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PubMed2006

Serum and urine inhibin A but not free activin A are endocrine biomarkers of severe pre-eclampsia.

OBJECTIVE: Elevation of total serum inhibin A and activin A has been interpreted as evidence of placental dysfunction in women who develop pre-eclampsia. We sought to evaluate serum and urine levels of inhibin A and free activin A in normal and hypertensive pregnancies. STUDY DESIGN: Inhibin A and free activin A were measured by immunoassay in simultaneously collected serum and urine samples from 75 women: (1) severe pre-eclampsia (n = 30); (2) mild pre-eclampsia (n = 11); (3) chronic hypertension (n = 9); (4) pregnant control women (n = 16); and (5) nonpregnant control women (n = 9). Urine levels were normalized to milligrams urine creatinine, and fractional excretions were calculated. RESULTS: Serum and urine inhibin A were increased and fractional excretion was decreased in pregnancy. Serum, urine, and fractional excretion of inhibin A were increased in severe pre-eclampsia, compared with other gravidas. The only difference observed in free activin A was a decrease in serum free activin A in chronic hypertension, compared with severe pre-eclampsia and pregnant control women. Urine inhibin A showed the greatest discrimination between severe pre-eclampsia and pregnant control women: a cut-off of 45 pg/mg urine creatinine had 96.8% sensitivity, 87.5% specificity, and 93.6% accuracy. Women with urine inhibin A greater than 90 pg/mg urine creatinine had a 17-fold relative risk (95% confidence interval 9.7-459.5) of a clinically indicated delivery due to pre-eclampsia. CONCLUSION: Serum and urine levels of inhibin A are altered in severe pre-eclampsia. Urine inhibin A may have application in the diagnosis and management of pre-eclampsia. Those with chronic hypertension have lower serum but not urine free activin A levels, compared with severe pre-eclampsia and mild pre-eclampsia.

Activins↗
PubMed2006

Placental ischaemia is a consequence rather than a cause of pre-eclampsia.

The aetiology or pre-eclampsia remains unknown, but it is widely accepted that the disorder is placental in origin. Failed trophoblast invasion of the maternal spiral arteries is accepted to be a central pathogenetic mechanism. However, the concept of failed trophoblast invasion is based on an assumption rather than direct scientific observation and there are other likely explanations for this phenomenon. The criteria for disease causation, such as the Bradford-Hill criteria are central to the ascertainment of causal relationships in modern medicine and these criteria are used here to assess the relationship between the placenta and pre-eclampsia. There is a strong association between pre-eclampsia and small (rather than large) placentas and an appropriate dose-response relationship does not exist. Failed trophoblast invasion of the spiral arteries is not specific to pre-eclampsia and occurs in other pregnancy complications and in up to 40% of biopsies from normal pregnancies and the relationship between placental ischaemia and pre-eclampsia is very inconsistent. A placental cause for pre-eclampsia is not consistent with the pathogenesis of other pregnancy complications like gestational diabetes mellitus. If pre-eclampsia was a disease of trophoblast origin, the risk of the disease should be determined by trophoblast rather than maternal factors. However, evidence from assisted reproduction shows that the risk of a woman developing pre-eclampsia is almost entirely dependent on maternal factors and independent of the embryo from which the placenta develops. There is currently no plausible proven mechanism by which the placenta causes pre-eclampsia. The syndrome typically gets worse, and can arise de-novo after the placenta has been removed, calling into question the role of the placenta in its causation. Uterine artery ligation in humans, unlike in animal experiments, is not associated with an increased incidence of pre-eclampsia, calling into question the role of poor utero-placental perfusion in the cause of the disease in humans. The signals that initiate maternal adaptive responses during pregnancy come from or through the placenta into the maternal milieu but as is the case with gestational diabetes mellitus, are not necessarily the cause of maternal disease. Pre-eclampsia causes renal, hepatic, myocardial, cerebral and adrenal ischaemia--that is ischaemia in all highly vascular organs. Placental ischaemia, like ischaemia in all other organs, is a consequence rather than a causal factor in the development of the syndrome and this has profound consequences for research strategies.

Female↗
PubMed2006

Eclampsia in Dar es Salaam, Tanzania -- incidence, outcome, and the role of antenatal care.

BACKGROUND: In order to assess the effectiveness of antenatal care for prevention of eclampsia, a retrospective case-control study was performed at the Muhimbili National Hospital (MNH), Dar es Salaam, Tanzania. All women with eclampsia seen at MNH during 1999-2000 and controls without eclampsia were included. METHODS: The study used a labor ward database and antenatal cards of eclamptic women and non-eclamptic controls. For each of the 741 eclamptic women who delivered at MNH, two non-eclamptic controls were chosen from the database. For 399 of the eclampsia cases and 420 non-eclamptic controls, the antenatal records could be traced and compared. Main outcome measures. Maternal and perinatal mortality, detection of antenatal risk factors, appropriate referrals, and incidence of eclampsia. RESULTS: Hospital and population-based incidences of eclampsia were 200/10,000 and 67/10,000, respectively. The case-fatality rate for eclampsia was 5.0% for women who delivered at MNH and 16% for those referred to MNH after being delivered elsewhere. The risk of low birth weight and perinatal death was significantly increased in eclamptic women (odds ratio = 6 and 10, respectively). The screening coverage for signs of pre-eclampsia was >85%, except for proteinuria (33%). Fewer than 50% of the women who developed eclampsia had been referred from the ANC clinic and <10% were admitted to the antenatal ward at MNH before onset of eclamptic fits. CONCLUSIONS: The current practice of antenatal care is insufficient as a prevention strategy for eclampsia in a low-resource setting with high incidence of eclampsia.

Delivery, Obstetric↗
PubMed2005

Plasma soluble vascular endothelial growth factor receptor-1 concentration is elevated prior to the clinical diagnosis of pre-eclampsia.

OBJECTIVE: Accumulating evidence suggests that the balance between vascular endothelial growth factor (VEGF), placental growth factor (PIGF), and their receptors is important for effective vasculogenesis, angiogenesis, and placental development. Recently, the soluble form of VEGFR-1 (sVEGFR-1), an antagonist to VEGF and PIGF, has been implicated in the pathophysiology of pre-eclampsia. Plasma sVEGFR-1 concentration is elevated in pre-eclampsia at the time of clinical diagnosis and correlates with the severity of the disease. The purpose of this study was to determine whether the concentrations of sVEGFR-1 in plasma of pre-eclamptic patients change prior to the clinical manifestations of the disease. METHODS: A longitudinal case-control study was conducted in normal pregnant women (n = 44) and patients with pre-eclampsia (n = 44). Blood sampling was performed at six intervals: (1) 7-16 weeks; (2) 16-24 weeks; (3) 24-28 weeks; (4)28-32 weeks; (5) 32-36 weeks; and (6) more than 37 weeks of gestation. To examine the relationship between plasmasVEGFR-1 concentration and interval to clinical diagnosis of pre-eclampsia, plasma samples of pre-eclamptic patients at different gestational ages were stratified according to the interval from blood sampling to clinical development of the disease into five groups: (1) at clinical manifestation; (2) 2-5 weeks; (3) 6-10 weeks; (4) 11-16 weeks; and (5) 17-25 weeks before clinical manifestations. Plasma concentrations of sVEGFR-1 were determined by enzyme-linked immunoassay. Parametric statistics and repeated measure procedures were used for the analysis. RESULTS: The mean plasma sVEGFR-1 concentration in pre-eclamptic patients before the clinical manifestation of the disease was significantly higher than in normal pregnant women at 24-28, 28-32, and 32-37 weeks of gestation (p = 0.02,p < 0.001, and p < 0.001, respectively). In contrast, no significant differences in the mean plasma sVEGFR-1 concentration between patients with pre-eclampsia and normal pregnant women were observed both at 7-16 weeks and 16-24 weeks of gestation (p= 0.1 and p= 0.9). Similarly, the mean plasma sVEGFR-1 concentration was significantly higher in pre-eclamptic patients than in normal pregnant women at clinical manifestation, at 2-5 weeks (mean 3.8 weeks), and at 6-10 weeks (mean 8.2 weeks) prior to the development of clinical pre-eclampsia (p < 0.001, p < 0.001, and p = 0.002,respectively). Among patients with early-onset pre-eclampsia (defined as gestational age of 34 weeks or less), the mean plasma sVEGFR-1 concentration was significantly higher in pre-eclampsia (before clinical diagnosis) than in normal pregnant women at 24-28 (mean 26.4) weeks of gestation (p = 0.008). In contrast, among patients with the late-onset disease(defined as gestational age of more than 34 weeks), plasma sVEGFR-1 concentration in pre-clinical pre-eclampsia was significantly higher than in normal pregnant women at 28-32 (mean 30.2) weeks of gestation (p < 0.001). CONCLUSIONS: Plasma sVEGFR-1 concentration is elevated in pre-eclampsia prior to the clinical diagnosis of the disease. This elevation began 6-10 weeks prior to the clinical manifestations, and the increase was more pronounced at 2-5 weeks before the diagnosis, as well as at clinical presentation. Furthermore, in early-onset pre-eclampsia, plasma concentration ofsVEGFR-1 is elevated earlier than the late-onset disease.

Adult↗
PubMed1994

The definition of pre-eclampsia.

BACKGROUND: Redman and Jefferies have proposed a revised definition of pre-eclampsia which is based on absolute blood pressure levels and an increment from the baseline in the first half of pregnancy. There is no requirement for proteinuria. This definition should facilitate the distinction between nonproteinuric pre-eclampsia and other causes of nonproteinuric gestational hypertension, such as chronic essential hypertension. OBJECTIVES: 1. To determine whether the blood pressure criteria of Redman and Jefferies can select women with characteristics of pre-eclampsia from the group of women with gestational hypertension by the current criteria of the International Society for the Study of Hypertension in Pregnancy (ISSHP). 2. To determine the level of agreement between the classification system proposed by Redman and Jefferies and that of the ISSHP. DESIGN: A prospective study. SETTING: Obstetric unit, Dudley Road Hospital, Birmingham, UK. SUBJECTS: Six hundred and ninety-two healthy nulliparous women and 11 women with chronic hypertension antedating pregnancy. MAIN OUTCOME MEASURES: 1. Differences in maternal characteristics and obstetric outcome among women with gestational (nonproteinuric) hypertension by the ISSHP criteria, meeting (and failing to meet) the Redman and Jefferies' blood pressure criteria. 2. The proportion of women classified as normal, proteinuric pre-eclampsia, and chronic hypertension on the basis of both Redman and Jefferies' criteria and the current ISSHP criteria. RESULTS: There were 55 women with gestational hypertension alone by the ISSHP criteria, of whom 33 met Redman and Jefferies' blood pressure criteria for pre-eclampsia. This group of 33 women had characteristics of nonproteinuric pre-eclampsia, compared with the remaining 22 women in the ISSHP gestational hypertension category who had characteristics of chronic hypertension. The group of 33 were significantly younger and less obese, had significantly lower blood pressure at their first antenatal visit and their obstetric outcome was poorer. The Redman and Jefferies' blood pressure criteria identified as normal 99.5% (95% CI, 98.6% to 99.9%) of women who were also characterised as normal on the basis of the ISSHP criteria (622/625). There were 12 women with proteinuric pre-eclampsia by the ISSHP criteria of whom 11 (92%; 95% CI, 62% to 99.8%) met Redman and Jefferies' blood pressure criteria for pre-eclampsia. None of the 11 women with chronic hypertension antedating pregnancy met these criteria. CONCLUSIONS: In this population the blood pressure criteria for pre-eclampsia proposed by Redman and Jefferies select women with features of pre-eclampsia (i.e., proteinuria and relatively poor outcome) and, in particular, they enable a distinction to be made between nonproteinuric pre-eclampsia and other causes of gestational hypertension.

Adult↗
PubMed2001

Long term mortality of mothers and fathers after pre-eclampsia: population based cohort study.

OBJECTIVE: To assess whether mothers and fathers have a higher long term risk of death, particularly from cardiovascular disease and cancer, after the mother has had pre-eclampsia. DESIGN: Population based cohort study of registry data. SUBJECTS: Mothers and fathers of all 626 272 births that were the mothers' first deliveries, recorded in the Norwegian medical birth registry from 1967 to 1992. Parents were divided into two cohorts based on whether the mother had pre-eclampsia during the pregnancy. Subjects were also stratified by whether the birth was term or preterm, given that pre-eclampsia might be more severe in preterm pregnancies. MAIN OUTCOME MEASURES: Total mortality and mortality from cardiovascular causes, cancer, and stroke from 1967 to 1992, from data from the Norwegian registry of causes of death. RESULTS: Women who had pre-eclampsia had a 1.2-fold higher long term risk of death (95% confidence interval 1.02 to 1.37) than women who did not have pre-eclampsia. The risk in women with pre-eclampsia and a preterm delivery was 2.71-fold higher (1.99 to 3.68) than in women who did not have pre-eclampsia and whose pregnancies went to term. In particular, the risk of death from cardiovascular causes among women with pre-eclampsia and a preterm delivery was 8.12-fold higher (4.31 to 15.33). However, these women had a 0.36-fold (not significant) decreased risk of cancer. The long term risk of death was no higher among the fathers of the pre-eclamptic pregnancies than the fathers of pregnancies in which pre-eclampsia did not occur. CONCLUSIONS: Genetic factors that increase the risk of cardiovascular disease may also be linked to pre-eclampsia. A possible genetic contribution from fathers to the risk of pre-eclampsia was not reflected in increased risks of death from cardiovascular causes or cancer among fathers.

Cardiovascular Diseases↗
PubMed1999

Eclampsia in Finland in 1990-1994.

BACKGROUND: Eclampsia is a serious threat to both maternal and fetal well-being. We started the present study because no recent data are available on the incidence of eclampsia and the outcome of patients with this serious disorder in Finland. METHODS: The incidence of eclampsia in Finland in 1990-1994 was studied retrospectively. The data were retrieved from the National Birth Register and the Finnish Hospital Discharge Register. Patient records were reviewed. RESULTS: Seventy-seven cases of eclampsia were found in the hospital records, which gave an eclampsia incidence of 2.4 per 10,000 deliveries (95% confidence intervals 1.9 to 2.9). Eclampsia was preceded by severe pre-eclampsia in 84% and by mild pre-eclampsia in 8% of the patients. Ten mothers suffered from severe eclampsia-related complications but, fortunately, none of the mothers died. Perinatal mortality was 5%, and 33% of the newborns were small for gestational age. CONCLUSIONS: Eclampsia is rare in Finland. Its low incidence is probably due to improved neonatal care that allows earlier deliveries before the progress of preeclampsia to eclampsia.

Adolescent↗
PubMed2005

[Associated factors of pre-eclampsia complicated in pregnant women with abnormal glucose metabolism].

OBJECTIVE: To investigate the incidence and associated factors of pre-eclampsia in women with abnormal glucose metabolism in pregnancy. METHODS: A retrospective study was conducted on 1202 pregnant women with abnormal glucose metabolism who delivered their babies in our hospital between 1981-2003. All women were divided into 2 groups: group I included 151 women with pre-eclampsia; group II consisted of 1050 women without pre-eclampsia. The risk factors of pre-eclampsia were analyzed. RESULTS: (1) The incidence of pre-eclampsia was 12.6% as a whole and was 34.8% (39/112), 11.8% (89/753) and 6.8% (23/337) in diabetes mellitus (DM), gestational diabetes mellitus (GDM) and gestational impaired glucose tolerance (GIGT) groups, respectively (P < 0.01). (2) The average pre-pregnant body mass index (BMI), the gestational age at the presence of elevated blood glucose and the parity in group I were significantly different from that of group II [(31 +/- 4) kg/m(2) vs (29 +/- 4) kg/m(2), P = 0.027; (27 +/- 11) weeks vs (30 +/- 7) weeks, P = 0.001; (1.0 +/- 0.6) vs (0.8 +/- 0.6), P = 0.01]. No difference was shown in these two groups in maternal age and gravida. (3) The incidence of pre-eclampsia was increased in women who had poor obstetric history and chronic hypertension (18.5% vs 11.6%, 41.9% vs 11.5%, P = 0.03, 0.000). (4) In group I, the glucose level of glucose challenge test (GCT), oral glucose tolerance test (OGTT, fasting, 2 hr and 3 hr) and the hemoglobin A(1)c (HbA(1)c) value were all higher than those of group II (P = 0.002, 0.000, 0.009, 0.001, 0.004, respectively). (5) Those with insulin treatment had a rate of 15.6% of pre-eclampsia, which was higher than those with diet control (9.9%, P = 0.009), and the glucose not well controlled women had a higher rate of pre-eclampsia than the well controlled ones (17.0% vs 10.0%, P = 0.000). (6) Logistic regression analysis showed that the independent risk factors of pre-eclampsia were pregnant women with chronic hypertension and the level of HbA(1)c. CONCLUSIONS: Types of abnormal glucose metabolism have significant effect on the incidence of pre-eclampsia. The occurrence of pre-eclampsia in these women is closely related to the plasma glucose level at GDM diagnosis and how well the maternal glucose level is controlled.

Adult↗
PubMed2006

[Expression of netrin-1 in placenta from patients with pre-eclampsia and the relation to placental angiogenesis].

OBJECTIVE: To investigate the expression of netrin-1 in placenta from patients with pre-eclampsia and the relation to placental angiogenesis. METHODS: Twenty patients with pre-eclampsia (12 mild cases and 8 severe cases) and 20 normal late pregnant women were investigated. The expression of netrin-1 mRNA and protein was determined with RT-PCR and Western blotting respectively. The placenta vascular density was examined by immunohistochemical F8 staining. RESULTS: (1) The values of netrin-1 mRNA in normal group and pre-eclampsia groups were 0.51 +/- 0.08 and 0.41 +/- 0.06; The values of netrin-1 protein in normal group and pre-eclampsia groups were 26.4 +/- 1.8 and 20.5 +/- 1.3 (P < 0.01). The values of netrin-1 mRNA in mild and severe pre-eclampsia groups were 0.48 +/- 0.08 and 0.34 +/- 0.07; The values of netrin-1 protein in mild and severe pre-eclampsia groups were 22.8 +/- 1.3 and 18.2 +/- 1.0 (P < 0.01). (2) The placenta vascular density in pre-eclampsia (54 +/- 8) was significantly reduced than in normal group (65 +/- 10) (P < 0.01); the decrease was even more obvious in severe group (48 +/- 7) than in mild group (60 +/- 9) (P < 0.01). (3) There was positive correlation between the expression of netrin-1 mRNA and protein and placenta vascular density in normal pregnancy (r = 0.67 and 0.71, P < 0.01), as well as in pre-eclampsia group (r = 0.61 and 0.70, P < 0.01), in mild pre-eclampsia group (r = 0.69 and 0.73, P < 0.01), and in severe pre-eclampsia group (r = 0.71 and 0.75, P < 0.01). CONCLUSION: The study shows that the decrease of netrin-1 in placenta of patients with pre-eclampsia is one of the possible reasons for the reduction of placenta vascular density.

Adult↗
PubMed1998

Dietary risk factors for pre-eclampsia among women attending Harare Maternity Hospital, Zimbabwe.

OBJECTIVE: To identify specific foods that predispose Zimbabwean women to a higher or lower risk of pre-eclampsia and/or eclampsia. DESIGN: A case control study was implemented. Participants were asked by questionnaire to recall the specific amounts of meats, poultry, fruits, fish, vegetables and dairy products they had consumed in the month prior to giving birth. SETTING: Harare Maternity Hospital, Harare, Zimbabwe between June of 1995 and April of 1996. SUBJECTS: 180 women clinically diagnosed with pre-eclampsia (144) or eclampsia (36), and 194 normotensive women without these conditions. MAIN OUTCOME MEASURES: Pre-eclampsia/eclampsia. RESULTS: There were few associations between consumption of specific food items and the occurrence of pre-eclampsia/eclampsia. Meat and fruit were the only foods found to be significantly associated with pre-eclampsia. Women who consumed 12 or more servings of meat per month were more likely to have pre-eclampsia/eclampsia when compared to women eating 11 servings of meat or less per month. While intake of bananas and mangos was unrelated to risk, women who consumed other fruits (i.e. apples, oranges, grapes, peaches, apricots, paw paw, and plums), were 1.7 (95% CI = 1.0 to 3.1) times more likely to develop pre-eclampsia/eclampsia as women who ate none of these fruits. However, women who consumed relatively large quantities of these fruits were not at a particularly high risk. Increased consumption of kapenta was modestly associated with a decrease in disease risk, but this finding was well within the limits of chance and no association was present with intake of other types of fish. CONCLUSIONS: Our findings suggest that variation in consumption of specific foods do not have a strong effect on the incidence of pre-eclampsia in this population. However, further research involving the use of a more comprehensive dietary measure, biochemical measurements of nutrients, pre-pregnancy assessment and ascertainment of dietary intake prior to the development of pre-eclampsia are needed.

Adult↗
PubMed2006

Endothelial nitric oxide synthase gene polymorphism (Glu298Asp) and development of pre-eclampsia: a case-control study and a meta-analysis.

BACKGROUND: Pre-eclampsia is thought to have an important genetic component. Recently, pre-eclampsia has been associated in some studies with carriage of a common eNOS gene Glu298Asp polymorphism, a variant that leads to the replacement of glutamic acid by aspartic acid at codon 298. METHOD: Healthy women with singleton pregnancies were recruited from 7 district general hospitals in London, UK. Women at high risk of pre-eclampsia were screened by uterine artery Doppler velocimetry at 22-24 weeks of gestation and maternal blood was obtained to genotype the eNOS Glu298Asp polymorphism. Odds ratios (OR) and 95%CI, using logistic regression methods, were obtained to evaluate the association between the Glu298Asp polymorphism and pre-eclampsia. A meta-analysis was then undertaken of all published studies up to November 2005 examining the association of eNOS Glu298Asp genotype and pre-eclampsia. RESULTS: 89 women with pre-eclampsia and 349 controls were included in the new study. The Glu298Asp polymorphism in a recessive model was not significantly associated with pre-eclampsia (adjusted-OR: 0.83 [95%CI: 0.30-2.25]; p = 0.7). In the meta-analysis, under a recessive genetic model (1129 cases & 2384 controls) women homozygous for the Asp298 allele were not at significantly increased risk of pre-eclampsia (OR: 1.28 [95%CI: 0.76-2.16]; p = 0.34). A dominant model (1334 cases & 2894 controls) was associated with no increase of risk of pre-eclampsia for women carriers of the Asp298 allele (OR: 1.12 [95%CI: 0.84-1.49]; p = 0.42). CONCLUSION: From the data currently available, the eNOS Glu298Asp polymorphism is not associated with a significant increased risk of pre-eclampsia. However, published studies have been underpowered, much larger studies are needed to confirm or refute a realistic genotypic risk of disease, but which might contribute to many cases of pre-eclampsia in the population.

Journal Article↗
PubMed2000

Antiplatelet agents for preventing and treating pre-eclampsia.

BACKGROUND: Pre-eclampsia is associated with deficient intravascular production of prostacyclin, a vasodilator, and excessive production of thromboxane, a platelet-derived vasoconstrictor and stimulant of platelet aggregation. These observations led to the hypotheses that antiplatelet agents, and low dose aspirin in particular, might prevent or delay the development of pre-eclampsia. OBJECTIVES: To assess the effectiveness and safety of antiplatelet agents when given to women at risk of developing pre-eclampsia, and to those with established pre-eclampsia. SEARCH STRATEGY: This review drew on the search strategy developed for the Pregnancy and Childbirth Group as a whole. The Cochrane Controlled Trials Register was also searched, The Cochrane Library 1999 Issue 1, Embase was searched from 1994-1999 and hand searches were performed of the congress proceedings of the International and European Societies for the Study of Hypertension in Pregnancy. SELECTION CRITERIA: All randomised trials comparing antiplatelet agents with either placebo or no antiplatelet agent during pregnancy. Quasi random study designs were excluded. Participants were pregnant women considered to be at risk of developing pre-eclampsia, and those with pre-eclampsia before delivery. Women treated postpartum were excluded. Interventions were any comparisons of an antiplatelet agent (such as low dose aspirin or dipyridamole) with either placebo or no antiplatelet agent. DATA COLLECTION AND ANALYSIS: Assessment of trials for inclusion in the review and extraction of data was performed independently and unblinded by two reviewers. Data were entered into the Review Manager software and double checked. MAIN RESULTS: Forty two trials involving over 32,000 women were included in this review, with 30,563 women in the prevention trials. There is a 15% reduction in the risk of pre-eclampsia associated with the use of antiplatelet agents [32 trials with 29,331 women; relative risk (RR) 0.85, 95% confidence interval (0.78, 0.92); Number needed to treat (NNT) 89, (59, 167)]. This reduction is regardless of risk status at trial entry or whether a placebo was used, and irrespective of the dose of asprin or gestation at randomisation. Twenty three trials (28,268 women) reported preterm delivery. There is a small (8%) reduction in the risk of delivery before 37 completed weeks [RR 0.92, (0.88, 0.97); NNT 72 (44, 200)]. Baby deaths were reported in 30 trials (30,093 women). Overall there is a 14% reduction in baby deaths in the antiplatelet group [RR 0.86, (0. 75, 0.98); NNT 250 (125, >10000)]. Small for gestational age babies were reported in 25 trials (20,349 women), with no overall difference between the groups, RR 0.92, (0.84, 1.01). There were no significant differences between treatment and control groups in any other measures of outcome. Five trials compared antiplatelet agents with placebo or no antiplatelet agent for the treatment of pre-eclampsia. There are insufficient data for any firm conclusions about the possible effects of these agents when used for treatment of pre-eclampsia. REVIEWER'S CONCLUSIONS: Antiplatelet agents, in this review largely low dose aspirin, have small-moderate benefits when used for prevention of pre-eclampsia. Further information is required to assess which women are most likely to benefit, when treatment should be started, and at what dose.

Aspirin↗
PubMed2000

Eclampsia. VIII. Risk factors for maternal morbidity.

OBJECTIVE: This study was undertaken to identify risk factors associated with adverse maternal outcome in pregnancies complicated by eclampsia. STUDY DESIGN: This was a descriptive study of 399 consecutive women with eclampsia whose cases were managed at one perinatal center between August 1977 and July 1998. Data were collected. Risk factors studied included maternal age, race, parity, preexisting medical complications, and clinical and laboratory findings. Outcome variables were maternal morbidities. Data were analyzed by either chi(2) analysis or the unpaired Student t test as appropriate. RESULTS: In the entire cohort of women with eclampsia major maternal complications included abruptio placentae (10%), HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome (11%), disseminated intravascular coagulopathy (6%), neurologic deficits and aspiration pneumonia (7%), pulmonary edema (5%), cardiopulmonary arrest (4%), acute renal failure (4%), and death (1%, n = 2 patients with antepartum onset). Women with antepartum eclampsia had significantly higher incidences of abruptio placentae (12% vs 6%; P <.05) and HELLP syndrome (14% vs 4%; P =. 005) than did those in whom eclampsia developed post partum. In contrast, women with postpartum eclampsia were more likely to have neurologic deficits develop (9% vs 2%; P =.0006) than were those with antepartum eclampsia. In addition, women in whom eclampsia developed at </=32 weeks' gestation had significantly higher incidences of abruptio placentae (17% vs 8%; P =.01), HELLP syndrome (20% vs 7%; P =.0005), and acute renal failure (8% vs 2%; P =.01) than did those in whom eclampsia developed later. CONCLUSION: Eclampsia remains a significant complication of pregnancy that carries high maternal mortality and morbidity rates. Antepartum onset carries greater risks, and onset at </=32 weeks' gestation is particularly dangerous to both mother and fetus.

Adult↗
PubMed1997

Activin A and inhibin A as possible endocrine markers for pre-eclampsia.

BACKGROUND: Inhibin A and activin A are produced by the placenta during human pregnancy. This study aimed to measure circulating concentrations of inhibin A, pro alpha C-containing inhibins, and activin A in the serum of women with pre-eclampsia and of healthy matched control pregnant women, and to establish the molecular-weight forms of circulating inhibin A and activin A in pre-eclampsia. METHODS: In a retrospective cross-sectional study, blood samples were taken from 20 women in hospital with established pre-eclampsia, and from 20 control pregnant women attending antenatal clinics, who were matched for duration of gestation (pre-eclampsia mean 29.15 [SD 3.75] weeks; controls 29.30 [3.93] weeks), parity, and maternal age. Serum samples were analysed for inhibin A, inhibin B, pro alpha C, and activin A. Pooled samples of control (n = 3) and pre-eclampsia serum (n = 3) subsequently underwent fast protein liquid chromatographic analysis to assess the molecular-weight forms of inhibin A and activin A. Results are expressed as mean and SD for all variables measured. FINDINGS: Serum concentrations of inhibin A, activin A, and pro alpha C were significantly higher in pre-eclampsia than in control normal pregnancy (inhibin A 3.05 [1.8] vs 0.36 [0.14] ng/mL, p < 0.001; activin A 38.08 [25.88] vs 3.95 [2.32] ng/mL, p < 0.001; pro alpha C-containing inhibins 2.2 [0.81] vs 0.71 [0.33] ng/mL, p < 0.001). Inhibin B concentrations in maternal serum were not increased. Molecular-weight forms of inhibin A (32 kDa) and activin A (> 100 kDa) were similar in pre-eclampsia and normal pregnancy. The mean concentrations of hCG were 59.05 [43.98] and 16.3 [8.72] ng/mL, respectively. INTERPRETATION: Higher maternal serum concentrations of inhibin A, pro alpha C, and total activin A in pre-eclampsia than in control pregnancies could be helpful in the diagnosis of pre-eclampsia. These changes are interpreted as further evidence for trophoblast dysfunction in pre-eclampsia.

Activins↗
PubMed2002

Late postpartum eclampsia: a preventable disease?

OBJECTIVE: The purpose of this study was to determine whether there is a shift in the timing of eclampsia in relation to delivery and whether traditional symptoms precede impending postpartum eclampsia. STUDY DESIGN: A multicenter analysis of data from patients with eclampsia from March 1996 through February 2001 at the University of Cincinnati, the University of Tennessee, Memphis, and Central Baptist Hospital, Lexington. Data were collected regarding the relationship of the patient's first seizure to delivery, prodromal symptoms, neuroimaging studies, use of magnesium sulfate, antihypertensive therapy, and follow-up medical care. The analysis focused on women who had late postpartum eclampsia. RESULTS: During the study period, 89 patients were diagnosed with eclampsia. Twenty-nine women (33%) had postpartum eclampsia, of whom 23 women (79%) had late onset (>48 hours). Interestingly, only 5 of these 23 women (22%) had been previously diagnosed with preeclampsia. Twenty-one patients (91%) with late postpartum eclampsia had at least 1 prodromal symptom, and 12 patients (52%) had >1 symptom that heralded the seizure: 20 women (87%) had headache; 10 women (44%) had visual changes; 5 women (22%) had nausea or vomiting; and 2 women (9%) experienced epigastric pain. Only 7 of these 21 women (33%) sought care for their symptoms, of whom 6 women (86%) had clinical evidence of preeclampsia that was not considered by the treating physician. Among all patients with eclampsia, there were 7 cases of aspiration pneumonia, 3 cases of pulmonary edema, 3 cases of pleural effusion, 2 cases of disseminated intravascular coagulation, and no cases of maternal death. CONCLUSION: Current obstetric treatment in the United States has resulted in a shift of eclampsia toward the postpartum period, with most cases being seen as late post partum. To reduce the rate of late postpartum eclampsia, efforts should be directed to the education of the health care providers and patients regarding the importance of prompt reporting and evaluation of symptoms of preeclampsia during the postpartum period.

Eclampsia↗
PubMed2000

Serum inhibin A and activin A are elevated prior to the onset of pre-eclampsia.

Serum inhibin A and activin A concentrations increase in pre-eclampsia. We investigated the time courses of the changes in relation to the onset of the maternal syndrome and if their measurement could be useful for clinical prediction particularly in relation to early onset disease, the most severe of the clinical presentations. Serial samples were taken from 1496 healthy nulliparae. Changes in activin A and inhibin A were analysed in women with: early onset pre-eclampsia (n = 11), pre-eclampsia delivering at 34-36 weeks (n = 14), term pre-eclampsia (n = 25) and gestational hypertension (n = 25); and in a subset with uncomplicated pregnancies (n = 25). Serum inhibin A and activin A were increased in all groups prior to pre-eclampsia, before 20 weeks in those with early onset pre-eclampsia. Screening efficacy was determined at 15-19 and 21-25 weeks in all women who developed pre-eclampsia (n = 70) and randomly selected controls (n = 240). Predictive sensitivities were low (16-59%) but much better for early onset pre-eclampsia: 67 and 44% at 15-19 weeks and 89 and 89% at 21-25 weeks for inhibin A and activin A respectively. Hence, serum inhibin A and activin A concentrations increase before the onset of pre-eclampsia at gestational ages that depend on when pre-eclampsia develops. On their own such measures are unlikely to prove efficient for screening.

Activins↗
PubMed2001

Higher risk of pre-eclampsia after change of partner. An effect of longer interpregnancy intervals?

Epidemiologic studies have shown that pre-eclampsia is mainly a disease of first pregnancy, possibly associated with primipaternity. The interpregnancy interval, which is strongly associated with change of partner, has received little attention. In this study, based on Danish hospital records, we evaluated whether the interpregnancy interval may confound or modify the paternal effect on pre-eclampsia. We studied the outcome of the second birth in a cohort of Danish women with pre-eclampsia in the previous birth (8,401 women) and in all women with pre-eclampsia in second (but not first) birth together with a sample of women with two births (26,596 women). A long interpregnancy interval was associated with a higher risk of pre-eclampsia in women with no previous pre-eclampsia when the father was the same. We estimated the risk of pre-eclampsia in second birth according to paternal change in different models. Although partner change was associated with an increased risk of pre-eclampsia in women with no history of pre-eclampsia, this effect disappeared after adjustment for the interpregnancy interval. We saw, however, different results when we stratified on the length of the interval. Our results indicate that the interval between births should be taken into consideration when studying the effect of changing partner on pre-eclampsia.

Adult↗
PubMed2005

Twenty-four-hour urine insulin as a measure of hyperinsulinaemia/insulin resistance before onset of pre-eclampsia and gestational hypertension.

OBJECTIVE: To evaluate levels of 24-hour urine insulin excretion before the onset of pre-eclampsia and gestational hypertension. DESIGN: Nested case-control study within the Calcium for Preeclampsia Prevention (CPEP) study cohort. SETTING: Five university medical centres in the United States. SAMPLE: Cases had developed pre-eclampsia (n= 70) or gestational hypertension (n= 142) in the absence of gestational diabetes. Controls (n= 429) had remained normotensive without gestational diabetes. METHODS: Subjects were required to have had an adequate baseline 24-hour urine collection prior to CPEP enrolment at 13-21 weeks. Controls were matched to cases by enrolment site and specimen storage time, without regard to gestational age or CPEP treatment. Adjusted mean 24-hour urine insulin excretion was, however, calculated using analysis of covariance, with adjustment models for pre-eclampsia considering body mass index, race and smoking status; and for gestational hypertension, gestational age at specimen collection, height, body mass index and smoking. Urine insulin was measured by radio-immunoassay. MAIN OUTCOME MEASURES: Twenty-four-hour urine insulin excretion. RESULTS: Adjusted 24-hour urine insulin excretion at baseline (mean 17 weeks of gestation) was greater in women who developed pre-eclampsia than in normotensive controls (mean [SE]: 15.6 [1.5] vs 13.1 [1.2] x 10(3)microIU/24 hour, P= 0.06), but not in women who developed gestational hypertension (14.7 [0.9] vs 15.0 [0.6] x 10(3)microIU/24 hour, P= 0.79, in cases vs controls). Among women who developed pre-eclampsia, adjusted urine insulin excretion was greater than controls only in women with mild pre-eclampsia and not in severe pre-eclampsia (mild pre-eclampsia vs controls: 17.3 [2.0] vs 13.7 [1.6] x 10(3)microIU/24 hour, P= 0.04; severe pre-eclampsia vs controls: 12.3 [2.2] vs 11.5 [1.2], P= 0.69). CONCLUSION: The data suggest that early hyperinsulinaemia, a marker of insulin resistance, may predispose to mild pre-eclampsia.

Adult↗