ObstetricsAdverse perinatal outcomes are significantly higher in severe gestational hypertension than in mild preeclampsia☆,☆☆,★
Abstract
Objective: The current literature emphasizes increased risk of adverse outcomes in the presence of proteinuria and hypertension. The objective of this study was to compare the frequency of adverse fetal outcomes in women who developed hypertensive disorders with or without proteinuria. Study Design: The study design was a secondary analysis of data from women who had preeclampsia in a previous pregnancy (n = 598) who were enrolled in a multicenter trial of aspirin for the prevention of preeclampsia. The women had no history of chronic hypertension or renal disease and were normotensive at study inclusion. The maternal and perinatal outcome variables assessed were preterm delivery at <37 and <35 weeks of gestation, rate of small-for-gestational-age infants, and abruptio placenta. Data were analyzed by using the chi-square test, and women who remained normotensive or who had mild gestational hypertension were considered as a single group because they had similar outcomes. Results: As compared to mild preeclampsia, women who developed severe gestational hypertension (without proteinuria) had higher rates of both preterm delivery at <37 weeks of gestation and small-forgestational-age infants. In addition, when compared to women with mild preeclampsia, for women with severe gestational hypertension, gestational age and birth weight were significantly lower at delivery (P <.003 for both age and birth weight). Moreover, women who developed severe gestational hypertension had higher rates of preterm delivery at <37 weeks of gestation (54.2% vs 17.8%, P =.001) and at <35 weeks of gestation (25.0% vs 8.4%, P =.0161), and delivery of small-for-gestational-age infants (20.8% vs 6.5%, P =.024) when compared to women who remained normotensive or those who developed mild gestational hypertension. There were no statistically significant differences in perinatal outcomes between the normotensive/mild gestational hypertension and the mild preeclampsia groups. Overall, women who had severe gestational hypertension had increased rates of preterm delivery and delivery of small-for-gestational-age infants than women with mild gestational hypertension or mild preeclampsia. In the presence of severe hypertension, proteinuria did not increase the rates of preterm delivery or delivery of small-for-gestational-age infants. Conclusions: In women who have gestational hypertension or preeclampsia, increased rates of preterm delivery and delivery of small-for-gestational-age infants are present only in those with severe hypertension. In these women, the presence of proteinuria does not influence perinatal outcome. (Am J Obstet Gynecol 2002;186:66-71.)
Section snippets
Study design
This study is a secondary analysis of women with singleton pregnancies who were enrolled in a multicenter randomized trial comparing low-dose aspirin with placebo for the prevention of preeclampsia.11 The trial was designed and conducted by members of the Network of Maternal-Fetal Medicine Units for the National Institutes of Child Health and Human Development. The subjects were women who had preeclampsia in a previous pregnancy and who were considered at high risk for recurrence. At enrollment
Results
Of the 598 women enrolled in the study, 304 were assigned to the aspirin group and 294 were assigned to the placebo group. There were no differences in the rates of preeclampsia between the aspirin and placebo groups (17% vs 19%, P =.47). Of these 598 women, 401 (67.1%) remained normotensive, 66 (11%) had mild gestational hypertension, and 24 (4.0%) had severe gestational hypertension. All 24 women had their urine checked at the time of diagnosis of severe hypertension and were found to have
Comment
Pregnancies complicated by preeclampsia are reported to be associated with high perinatal morbidity and mortality.5, 7 It is unfortunate that minimal information is available about perinatal outcomes in patients with severe gestational hypertension in the absence of proteinuria.10 However, Hauth et al10 investigated the outcome of women who were nulliparous. Therefore, this secondary analysis was designed to evaluate a cohort of women who had preeclampsia in a prior pregnancy and who were
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Cited by (298)
Preeclampsia: Guidelines for clinical practice from the French College of Obstetricians and Gynecologists
2024, Gynecologie Obstetrique Fertilite et SenologieDéterminer les stratégies permettant de réduire la morbidité maternelle et périnatale secondaire à la pré-éclampsie.
Méthodologie GRADE® avec questions formulées sous le format PICO (Patients, Intervention, Comparison, Outcome) et critères de jugement définis a priori et classifiés selon leur importance. Recherche bibliographique extensive: Medline, Cochrane, Embase et Google Scholar. Analyse de la qualité de la preuve (élevée, modérée, basse, très basse) et formulation d’une recommandation (i) forte ou (ii) faible ou (iii) absence de recommandation. Deux tours de relectures de type Delphi avec des relecteurs extérieurs ont été utilisés pour retenir les recommandations faisant consensus.
Une pré-éclampsie est définie par une hypertension artérielle (HTA) systolique ≥ 140 mmHg et/ou diastolique ≥ 90 mmHg associée à une protéinurie ≥ 0,3 g/24 h ou un ratio Protéinurie/Créatininurie ≥ 30 mg/mmol survenant après 20 semaines d’aménorrhée. Les données de la littérature ne montrent pas de bénéfice en termes de santé maternelle ou périnatale à implémenter une définition plus élargie de la pré-éclampsie. La totalité des 31 questions soumises au panel de relecteurs a fait l’objet d’un accord. En population générale, il est recommandé de ne pas réaliser en routine de dépistage précoce de la pré-éclampsie à l’aide d’algorithmes (Recommandation faible, Qualité de la preuve basse), ni de prescrire d’aspirine à faible dose (Recommandation forte, Qualité de preuve très basse) dans le but de réduire la morbidité maternelle ou périnatale, mais d’encourager la pratique d’une activité physique au cours de la grossesse pour réduire le risque de survenue d’une pré-éclampsie (Recommandation forte, Qualité de la preuve basse). En cas de diabète préexistant, de grossesse multiple, d’hypertension artérielle chronique, de pathologie rénale chronique, les données de la littérature sont insuffisantes en nombre et en qualité pour émettre une recommandation quant à l’intérêt de l’aspirine pendant la grossesse pour prévenir la morbidité maternelle ou périnatale (Absence de recommandation, Qualité de la preuve basse). Chez les femmes enceintes ayant un antécédent de pathologie vasculaire placentaire, il est recommandé de prescrire de l’aspirine pour prévenir la morbidité maternelle ou périnatale (Recommandation forte, Qualité de la preuve modérée), à une dose de 100 à 160 mg (Recommandation faible, Qualité de preuve basse), idéalement avant 16 semaines d’aménorrhée, et au plus tard avant 20 semaines d’aménorrhée (Recommandation forte, Qualité de la preuve basse), et de l’arrêter à partir de 36 semaines d’aménorrhée (Recommandation faible, Qualité de la preuve très basse.). Dans une population à risque, il est recommandé de ne pas administrer des HBPM en plus de l’aspirine (Recommandation faible, Qualité de la preuve modérée). En cas de suspicion de pré-éclampsie (Recommandation faible, Qualité de la preuve modérée) et de pré-éclampsie avérée (Recommandation faible, Qualité de la preuve basse), il est recommandé de ne pas utiliser en routine le dosage du PlGF ou du ratio sFLT-1/PlGF dans le seul but de réduire la morbidité maternelle ou périnatale. Dans une population de femmes ayant une pré-éclampsie non sévère, il est recommandé de prescrire un traitement antihypertenseur par voie orale en cas de pression artérielle systolique mesurée entre 140 et 159 mmHg et/ou de pression artérielle diastolique mesurée entre 90 et 109 mmHg à plusieurs reprises et au repos, pour réduire la morbidité maternelle ou périnatale (Recommandation faible, Qualité de la preuve basse). Chez les femmes présentant une pré-éclampsie non sévère, l’induction de naissance entre 34 et 36+6 semaines d’aménorrhée permet de réduire uniquement l’HTA maternelle sévère mais augmente l’incidence de la prématurité modérée. En tenant compte de la balance bénéfices/risques pour la mère et pour l’enfant, il est recommandé de ne pas induire systématiquement la naissance chez les femmes présentant une pré-éclampsie non sévère entre 34 et 36+6 semaines d’aménorrhée (Recommandation forte, Qualité de la preuve élevée). Chez les femmes avec une pré-éclampsie non sévère diagnostiquée entre 37+0 et 41 semaines d’aménorrhée, il est recommandé d’induire la naissance pour réduire la morbidité maternelle (Recommandation forte, Qualité de la preuve basse), et de réaliser une tentative de voie basse en l’absence de contre-indication obstétricale (Recommandation forte, Qualité de la preuve très basse). Chez les femmes ayant un antécédent de pré-éclampsie isolée, il est recommandé de ne pas réaliser de bilan à la recherche d’une thrombophilie héréditaire (Recommandation forte, Qualité de la preuve modérée). En raison du risque élevé de développer une hypertension artérielle chronique à moyen terme et du risque accru de complications cardiovasculaires à long terme, il est recommandé d’informer les femmes ayant présenté une pré-éclampsie de la nécessité d’un suivi médical pour surveiller la pression artérielle et prendre en charge de possibles autres facteurs de risque cardiovasculaires (Recommandation forte, Qualité de la preuve modérée).
Le but de ces recommandations a été de réévaluer la définition de la pré-éclampsie, et de déterminer les stratégies permettant de réduire la morbidité maternelle et périnatale en lien avec la pré-éclampsie, pendant la grossesse mais aussi à distance de l’accouchement. Elles visent à aider dans leur pratique clinique quotidienne les professionnels de santé amenés à informer ou prendre en charge les patientes ayant eu ou ayant une pré-éclampsie. Des documents d’information synthétiques sont également proposés à destination des professionnels et du grand public.
To identify strategies to reduce maternal and neonatal morbidity related to preeclampsia.
The quality of evidence of the literature was assessed following the GRADE® method with questions formulated in the PICO format (Patients, Intervention, Comparison, Outcome) and outcomes defined a priori and classified according to their importance. An extensive bibliographic search was performed on PubMed, Cochrane, EMBASE and Google Scholar databases. The quality of the evidence was assessed (high, moderate, low, very low) and recommendations were formulated as a (i) strong, (ii) weak or (iii) no recommendation. The recommendations were reviewed in two rounds with external reviewers (Delphi survey) to select the consensus recommendations.
Preeclampsia is defined by the association of gestational hypertension (systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg) and proteinuria ≥ 0.3 g/24 h or a Proteinuria/Creatininuria ratio ≥ 30 mg/mmol occurring after 20 weeks of gestation. Data from the literature do not show any benefit in terms of maternal or perinatal health from implementing a broader definition of preeclampsia. Of the 31 questions, there was agreement between the working group and the external reviewers on 31 (100%). In general population, physical activity during pregnancy should be encouraged to reduce the risk of preeclampsia (Strong recommendation, Quality of the evidence low) but an early screening based on algorithms (Weak recommendation, Quality of the evidence low) or aspirin administration (Weak recommendation, Quality of the evidence very low) is not recommended to reduce maternal and neonatal morbidity related to preeclampsia. In women with preexisting diabetes or hypertension or renal disease, or multiple pregnancy, the level of evidence is insufficient to determine whether aspirin administration during pregnancy is useful to reduce maternal and perinatal morbidity (No recommendation, Quality of the evidence low). In women with a history of vasculo-placental disease, low dose of aspirin (Strong recommendation, Quality of the evidence moderate) at a dosage of 100–160 mg per day (Weak recommendation, Quality of the evidence low), ideally before 16 weeks of gestation and not after 20 weeks of gestation (Strong recommendation, Quality of the evidence low) until 36 weeks of gestation (Weak recommendation, Quality of the evidence very low) is recommended. In a high-risk population, additional administration of low molecular weight heparin is not recommended (Weak recommendation, Quality of the evidence moderate). In case of preeclampsia (Weak recommendation, Quality of the evidence low) or suspicion of preeclampsia (Weak recommendation, Quality of the evidence moderate, the assessment of PlGF concentration or sFLT-1/PlGF ratio is not routinely recommended) in the only goal to reduce maternal or perinatal morbidity. In women with non-severe preeclampsia antihypertensive agent should be administered orally when the systolic blood pressure is measured between 140 and 159 mmHg or diastolic blood pressure is measured between 90 and 109 mmHg (Weak recommendation, Quality of the evidence low). In women with non-severe preeclampsia, delivery between 34 and 36+6 weeks of gestation reduces severe maternal hypertension but increases the incidence of moderate prematurity. Taking into account the benefit/risk balance for the mother and the child, it is recommended not to systematically induce birth in women with non-severe preeclampsia between 34 and 36+6 weeks of gestation (Strong recommendation, Quality of evidence high). In women with non-severe preeclampsia diagnosed between 37+0 and 41 weeks of gestation, it is recommended to induce birth to reduce maternal morbidity (Strong recommendation, Low quality of evidence), and to perform a trial of labor in the absence of contraindication (Strong recommendation, Very low quality of evidence). In women with a history of preeclampsia, screening maternal thrombophilia is not recommended (Strong recommendation, Quality of the evidence moderate). Because women with a history of a preeclampsia have an increased lifelong risk of chronic hypertension and cardiovascular complications, they should be informed of the need for medical follow-up to monitor blood pressure and to manage other possible cardiovascular risk factors (Strong recommendation, Quality of the evidence moderate).
The purpose of these recommendations was to reassess the definition of preeclampsia, and to determine the strategies to reduce maternal and perinatal morbidity related to preeclampsia, during pregnancy but also after childbirth. They aim to help health professionals in their daily clinical practice to inform or care for patients who have had or have preeclampsia. Synthetic information documents are also offered for professionals and patients.
Hypertensive Disorders of Pregnancy
2023, Emergency Medicine Clinics of North AmericaContribution of Preterm Birth to Mortality Among Neonates with Birth Defects
2023, Journal of PediatricsTo estimate the proportion of neonatal mortality risk attributable to preterm delivery among neonates with birth defects.
Using a statewide cohort of live born infants from the Texas Birth Defects Registry (1999-2014 deliveries), we estimated the population attributable fraction and 95% CI of neonatal mortality (death <28 days) attributable to prematurity (birth at <37 weeks vs ≥37 weeks) for 31 specific birth defects. To better understand the overall population burden, analyses were repeated for all birth defects combined.
Our analyses included 169 148 neonates with birth defects, of which 40 872 (24.2%) were delivered preterm. The estimated proportion of neonatal mortality attributable to prematurity varied by birth defect, ranging from 12.5% (95% CI: 8.7-16.1) for hypoplastic left heart syndrome to 71.9% (95% CI: 41.1-86.6) for anotia or microtia. Overall, the proportion was 51.7% (95% CI: 49.4-54.0) for all birth defects combined.
A large proportion of deaths among neonates with birth defects are attributable to preterm delivery. Our results highlight differences in this burden across common birth defects. Our findings may be helpful for prioritizing future work focused on better understanding the etiology of prematurity among neonates with birth defects and the mechanisms by which prematurity contributes to neonatal mortality in this population.
Perinatal outcomes of 221,709 singleton and twin pregnancies after the use of donor versus partner sperm
2022, Fertility and SterilityTo study the association of donor sperm on perinatal outcomes of livebirths conceived via in vitro fertilization (IVF) when compared with partner sperm.
Retrospective cohort study
National Human Fertilisation and Embryology Authority assisted reproductive technology registry
All live born singletons and twins conceived through IVF with or without intracytoplasmic sperm injection in the United Kingdom between 1991 and 2016
Donor sperm compared to partner sperm
Perinatal outcomes were assessed. The primary outcomes were preterm and very preterm birth; low, very low, high, and very high birthweight; Secondary outcomes were congenital anomaly and health baby. These were assessed for singletons and twins separately.
For singleton livebirths, compared to partner sperm, those conceived with donor sperm were at reduced odds of very preterm (odds ratio [OR], 0.76; 95% confidence interval [CI], 0.63–0.91; adjusted OR [aOR], 0.80; 95% CI, 0.66–0.96), and preterm (OR, 0.90; 95% CI, 0.83–0.98; aOR, 0.93; 95% CI, 0.85–1.01) birth. For birthweight outcomes, donor sperm showed a reduced odds of low (OR, 0.83; 95% CI, 0.76–0.91; aOR, 0.86; 95% CI, 0.78–0.94) and an increased odds of high (OR, 1.15; 95% CI, 1.07–1.23; aOR, 1.09; 95% CI, 1.01–1.17) birthweight. There was no confirmed difference in the odds ratios of very low (OR, 0.88; 95% CI, 0.74–1.06; aOR, 0.94; 95% CI, 0.78–1.13) or very high (OR, 1.21; 95% CI, 1.04–1.40; aOR, 1.15; 95% CI, 0.98–1.34) birthweight.
Liveborn twins conceived with donor sperm, compared to partner sperm, were at reduced odds of very low (OR, 0.76; 95% CI, 0.66–0.88; aOR, 0.83; 95% CI, 0.72–0.96) and low (OR, 0.87; 95% CI, 0.81–0.93; aOR, 0.91; 95% CI, 0.85–0.98) birthweight. There was a suggestion of a reduced odds of very preterm (OR, 0.81; 95% CI, 0.70–0.95; aOR, 0.86; 95% CI, 0.74–1.01) and preterm (OR, 0.93; 95% CI, 0.86–1.01; aOR, 0.96; 95% CI, 0.88–1.04) birth. There was considerable uncertainty around the ORs for high (OR, 0.73; 95% CI, 0.31–1.72; aOR, 0.72; 95% CI, 0.29–1.80) and very high (OR, 1.02; 95% CI, 0.39–2.67; aOR, 1.34; 95% CI, 0.50–3.60) birthweight.
Although unmeasured confounding remains a possibility, as paternal age, body mass index, and smoking status were unavailable for analysis, women, couples, service providers can be reassured that IVF livebirths conceived with donor sperm have no greater chance of adverse outcomes when compared to partner sperm.
Resultados perinatales de 221,709 embarazos únicos y gemelares después del uso semen donado o semen de pareja.
Estudiar la asociación de semen donado en los resultados perinatales de nacidos vivos concebidos vía fecundación in vitro (IVI comparados con semen de pareja.
Estudio de cohorte retrospectivo.
Registro de la Autoridad Nacional de Fertilización Humana y Embriología.
Todos los nacidos vivos únicos y gemelares concebidos a través de IVF con o sin inyección intracitoplasmática en el Reino Unido entre 1991 y 2006.
Semen donado comparado con semen de pareja.
Se valoró el resultado perinatal. Los resultados primarios fueron parto pretérmino y parto muy pretérmino; pesos bajo, muy bajo, alto y muy alto; resultados secundarios fueron anomalías congénitas y la salud del niño. Todo esto se valoró en embarazos únicos y gemelares por separado.
Para nacidos vivos únicos, comparado con semen de parejas, los que concibieron con semen donado tuvieron menor probabilidad de muy pretérmino (odds ratio [OR], 0.76; 95% intervalo de confianza [CI], 0.63-0.91; OR ajustado [aOR], 0.80;95% CI, 0.66-0.96), y de pretérmino (OR, 0.90; 95% CI, 0.76-0.91; aOR, 0.86; 95% CI, 0.78-0.94) y una probabilidad aumentada de alto (OR, 1.15;95% CI, 1.07-1,23; aOR, 1.09; 95% CI, 1.01-1.17) peso al nacer. No hubo diferencias confirmadas en los odds ratio de muy bajo (OR, 0.88; 95% CI, 0.74-1.06; aOR, 0.94; 95% CI, 0.78-1.13) o de muy alto (OR, 1.21; 95% CI, 1.04-1.40; aOR, 1.15; 95% CI, 0.98-1.34) peso al nacer.
Los gemelos nacidos vivos concebidos con semen donado, comparado con semen de pareja, tuvieron menor probabilidad de muy bajo (OR, 0.76; 95% CI, 0.66-0.88; aOR, 0.83; 95% CI, 0.72-0.96) y bajo (OR, 0.87; 95% CI, 0.81-0.93; aOR, 0.91; 95% CI, 0.85-0.98) peso al nacer. Hubo una sugestión de una probabilidad reducida de nacimientos muy pretérminos (OR, 0.81; 95% CI, 0.70-0.95; aOR, 0.86; 95% CI, 0.74-1.01) y de nacimientos pretérminos (OR, 0.93; 95% CI, 0.86-1.01; aOR, 0.96; 95% CI, 0.88-1.04). Hubo una duda considerable sobre el ORs para pesos al nacer alto (OR, 0.73; 95% CI, 0.31-1.72; aOR, 0.72; 95% CI, 0.29-1.80) y pesos al nacer muy altos (OR, 1.02; 95% CI, 0.39-2.67; aOR, 1.34; 95% CI, 0.50-3.60).
A pesar de las confusiones no medibles es una posibilidad, como edad paterna, índice de masa corporal y tabaquismo no estuvieron disponibles para la análisis, las mujeres, parejas y proveedores de servicio puedes estar confiados que los nacidos vivos por IVF concebidos con semen de donante no tiene mas oportunidades de resultados adversos comparados con semen de pareja.
A comparative analysis of neonatal outcomes in pregnancies complicated by preeclampsia and eclampsia in Ghana
2022, AJOG Global ReportsWorldwide, hypertensive disorders of pregnancy are a serious complication of pregnancy, and contribute to poor maternal and neonatal outcomes. The most significant consequences of hypertensive disorders of pregnancy are observed in sub-Saharan Africa, where neonatal outcomes have not been fully described. Understanding relationships between maternal disease severity and neonatal outcomes can guide patient counseling and allow the targeting of limited resources to the most at-risk neonates.
To describe and compare neonatal outcomes in pregnancies complicated by preeclampsia with severe features and eclampsia.
This study is a secondary analysis of data collected as part of a randomized controlled trial at the Korle-Bu Teaching Hospital in Ghana. Participants were adult pregnant women with preeclampsia with severe features or eclampsia and their neonates. Data include prospectively collected medical and obstetrical history, intrapartum events, and neonatal outcomes. The main outcome of this secondary analysis was a composite of poor neonatal outcomes, defined as 1 or more of the following: stillbirth, very low birthweight (<1500 g), 5-minute Apgar score <7, neonatal intensive care unit admission, or a live birth with a subsequent death before discharge.
Median gestational age at delivery was 36.6 weeks (interquartile range, 33.3–38.9). Median birthweight was 2.3 kg (interquartile range, 1.6–3.0), with 227 (19.0%) birthweights <1500 g. There were 162 neonates (15.5%) with an Apgar score <7 at 5 minutes and 144 (11.9%) were stillbirths. Of live births, half (n=524, 50.3%) were admitted to the neonatal intensive care unit and 7.9% (n=91) died before discharge. A composite of poor neonatal outcomes was experienced by 58.2% (n=707) of neonates and was twice as likely with a maternal diagnosis of eclampsia (odds ratio, 1.91; P=.04). For each additional week of gestational age, the probability of a poor neonatal outcome was reduced by 39% (odds ratio, 0.61; P<.0001).
Poor neonatal outcomes were experienced by more than half of pregnancies complicated by preeclampsia with severe features or eclampsia. Even after controlling for gestational age, pregnancies complicated by eclampsia were twice as likely to have poor neonatal outcomes.
Preeclampsia and eclampsia: the conceptual evolution of a syndrome
2022, American Journal of Obstetrics and GynecologyPreeclampsia, one of the most enigmatic complications of pregnancy, is considered a pregnancy-specific disorder caused by the placenta and cured only by delivery. This article traces the condition from its origins—once thought to be a disease of the central nervous system, recognized by the occurrence of seizures (ie, eclampsia)—to the present time when preeclampsia is conceptualized primarily as a vascular disorder. We review the epidemiologic data that led to the recommendation to use diastolic hypertension and proteinuria as diagnostic criteria, as their combined presence was associated with an increased risk of fetal death and the birth of small-for-gestational-age neonates. However, preeclampsia is a multisystemic disorder with protean manifestations, and the condition can be present even in the absence of hypertension and proteinuria. Toxins gaining access to the maternal circulation have been proposed to mediate the clinical manifestations—hence, the term “toxemia of pregnancy,” which was used for several decades. The search for putative toxins has challenged investigators for more than a century, and a growing body of evidence suggests that products of an ischemic or a stressed placenta are responsible for the vascular changes that characterize this syndrome. The discovery that the placenta can produce antiangiogenic factors, which regulate endothelial cell function and induce intravascular inflammation, has been a major step forward in the understanding of preeclampsia. We view the release of antiangiogenic factors by the placenta as an adaptive response to improve uterine perfusion by modulating endothelial function and maternal cardiovascular performance. However, this homeostatic response can become maladaptive and lead to damage of target organs during pregnancy or the postpartum period. Early-onset preeclampsia has many features in common with atherosclerosis, whereas late-onset preeclampsia seems to result from a mismatch of fetal demands and maternal supply, that is, a metabolic crisis. Preeclampsia, as it is understood today, is essentially vascular dysfunction unmasked or caused by pregnancy. A subset of patients diagnosed with preeclampsia are at greater risk of the subsequent development of hypertension, ischemic heart disease, heart failure, vascular dementia, and end-stage renal disease. However, these adverse events may be the result of a preexisting vascular pathologic process; it is not known if the occurrence of preeclampsia increases the baseline risk. Therefore, the understanding, prediction, prevention, and treatment of preeclampsia are healthcare priorities.
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Supported by grants (HD 19897, HD21410, HD 21414, HD 21434, HD 27860, HD 27861, HD 27869, HD 27883, HD 27889, HD 27905, HD 27915, and HD 27917) from the National Institute of Child Health and Human Development.
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*A complete list of members of the Network and their institutional affiliations appears at the end of this article.
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Reprint requests: Baha M. Sibai, MD, Professor and Chairman, Department of Obstetrics and Gynecology, University of Cincinnati Medical Center, PO Box 670526, Cincinnati, OH 45267-0526.