los vasos fetales (ductus venoso) por lo que mejora la perfusión. Conclusión. La administración desde el inicio y a baja dosis, elimina el síndrome materno de la PE y mejora la condición fetal. más estudios son necesarios para poder administrarlo a pacientes con PE temprana o con antecedentes de insuficiencia placentaria como profilaxis.
Preeclampsia (PE) is a pregnancy specific disease that affects 5-10% of pregnancies and remains one of the major causes of maternal and fetal mortality. Maternal syndrome involves endothelial dysfunction, hypertension and proteinuria and fetal syndrome produces intrauterine growth restriction. All due to an ineffective trophoblast invasion of uterine arteries that produce a restricted placental blood flow. In normal pregnancies vasodilatation in uterine arteries improves trophoblast invasion but in PE vasoconstriction disturbs uterine artery remodelling. Vasodilatant effects occurs via nitric oxide (NO) and cGMP that prevents contraction of muscular cells around the vessels producing vasodilatation. In PE a decrease of cGMP levels was described and its known that vasoconstriction is produced by a reduction of vasodilatant substances as NO and cGMP. Sildenafil (SC) is a phosphodiesterase 5 (PDE5) inhibitor that acts as a vasodilatant agent increasing the amount of cGMP. Therefore, it is a potential therapeutic tool to maintain vasodilatation in complicated pregnancies. In an animal model of PE developed by chronic inhibition of nitric oxide synthesis by L-NAME administration be test the effects of SC administration in rats. SC administration starts in a low dose manner at the onset of pregnancy in order to test the effect during placental development and uterine artery remodelling. We evaluate maternal blood pressure, weight and mortality during pre and post natal development, neurological development in the offspring and maternal and fetal hemodynamic function by Doppler scan. SC administration at low dose since the onset of pregnancy improves maternal syndrome because restores normal values of blood pressure and proteinuria. In hemodynamics, SC restores resistance index of uterine arteries through its vasodilatant effect. In the offspring when was administered in PE, SC improves weight gain and increases survival rates. When hemodynamic function was analyzed SC produces a decrease of resistances in fetal vessels producing an increase of fetal perfusion. Chronic administration of SC during the pregnancy restores maternal effects of PE and improved fetal growth and neurological development of the offspring.

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Peters, Paula Kay. "Calcium intake and bone mass in women with preeclampsia /". The Ohio State University, 1991. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487687485810412.

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Kedia, Komal. "Placental ‘Omics’ Study to Understand the Pathogenesis of Preeclampsia". BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/5876.

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Preeclampsia (PE) is a potentially fatal complication of pregnancy characterized by an increase in blood pressure (>140/90 mmHg) and proteinuria (>300 mg/24 hrs), often accompanied by edema. Symptoms of PE start after 20 weeks of gestation. If PE remains untreated, it can lead to eclampsia, grand-mal seizures responsible for most fatalities. PE is believed to affect 2-10% of pregnancies worldwide, and claims the lives of over 75,000 mothers and 500,000 newborns yearly. No therapeutic agents have been developed to prevent or cure PE. Part of the reason for this is the absence of a complete understanding of the pathogenesis of this disease. PE has long been regarded as a “disease of theories”, and the pathophysiology of PE continues to be the subject of debate. Nonetheless, several abnormalities have been observed to precede established, clinical PE and have in turn been proposed to be involved in the causation of this disease, all with involvement of the mother's placenta as a central feature. Removal of placenta is the only cure for PE and results in a rapid resolution of the symptoms. Thus, the placenta remains an organ of substantial interest and many research groups have attempted to identify abnormal placental features occurring in PE. None of these studies have focused on less abundant, low molecular weight (LMW) biomolecules, which play important roles in the pathophysiology of many diseases. There are a number of alterations that are believed to affect the placenta and contribute to the pathogenesis of PE. The most widely accepted ones include hypoxia, oxidative stress, and an increase of pro-inflammatory mediators in the mother's placenta. The goal of my initial study was to identify which of these hypothesized causative pathways has a significance in the etiology of this syndrome as well as to investigate which less abundant, low molecular weight biomolecules change in response to these abnormalities. For this purpose, we first adapted and optimized a previously developed methodology that studied LMW biomolecules in tissue specimens to study placental biomolecules. This approach involved a tissue homogenization step followed by protein depletion using acetonitrile. We compared two regions of human placenta: the chorionic plate and the basal plate to find differences in the LMW fraction. We discovered 16 species with statistically significant differences between the two sides, and identified 12 of them using tandem mass spectrometry. In the second study we collected normal human term placentas from elective C-section deliveries and exposed explants to each of the above-mentioned provocative agents or stress conditions for 48 hrs. Other explants without any stressors were cultured in parallel for the same amount of time. The processing of explants was divided into five steps: 1) explant culture; 2) tissue homogenization; 3) acetonitrile precipitation to remove high abundance, high molecular weight proteins; 4) injection of the protein-depleted specimen into a capillary liquid chromatography–mass spectrometer; 5) analysis of MS data to identify quantitative differences between cases (stressed explants) and controls (normal explants). In total, we observed 146 molecules changed in abundance between the treated explants and the controls with 75 of these molecules changed in response to hypoxic treatment, 23 changed due to hypoxia-reoxygenation, a process generating reactive oxygen species, and 48 changed due to tumor necrosis factor–alpha (TNFα), a pro-inflammatory cytokine. We were successful in identifying 45% of all these molecules by tandem MS. Statistical modeling that applied LASSO analysis allowed for the development of a model that used 16 of the 146 differentially expressed biomolecules to accurately classify and differentiate each of the 4 stressed conditions. In my third study, I then submitted actual preeclamptic and non-diseased placental tissue to our established homogenization and acetonitrile precipitation protocol to see if any of the differences in LMW biomolecules produced under stress conditions in normal placenta were recapitulated in actual diseased placenta. In a preliminary statistical analysis, 8 of the original 146 differentially expressed species, displayed significant or near significant changes in the actual disease placenta. After applying two stringent statistical tests that eliminated any potential influence of gestational age, four out of the 146 biomarkers previously studied, continued to be differentially expressed in both stringent analyses. Of the four, 1 biomarker (m/z 649.49 (+1)) showed an increased abundance in hypoxic placental explants as well as in PE placenta; 2 (461.06 (+1), 476.24 (+1)) were increased in response to TNFα-exposed placental explants and in these PE placentas and 1 (426.35 (+1)) increased in response to hypoxia-reoxygenation-treated placental explants was also increased in PE placenta. We have chemically characterized 2 of the 4 biomarkers. One was a phospholipid (m/z 476.24) while the other was an acyl-carnitine (m/z 426.35). This suggests that features of PE appear to arise from the predicted early abnormalities that affect the placenta. In conclusion, I was successful in developing an ‘omics’ approach to study less abundant, low molecular weight biomolecules in human placenta as well as investigate which biomarkers show differential expression in human placenta when exposed to proposed abnormalities of PE and have data to suggest that these same responses are present in PE placenta.

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Bonifacio, Mezuma Shandrelly Yesenia. "Relación entre el nivel de conocimientos y las fuentes de información sobre preeclampsia en gestantes con este trastorno atendidas en el Instituto Nacional Materno Perinatal durante mayo-julio 2015". Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2015. https://hdl.handle.net/20.500.12672/4570.

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OBJETIVO: Determinar la relación entre el nivel de conocimientos y las fuentes de información sobre preeclampsia en gestantes con este trastorno atendidas en el Instituto Nacional Materno Perinatal durante Mayo - Julio 2015. METODOLOGÍA: Estudio de tipo observacional, correlacional, prospectivo y de corte transversal, en el que se tomó a 184 gestantes con preeclampsia que hayan recibido información sobre este trastorno y que cumplían con los criterios de inclusión y exclusión. El grado de relación entre el nivel de conocimientos y las fuentes de información se estimó a través de la prueba Chi-cuadrado, con un nivel de confianza (IC) del 95%, el cual se consideró significativo cuando tenía un valor p<0.05. RESULTADOS: Las fuentes de información que recibieron las gestantes con preeclampsia fueron a través de medios de información como el Obstetra en el 39.1% y el Médico ginecólogo en el 29.3%; el lugar de información fue el Hospital en el 47.8% y el momento de información fue durante el control prenatal en el 53.8%. El nivel de conocimientos que presentan las gestantes con preeclampsia es “Medio” en el 60.3% y “Alto” en el 22.3%. El nivel de conocimientos sobre preeclampsia se relaciona con el medio de información (p=0.000), el lugar de información (p=0.000) y el momento de información (p=0.025) en las gestantes con este trastorno. CONCLUSIÓN: El nivel de conocimiento se relaciona con el medio, el lugar y el momento de información sobre preeclampsia en las gestantes con este trastorno atendidas en el Instituto Nacional Materno Perinatal durante Mayo - Julio 2015. PALABRAS CLAVES: Preeclampsia, conocimientos, fuentes de información.
OBJECTIVE: To determine the relationship between the level of knowledge and the sources of information about preeclampsia in pregnant women with this disorder attended in the National Institute Maternal Perinatal during May-July 2015. METHODOLOGY: Observational study, correlational, prospective and cross-sectional in which was taken in 184 pregnant women with preeclampsia who have received information about this disorder and who met the inclusion and exclusion criteria. The degree of relationship between the level of knowledge and the sources of information is estimated using the Chi-square test, with a confidence interval (CI) of 95%, which is considered significant when p value was <0.05. RESULTS: The sources of information they received pregnant women with preeclampsia were through the mass media such as the 39.1% Obstetrician and gynecologist at 29.3%; the place of information was the Hospital in 47.8% and the moment information during antenatal care was at 53.8%. The present level of knowledge that pregnant women with preeclampsia are "Medium" at 60.3% and "High" at 22.3%. The level of knowledge about the information medium preeclampsia (p = 0.000), the location information (p = 0.000) and the time information (p = 0.025) in pregnant women are associated with this disorder. CONCLUSIONS: The level of knowledge is related to the medium, location and timing information about preeclampsia in pregnant women with this disorder attended in the National Institute Maternal Perinatal during May to July 2015. KEYWORDS: Preeclampsia, knowledge, information sources.
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He, Shu. "Hypercoagulation in preeclampsia : implications for maternal health and foetal growth /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3647-1/.

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Belfort, Michael A. "The cerebral circulation in preeclampsia : abnormalities in autoregulation and perfusion /". Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4622-1/.

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Martínez, Ruiz Ana. "Biomarcadores predictores de preeclampsia en gestantes con factores de riesgo". Doctoral thesis, Universidad de Murcia, 2013. http://hdl.handle.net/10803/117522.

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En este trabajo se evaluó la utilidad de una serie de marcadores: triglicéridos, ácido úrico, forma soluble de la tirosín kinasa 1 (sFlt-1), factor de crecimiento placentario (PlGF), múltiplo de la mediana de la proteína plasmática A asociada al embarazo (MoM PAPP-A), antígeno sérico CA125 (CA125), enzima convertidora de angiotensina (ECA) y el estudio ecográfico Doppler, como posibles predictores de preeclampsia en el primer y segundo trimestre de gestación. Se incluyeron un total de 68 gestantes con “riesgo a priori” de desarrollar preeclampsia (diabetes mellitus tipo I, enfermedad renal preexistente, hipertensión crónica sin proteinuria, etc) y un grupo control. De esas 68 gestantes, 8 desarrollaron preeclampsia. La combinación de marcadores más eficiente fue utilizando el PlGF del primer trimestre con un punto de corte ≤37,6 pg/ml, un índice de resistencia ≥0,7 y la ECA≥ 40,4 U/L del segundo trimestre, pudiendo predecir el 87,5% de las gestantes que desarrollarían preeclampsia.
This study evaluated the usefulness of several biomarkers: triglycerides, uric acid, soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), multiple of the median of pregnancy associated plasma protein-A (PAPP-A MoM), serum antigen CA125 (CA125), angiotensin converting enzyme (ACE) and the Doppler ultrasound as predictors of preeclampsia in the first and second trimester of pregnancy. We included a total of 68 pregnant women with "a priori risk" of develop preeclampsia (type I diabetes mellitus, preexisting renal disease, chronic hypertension without proteinuria, etc) and a control group. Of those 68 pregnant women, 8 developed preeclampsia. The most efficient combination of the studied biomarkers was the use of PlGF in the first-trimester with a cut-off ≤37.6 pg/ml, a resistance index ≥0.7 and ACE ≥40,4 U/L in the second trimester which can predict 87,5% of pregnant women who develop preeclampsia.

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