Diagnosis and Management of Gestational Hypertension and Preeclampsia

Department of Obstetrics & Gynecology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0526, USA.
Obstetrics and Gynecology (Impact Factor: 5.18). 08/2003; 102(1):181-92. DOI: 10.1016/S0029-7844(03)00475-7
Source: PubMed


Gestational hypertension and preeclampsia are common disorders during pregnancy, with the majority of cases developing at or near term. The development of mild hypertension or preeclampsia at or near term is associated with minimal maternal and neonatal morbidities. In contrast, the onset of severe gestational hypertension and/or severe preeclampsia before 35 weeks' gestation is associated with significant maternal and perinatal complications. Women with diagnosed gestational hypertension-preeclampsia require close evaluation of maternal and fetal conditions for the duration of pregnancy, and those with severe disease should be managed in-hospital. The decision between delivery and expectant management depends on fetal gestational age, fetal status, and severity of maternal condition at time of evaluation. Expectant management is possible in a select group of women with severe preeclampsia before 32 weeks' gestation. Steroids are effective in reducing neonatal mortality and morbidity when administered to those with severe disease between 24 and 34 weeks' gestation. Magnesium sulfate should be used during labor and for at least 24 hours postpartum to prevent seizures in all women with severe disease. There is an urgent need to conduct randomized trials to determine the efficacy and safety of antihypertensive drugs in women with mild hypertension-preeclampsia. There is also a need to conduct a randomized trial to determine the benefits and risks of magnesium sulfate during labor and postpartum in women with mild preeclampsia.

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    • "Recognition of sensitive, specific, cost-effective, and easy to perform biomarkers would allow not only detection of women at risk of PE, but it would also allow a close surveillance, a precise PE diagnosis and a timely intervention. Because PE can progress rapidly, it requires prompt intervention that may include observation in a tertiary care setting and termination of pregnancy, either by inducing labor or by Cesarean section, which is the only known cure for this condition [5]-[8]. As it affects multiple organs, no single, specific and cost-effective marker to predict PE has yet been proposed [9]. "
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    ABSTRACT: Objective: To assess whether changes in platelet indices, detectable by simple complete blood count (CBC), during pregnancy could be used as markers for prediction of development of preeclampsia (PE). Methods: A total of 2813 pregnant women who received regular antenatal care until delivery were included. Participants were divided into 3 groups: normotensive pregnant women (n = 2621), women with PE without severe features (n = 169), and women with PE with severe features (n = 23). Blood samples were collected during antenatal visits and/or during the period of in-patient hospital stay, and changes in platelet indices were compared among the three groups. Results: Platelet count (PC) was decreasing while mean platelet volume (MPV) and platelet distribution width (PDW) were increasing as PE progressed. Receiver operating characteristics (ROC) curve analysis showed that PDW had the largest area under curve (AUC) [0.980 (95% CI: 0.964-1.000)], making it the best marker for predicting development of PE. Also, PDW showed the most statistically significant correlation with mean arterial pressure (MAP) (r = 0.902, p = 0.000), making it the best marker for predicting severity of hypertension. Conclusion: This study provides evidence that PC decreases while MPV and PDW increase as pregnancy advances, and these changes are more pronounced in PE than normotensive pregnancy. These changes predate development of PE by 2-8 weeks and are proportional to the progress of this disorder. The selected platelet indices, especially PDW, have the potential to be utilized as markers for not only prediction of PE development but also severity of hypertension.
    Open Journal of Obstetrics and Gynecology 10/2015; 5(12):703-712. DOI:10.4236/ojog.2015.512099
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    • "Severe early-onset PE exerts a substantial impact on maternal health and is often associated with fetal complications such as prematurity and low birth weight (Sibai, 2003). "
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    ABSTRACT: Several gap junction connexins have been shown to be essential for appropriate placental development and function. It is known that the expression and distribution of connexins change in response to environmental oxygen levels. The placenta develops under various oxygen levels, beginning at a low oxygen tension of approximately 2% and increasing to a tension of 8% after the onset of the uteroplacental circulation. Moreover, it has been shown that during preeclampsia placentas are subjected to chronic hypoxia. Therefore, we investigated oxygen sensitivity of placental connexins 43 and 46. Using the trophoblast cell line Jar we demonstrated that the expression of connexin43 increased during acute hypoxia but decreased during chronic hypoxia. Chronic hypoxia resulted in the translocation of connexin43 from the membrane to the cytoplasm and in a reduction in its communication properties. In contrast, the expression of connexin46 was down-regulated during chronic hypoxia and was translocated from perinuclear areas to the cell membrane. Hypoxia-inducible factor (HIF) knockdown showed that the translocation of connexin43 but not that of connexin46 was HIF-2α dependent and was mediated by phosphoinositide 3-kinase. The upregulation of connexin43 in combination with the down-regulation of connexin46 was confirmed in placental explants cultivated under low oxygen and in placentas with early-onset preeclampsia. Taken together, in Jar cells placental connexins 43 and 46 are regulated during periods of low oxygen in opposite manners. The oxygen sensing of connexins in the trophoblast may play a role in physiological and pathophysiological oxygen conditions and thus may contribute to preeclampsia. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Cellular Biochemistry 05/2015; 116(12). DOI:10.1002/jcb.25240 · 3.26 Impact Factor
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    • "Currently the preeclampsia management is the pregnancy termination [3] supported by the control of blood pressure and coagulation administrating aspirin and methyldopa [20] however, this strategy does not improve significantly the clinical outcome and their use is associated with several side effects [21]. Even when the management of RAS alterations appears to be a logical choice, given the strong evidence about an excessive AT1 receptor activation during preeclampsia and the studies carried on animal models [22] [23] [24], there is a complete lack of clinical studies testing low doses of Losartan in preeclampsia patients. "
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    ABSTRACT: Preeclampsia affects 2-3% of the pregnancies worldwide and is one of the main causes of maternal death and premature birth. Its first stage is related to the invasion of the maternal decidua and the remodeling of the uterine spiral arteries by the extravillous trophoblast. An enhancement of the systemic and local renin-angiotensin system has been identified in PE patients, and the RAS counter-regulatory kallikrein–kinin system is expressed in extravillous trophoblasts. The aim of the present study was to evaluate the effect of a misbalance provoked by exogenous Angiotensin II (AII) and blockade of the B2R receptor by the non-peptide antagonist Bradyzide (BDZ) on the migratory phenotype and and on invasive capacity of HRT8/SVneo cells, a well accepted trophoblast in vitro model. HTR-8/SVneo cells express Kalicrein, Kininogen, AT1, AT2, B1R and B2R. AII, AII+BDZ and losartan induced marked changes in the length and shape of filopodias. AII and AII+BDZ reduced significantly the number of filopodias, the migration and invasion capacity. Losartan reverted the effect of AII on the number of filopodias and the invasion index. In conclusion an induced disequilibrium between the AT1 and B2R alters morphological and motile characteristics that could explain in part the cellular aspects of the impaired trophoblastic invasion present on preeclampsia and could be a potential treatment target for preeclampsia.
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