Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ECLAMPSIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMedDate not supplied

Correlation between second trimester maternal serum inhibin-A and human chorionic gonadotrophin for the prediction of pre-eclampsia.

We aimed to investigate the relationship between inhibin-A and human chorionic gonadotrophin (hCG) concentrations in the second trimester in the same cohort of women and compare their screening efficiency for the subsequent development of pre-eclampsia. The main outcome measures were pre-eclampsia and pre-eclampsia requiring delivery before 37 weeks.We carried out a retrospective examination of inhibin-A and free beta-hCG levels taken between 15 and 19 weeks of gestation, from 685 women. The values were corrected for weight and gestation and presented as multiples of the median (MoM). Receiver operator characteristic (ROC) curves for the prediction of pre-eclampsia and pre-eclampsia requiring delivery before 37 weeks were created for both analytes alone and in combination. Based on this data the sensitivities for the prediction of pre-eclampsia using inhibin-A and hCG, alone and in combination were examined for a specificity of 90 per cent.Thirty-five (5.5 per cent) women developed pre-eclampsia, of whom 15 (2.7 per cent) required delivery before term as a result of pre-eclampsia. There was no correlation between inhibin-A and hCG for the whole population (r=0.08) but there was a significant correlation for women who subsequently developed pre-eclampsia (r=0.648) or preterm pre-eclampsia (r=0.84). For a specificity of 90 per cent the sensitivity using inhibin-A was significantly better than for hCG (48.6 per cent versus 31.4 per cent, P< 0.05). The results were similar for preterm pre-eclampsia (P< 0.05). The addition of hCG data to inhibin-A data did not improve the sensitivity for pre-eclampsia compared to inhibin-A alone (42.9 per cent versus 48.6 per cent, P< 0.20).Inhibin-A is a more sensitive marker for the subsequent development of pre-eclampsia than hCG. Addition of hCG data to inhibin-A did not improve the screening efficacy for pre-eclampsia suggesting that inhibin-A and hCG are markers of the same underlying pathological process.

Adult↗
PubMed2000

Risk factors and clinical manifestations of pre-eclampsia.

OBJECTIVE: To study associations between established risk factors for pre-eclampsia and different clinical manifestations of the disease. DESIGN: A population-based, nested case-control study. SETTING: Information from 12,804 consecutive deliveries that took place over three years at a birth clinic, which alone serves a population of nearly 240,000 in Rogaland county, Norway. SUBJECTS: Cases of pre-eclampsia (n = 323) and healthy controls (n = 650) were selected. Pre-eclampsia was defined as increase in diastolic blood pressure (> or = 25 mmHg to > or = 90 mmHg) and proteinuria (> or = 1+ by dipstick testing) after 20 weeks of pregnancy. MAIN STUDY MEASURES: Parity, previous pre-eclampsia, blood pressure, maternal weight, and maternal smoking were included as study variables. Women with pre-eclampsia were grouped according to clinical manifestations of the disease (i.e. severity [mild, moderate or severe]) and time of onset (early or late gestation). Associations with the study factors were estimated as relative risks (odds ratio, OR). RESULTS: Both nulliparity and hypertension increased pre-eclampsia risk, with no clear preference for any clinical subtype. High maternal weight was related to a higher risk of mild and moderate, but not severe, pre-eclampsia. Previous pre-eclampsia strongly increased the risk for pre-eclampsia in the current pregnancy, and the risk of early onset disease was especially high (OR 42.4; 95% CI 11.9-151.6). Overall, smoking was associated with a reduced risk for pre-eclampsia (OR 0.6; 95% CI 0.4-0.9). However, no effect of smoking was observed in the early onset disease group and among women with repeated pre-eclampsia. CONCLUSION: Nulliparity and hypertension increased the risk for each subgroup of pre-eclampsia, but high maternal weight, previous pre-eclampsia and smoking were not consistently associated with each clinical subtype. This observation may suggest that heterogeneous clinical manifestations of pre-eclampsia may be preceded by different pathological mechanisms.

Body Weight↗
PubMed2000

Mid-trimester beta-hCG levels incorporated in a multifactorial model for the prediction of severe pre-eclampsia.

Pre-eclampsia remains a major cause of perinatal morbidity and mortality worldwide. Proposed predicting tests for early detection of pregnant women destined to develop pre-eclampsia remain unsatisfactory. The aim of this study was to investigate the clinical utility of combining mid-trimester maternal serum beta-human chorionic gonadotrophin (MShCG) levels with selected clinical determining factors as a multifactorial predictive test for pre-eclampsia. Thirty-nine cases with mild pre-eclampsia and 56 with severe pre-eclampsia were recruited as the study groups. Normotensive women (957) were enrolled as controls. Potential determining risk factors for severe pre-eclampsia were selected using a multiple logistic regression to build various combined prediction models. A receiver-operator characteristic curve was employed to assess the performance of each prediction test for pre-eclampsia. The prediction efficacy of each test was examined by the area under the curve (AUC). Our data show that mid-trimester MShCG levels significantly correlated with severity of pre-eclampsia (Spearman rank correlation coefficient=0.195, p<0.001). Women with mild pre-eclampsia had a 2.61-times greater chance, while women with severe pre-eclampsia had a 6.13-times greater chance of having MShCG exceeding 2.0 multiples of the median than did women with a normal pregnancy. A combined prediction model composed of MShCG levels, body mass index (BMI), parity, and age as a predictive test for severe pre-eclampsia was superior to MShCG levels alone (AUC 0.765 versus 0.648). The integrated multifactorial model could identify women at risk early on for developing severe pre-eclampsia, with a sensitivity of 70% and a specificity of 71%. Thus, we demonstrate a potentially effective and convenient method by which women at risk for developing severe pre-eclampsia can be identified early, based on a multifactorial predictive model composed of midtrimester MShCG levels, BMI, parity, and age.

Adult↗
PubMed2005

The role of lipoprotein (a) in pregnancies complicated by pre-eclampsia.

Endothelial cell dysfunction is a key feature of the pathogenesis of pre-eclampsia. The cause of the endothelial cell injury is probably multifactorial, but poor placenta perfusion plays a major role. In pre-eclampsia, characteristic pathological lesions in the placenta are fibrin deposits, acute atherosis and thrombosis. The similarity between the lesions of pre-eclampsia and atherosclerosis has led to speculations of a common pathophysiological pathway. An abnormal lipid profile is known to be strongly associated with atherosclerotic cardiovascular disease and has a direct effect on endothelial function. Abnormal lipid metabolism seems important in the pathogenesis of pre-eclampsia too. An elevated plasma lipoprotein (a) concentration is a known risk factor for atherosclerotic cardiovascular disease. In this paper, we discuss three hypotheses about the mechanisms by which lipoprotein (a) may be associated with pre-eclampsia: 1. Lp(a), as an acute-phase reactant, transporting cholesterol to sites of endothelial damage for reparation, temporarily increases during pregnancy and increases more during a pregnancy complicated by mild to moderate pre-eclampsia as compared to an uncomplicated pregnancy, in response to a greater extend of endothelial injury in pre-eclampsia. After delivery, pre-eclampsia subsides and Lp(a) concentrations return to baseline levels. 2. In cases of severe pre-eclampsia, there is even more extensive endothelial damage and consequently a higher consumption of Lp(a) in reparation of this vascular damage. These women will have lower concentrations of Lp(a). 3. High baseline concentrations of Lp(a), which are genetically determined, may induce or contribute to the development of pre-eclampsia by promoting endothelial dysfunction. In this line of reasoning one would expect to find higher concentrations of Lp(a) in women at risk for developing pre-eclampsia in a future pregnancy or with a history of pre-eclampsia. As discussed above, these women are also at increased risk for future cardiovascular disease as compared to women with a history of normal pregnancy. The pathophysiologic changes associated with cardiovascular disease may also be responsible for the increased incidence of pre-eclampsia in these women.

Biomarkers↗
PubMed1999

Does a predisposition to the metabolic syndrome sensitize women to develop pre-eclampsia?

OBJECTIVE: This study aimed to identify those factors in the non-pregnant state that distinguished women who developed pre-eclampsia from those who had normotensive pregnancies. DESIGN AND SETTING: This was a retrospective analysis of anthropometry, blood pressure, biochemical and haematological variables in 62 women with pre-eclampsia and 84 normotensive pregnant women who took part in studies of the pathophysiology of pre-eclampsia. Pregnant volunteers were seen, after admission to hospital or in the outpatient clinic, and followed-up at 6 weeks and 6 months post-partum in the outpatient clinic or their home. Participants Proteinuric pre-eclampsia was defined as blood pressure > or = 140/90 mmHg with proteinuria of at least 300 mg/24 h after 20 weeks gestation, in women with no history of hypertension and whose blood pressure returned to normal levels by 6 months post-partum. Normotensive pregnancy was defined as blood pressure < 130/90 mmHg without proteinuria. MAIN OUTCOME MEASURES: The primary outcome measures were blood pressure, body mass index (BMI), triglycerides, total cholesterol, low density lipoprotein (LDL) and high density lipoprotein cholesterol and markers of severity of pre-eclampsia. RESULTS: Regardless of parity, women with pre-eclampsia had elevated BMI before, during and after pregnancy compared with women who had normotensive pregnancies. Triglycerides were significantly elevated in women who had pre-eclampsia both before and after delivery, while total and LDL cholesterol were elevated significantly at both visits after delivery. Systolic and diastolic blood pressure, which by definition were elevated antepartum in women with pre-eclampsia, remained higher at post-partum visits compared with women who had normotensive pregnancies. Women with pre-eclampsia reported a greatly increased frequency of both maternal hypertension and pre-eclampsia. Markers of severity of pre-eclampsia, which normalized by 6 months postpartum, included plasma creatinine, uric acid, albumin, endothelin 1 and urinary protein, 2,3, dinor-6-keto-PGF1alpha, blood platelet and neutrophil counts. CONCLUSION: The relative elevation of blood pressure, BMI and lipids in the non-pregnant state are features of the metabolic syndrome and may be important sensitizing factors contributing to the pathogenesis of pre-eclampsia. A familial predisposition to pre-eclampsia may operate partly through these mechanisms.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

Cost-effectiveness of prophylactic magnesium sulphate for 9996 women with pre-eclampsia from 33 countries: economic evaluation of the Magpie Trial.

OBJECTIVE: To assess the cost-effectiveness of using magnesium sulphate for pre-eclampsia to prevent eclampsia. DESIGN: Multinational trial-based economic evaluation. SETTING: Thirty-three countries participating in the Magnesium Sulphate for Prevention of Eclampsia (Magpie) Trial. POPULATION: Women (9996) with pre-eclampsia from the Magpie Trial. METHODS: Outcome and hospital resource use data were available for the trial period from the Magpie Trial. Country-specific unit costs (U.S. dollar, year 2001) were obtained subsequently from participating hospitals by questionnaire. Cost-effectiveness was estimated for three categories of countries grouped by gross national income (GNI) into high, middle and low GNI countries using a regression model. Uncertainty was explored in sensitivity analyses. MAIN OUTCOME MEASURES: Eclampsia, hospital care costs and the incremental cost per case of eclampsia prevented. RESULTS: The number of women with pre-eclampsia who needed to receive magnesium sulphate to prevent one case of eclampsia was 324 [95% confidence interval (CI) 122, infinity] in high, 184 (95% CI 91, 6798) in middle and 43 (95% CI 30, 68) in low GNI countries. The additional hospital care cost per woman receiving magnesium sulphate was $65, $13 and $11, respectively. The incremental cost of preventing one case of eclampsia was $21,202 in high, $2473 in middle and $456 in low GNI countries. Reserving treatment for severe pre-eclampsia would lower these estimates to $12,942, $1179 and $263. CONCLUSIONS: Magnesium sulphate for pre-eclampsia costs less and prevents more eclampsia in low GNI than in high GNI countries. Cost-effectiveness substantially improves if it is used only for severe pre-eclampsia, or the purchase price is reduced in low GNI countries.

Anticonvulsants↗
PubMed2006

[Expression of transforming growth factor-beta 1, vascular cell adhesion molecule-1 and endothelium-selectin in placenta of patients with pre-eclampsia].

OBJECTIVE: To study the change and significance of the expression of transforming growth factor-beta 1 (TGF-beta1), vascular cell adhesion molecule-1 (VCAM-1) and endothelium-selectin (E-selectin) in placenta of patients with pre-eclampsia. METHODS: Twenty normal pregnant women (control group) and 40 women with pre-eclampsia (pre-eclampsia group, including 16 women with mild pre-eclampsia and 24 women with severe pre-eclampsia) were selected. The cellular distribution of TGF-beta1, VCAM-1 and E-selectin in placenta in both groups was determined by immunohistochemistry, and the mean density was measured by computer image analysis system. RESULTS: (1) The level of TGF-beta1 in placental villous syncytiotrophoblast of pre-eclampsia group (70.7 +/- 0.5) was significantly higher than that of control group (70.3 +/- 0.6), while the level of VCAM-1 and E-selectin in pre-eclampsia group (VCAM-1: 82.5 +/- 0.5, E-selectin: 53.5 +/- 0.5) was significantly lower than that of control group (VCAM-1: 82.8 +/- 0.3, E-selectin: 53.8 +/- 0.4) (P < 0.05). However, there were no significant differences in women with mild pre-eclampsia (TGF-beta1: 70.6 +/- 0.6, VCAM-1: 82.4 +/- 0.6, E-selectin: 53.4 +/- 0.5) and severe ones (TGF-beta1: 70.8 +/- 0.4, VCAM-1: 82.6 +/- 0.5, E-selectin: 53.6 +/- 0.5) (P > 0.05); (2) The level of E-selectin in placental villous capillary endothelial cells of pre-eclampsia group (63.0 +/- 0.5) was significantly higher than that of control group (62.6 +/- 0.4) (P < 0.05), while there was no significant difference in women with mild pre-eclampsia (63.2 +/- 0.4) and severe pre-eclampsia (62.9 +/- 0.5) (P > 0.05). CONCLUSION: TGF-beta1, VCAM-1 and E-selectin are not only related to placenta shallow bed of pre-eclampsia, but also participate in pathogenic process of vascular endothelial damage of pre-eclampsia.

Adult↗
PubMed2001

Pregnancy-related mortality from preeclampsia and eclampsia.

OBJECTIVE: To examine the role of preeclampsia and eclampsia in pregnancy-related mortality. METHODS: We used data from the Centers for Disease Control and Prevention's Pregnancy Mortality Surveillance System to examine pregnancy-related deaths from preeclampsia and eclampsia from 1979 to 1992. The pregnancy-related mortality ratio for preeclampsia-eclampsia was defined as the number of deaths from preeclampsia and eclampsia per 100,000 live births. Case-fatality rates for 1988-1992 were calculated for preeclampsia and eclampsia deaths per 10,000 cases during the delivery hospitalization, using the National Hospital Discharge Survey. RESULTS: Of 4024 pregnancy-related deaths at 20 weeks' or more gestation in 1979-1992, 790 were due to preeclampsia or eclampsia (1.5 deaths/100,000 live births). Mortality from preeclampsia and eclampsia increased with increasing maternal age. The highest risk of death was at gestational age 20-28 weeks and after the first live birth. Black women were 3.1 times more likely to die from preeclampsia or eclampsia as white women. Women who had received no prenatal care had a higher risk of death from preeclampsia or eclampsia than women who had received any level of prenatal care. The overall preeclampsia-eclampsia case-fatality rate was 6.4 per 10,000 cases at delivery, and was twice as high for black women as for white women. CONCLUSION: The continuing racial disparity in mortality from preeclampsia and eclampsia emphasizes the need to identify those differences that contribute to excess mortality among black women, and to develop specific interventions to reduce mortality from preeclampsia and eclampsia among all women.

Adult↗
PubMed2001

Oxidative stress in pre-eclampsia.

BACKGROUND: The objective of this study was to test the hypothesis that maternal plasma, cord plasma and placental tissue lipid peroxidation products are increased and antioxidants are decreased in women with pre-eclampsia. METHODS: Placenta, maternal and cord plasma were collected at delivery from 29 normal, 21 pre-eclamptic and six eclamptic women. Plasma was collected from 21 non-pregnant matched controls. The analyses were measured by HPLC and colorimetric assay. RESULTS: Plasma maternal concentrations of uric acid, LPO, MDA, ascorbic acid, vitamin E and cholesterol were not significantly different in pre-eclampsia as compared with normal pregnancy. Plasma concentrations of ascorbic acid and vitamin E were not significantly different in normal pregnancy as compared with the non-pregnant controls. Cord plasma concentrations of MDA were significantly higher in eclampsia (1.16+/-0.26 micromol/l) as compared with normal pregnancy (0.79+/-0.05 micromol/l, p<0.02) and pre-eclampsia (0.83+/-0.05 micromol/l, p<0.05). Cord plasma concentrations of vitamin E were significantly higher in eclampsia (21.3+/-7.5 micromol/l) as compared with normal pregnancy (10.2+/-1.1 micromol/l, p<0.01) and pre-eclampsia (10.4+/-1.8 micromol/l, p<0.04). Placental concentrations of LPO, MDA and ascorbic acid were not significantly different in pre-eclampsia as compared with normal pregnancy. Plasma cord concentrations of LPO and placental concentrations of vitamin E were undetected for normal pregnant, pre-eclamptic and eclamptic women respectively. Uric acid concentrations were significantly increased in eclampsia as compared with the non-pregnant controls (p<0.0001), normal pregnant controls (p<0.0001) and pre-eclampsia (p<0.008). CONCLUSIONS: The findings in this study do not show any evidence of deficiency in the maternal protective antioxidant systems or increased production of lipid peroxidation products, LPO and MDA in African women with pre-eclampsia as compared with normal pregnancy. However, there was evidence of increased cord plasma concentrations of MDA and vitamin E in eclampsia as compared with normal pregnancy and pre-eclampsia. The placenta may be effective in removing MDA. The antioxidant uric acid serves as a protective role whilst the antioxidant and oxidant capacity in the different study groups remained unchanged.

Adolescent↗
PubMed2005

Diagnosis, prevention, and management of eclampsia.

The pathogenesis of eclamptic convulsions remains unknown. Cerebral imaging suggests that cerebral abnormalities in eclampsia (mostly vasogenic edema) are similar to those found in hypertensive encephalopathy. However, cerebral imaging is not necessary for the diagnosis or management of most women with eclampsia. The onset of eclamptic convulsions can be antepartum (38-53%), intrapartum (18-36%), or postpartum (11-44%). Recent data reveal an increase in the proportion of women who develop eclampsia beyond 48 hours after delivery. Other than early detection of preeclampsia, there are no reliable tests or symptoms for predicting the development of eclampsia. In developed countries, the majority of cases reported in recent series are considered unpreventable. Magnesium sulfate is the drug of choice for reducing the rate of eclampsia developing intrapartum and immediately postpartum. There are 4 large randomized trials comparing magnesium sulfate with no treatment or placebo in patients with severe preeclampsia. The rate of eclampsia was significantly lower in those assigned to magnesium sulfate (0.6% versus 2.0%, relative risk 0.39, 95% confidence interval 0.28-0.55). Thus, the number of women needed to treat to prevent one case of eclampsia is 71. Magnesium sulfate is the drug of choice to prevent recurrent convulsions in eclampsia. The development of eclampsia is associated with increased risk of adverse outcome for both mother and fetus, particularly in the developing nations. Pregnancies complicated by eclampsia require a well-formulated management plan. Women with a history of eclampsia are at increased risk of eclampsia (1-2%) and preeclampsia (22-35%) in subsequent pregnancies. Recommendations for diagnosis, prevention, management, and counseling of these women are provided based on results of recent studies and my own clinical experience.

Adult↗
PubMed1993

Whole blood platelet aggregation in moderate and severe pre-eclampsia.

OBJECTIVE: To compare whole blood platelet aggregation in moderate and severe pre-eclampsia with normal pregnancy. DESIGN: Whole blood platelet aggregation in response to collagen, ADP, PAF, adrenalin and arachidonic acid was measured in the pre-eclampsia group at 36 weeks gestation and at 1, 24 and 48 h and at five days and six weeks post delivery. The normal pregnancy group were studied serially at 12, 20, 28, 32, and 36 weeks gestation and at 1, 24, 48 h and six weeks post delivery. SETTING: Trinity College Medical School, St James's Hospital, Dublin. SUBJECTS: Thirty women with diagnosed pre-eclampsia were recruited for the study. Fifteen of these women had severe pre-eclampsia and the remaining 15 had moderate disease. The pre-eclampsia group were compared with 20 healthy primigravid women with uncomplicated pregnancies and deliveries. RESULTS: In women with severe pre-eclampsia, platelet aggregation in response to collagen, ADP, adrenalin and arachidonic acid was significantly lower at 36 weeks gestation compared with normal pregnancy. Lower levels of collagen induced aggregation were also found at 1 h post delivery when compared with normal pregnancy. Women with moderate pre-eclampsia showed a decreased response to aggregating agents at 36 weeks gestation but this was not significant. ADP, collagen and PAF induced aggregation was higher in women with moderate pre-eclampsia at 36 weeks gestation and during the early puerperium compared with severe pre-eclampsia. CONCLUSIONS: The clinical signs of pre-eclampsia are accompanied by a reduction in platelet responsiveness, the extent of which is related to the severity of the disease. This suggests that an abnormal platelet activation occurs early in pregnancies destined to be complicated by pre-eclampsia. This activation may be involved in the pathogenesis of pre-eclampsia since its inhibition using low dose aspirin has been shown to modify the disease in high risk pregnancies.

Adenosine Diphosphate↗
PubMed2000

Eclampsia in dogs: 31 cases (1995-1998).

OBJECTIVE: To compare clinical characteristics and laboratory findings of dogs with eclampsia with those of dogs without eclampsia. DESIGN: Retrospective study. ANIMALS: 31 dogs with eclampsia (affected) and 31 with dystocia (controls). PROCEDURE: Information on signalment, type of diet, reproductive history, litter size, time from whelping to eclampsia, body weight, clinical signs, results of physical examination and hematologic and biochemical analyses, response to calcium supplementation, and recurrence was obtained from the medical records of all dogs with eclampsia evaluated between 1995 and 1998 and compared with information from medical records of 31 of 102 dogs with dystocia evaluated during the same period. RESULTS: Dogs with eclampsia weighed less, had a smaller body weight-to-litter size ratio, higher rectal temperature and heart and respiratory rates, and lower plasma total solids concentration than control dogs. Ionized calcium concentration was < or = 0.8 mmol/L for all but 1 of the affected dogs; median concentration for the affected dogs was significantly less than that for control dogs. Six (19%) dogs did not manifest typical clinical signs associated with eclampsia. Twelve (39%) dogs with eclampsia had previous litters; none had a history of eclampsia. Affected dogs were discharged from the hospital within hours after admission, but 3 dogs returned 1 to 3 weeks later because of recurrence of eclampsia. CONCLUSIONS AND CLINICAL RELEVANCE: Eclampsia develops primarily in small-breed dogs with large litters. Plasma ionized calcium concentrations > 0.8 mmol/L in dogs with clinical signs typical of hypocalcemia may indicate that other causes of clinical signs should be considered. In addition, some dogs with eclampsia may have low ionized calcium concentrations and not manifest typical clinical signs.

Animals↗
PubMed1997

The changing pattern of eclampsia over a 60-year period.

OBJECTIVE: To determine changes in the incidence and pattern of eclampsia within the same geographical area over a 60-year period. DESIGN: A retrospective, descriptive study of 1259 consecutive women classified, at the time, as having had an eclamptic convulsion between the years 1931 and 1990. SETTING: A large city centre teaching hospital and the surrounding catchment area. MAIN OUTCOME MEASURES: The changes in the incidence and timing of the convulsion and the outcomes for the mother and baby. RESULTS: Over the study period, the incidence of eclampsia fell by more than 90%, from 74.1/10,000 in the 1930s to 7.2/10,000 in the 1980s. Most of the reduction occurred over the first four decades, with little change in the last 20 years. Overall, 44% of the cases of eclampsia occurred in the antenatal period, 33% intrapartum and 23% postpartum. Since the biggest decreases were seen in the incidence of antenatal and particularly intrapartum eclampsia, there has been a relative increase in the proportion of eclampsia occurring postpartum. Maternal death from eclampsia occurred in 15.1% of cases between 1931 and 1940, 13.4% between 1941 and 1950, but fell dramatically to < or = 3.9% after 1950. There has been no maternal death since 1964. Apart from the first decade, postpartum eclampsia was associated with significantly less risk of death to the mother throughout the study period. Perinatal death rate has fallen steadily from 432.6/1000 cases of eclampsia between 1931 and 1940 over the first three decades, to 168.7/1000 between 1961 and 1970. There has been little change since, although a lower proportion of neonatal deaths occurred as stillbirths. CONCLUSIONS: We found a significant reduction in both the incidence of eclampsia and associated morbidity in this population over the last 60 years. This has occurred in association with the introduction of the National Health Service, widespread antenatal care for all and a general improvement in health and welfare. Any further reduction in the incidence in the UK may be difficult to achieve. Since the incidence of eclampsia is now low, efforts should perhaps be directed at minimising the morbidity associated with severe pre-eclampsia rather than prevention of convulsions.

Adult↗
PubMed2000

Is the prophylactic administration of magnesium sulphate in women with pre-eclampsia indicated prior to labour?

OBJECTIVE: To determine whether prophylactic magnesium sulphate is necessary to prevent eclampsia and associated complications among women with pre-eclampsia prior to labour. DESIGN: Case series. SETTING: Tertiary referral centre. POPULATION: Three hundred and eighteen women with pre-eclampsia (blood pressure > or = 140/90 mmHg and > or = 2+ proteinuria) who were not in labour or for planned induction thereof and had not received magnesium sulphate during transfer. METHODS: Clinical evaluation of the pregnant women with careful blood pressure control. Magnesium sulphate was withheld even in the presence of imminent eclampsia. During labour, the option of magnesium sulphate prophylaxis was left to the clinician, but magnesium sulphate was administered in cases of eclampsia. MAIN OUTCOME MEASURES: Eclampsia and related complications. RESULTS: Five women (1.5%) developed eclampsia, although none developed related complications. Women presented at an early gestational age (mean 30 weeks), with high blood pressure, often suffering from headaches. Twenty pregnancies were terminated prior to viability, of which half were terminated for maternal reasons. Ten intrauterine deaths occurred. Most often fetal distress (38.6%) initiated the delivery process, which was mainly by caesarean section (68.5%). With the exception of epigastric discomfort, symptoms and signs of imminent eclampsia decreased after admission. Blood pressure values were significantly lower at delivery although biochemistry results deteriorated from admission to delivery. CONCLUSION: In women with pre-eclampsia prior to labour, where blood pressure control was carefully applied but magnesium sulphate not given, the eclampsia rate was low and eclampsia did not appear to worsen the existing prognosis for mother or fetus.

Adult↗
PubMed2006

Screening in early pregnancy for pre-eclampsia using Down syndrome quadruple test markers.

OBJECTIVES: To estimate the screening performance of early second-trimester prenatal serum markers for Down syndrome, in screening for the development of pre-eclampsia, and analyse the uncertainty over its screening performance. METHODS: A nested case-control study was carried out on 96 women with pre-eclampsia and 5 controls for each case from among the women attending three hospitals in London for their prenatal care. Record linkage between computerized obstetric and screening databases identified women with pre-eclampsia and unaffected control women. The stored frozen serum samples collected from these pregnancies between 15 and 22 weeks' gestation were retrieved and assayed for alpha-fetoprotein (AFP), unconjugated estriol (uE(3)), total human chorionic gonadotrophin (hCG), free beta-hCG and inhibin-A. RESULTS: Pre-eclampsia was identified from the computerized obstetric records and confirmed by examination of the medical notes. In the pregnancies that went on to develop pre-eclampsia, early second trimester inhibin-A and hCG values were significantly raised and uE(3) values were significantly lowered, while AFP values were not significantly altered. Using the Quadruple test markers (AFP, uE(3), hCG (total or free beta) and inhibin-A), an estimated 34% of pregnancies that developed pre-eclampsia were detected at a 5% false-positive rate. If all the women who had pre-eclampsia in a previous pregnancy (assuming a pre-eclampsia prevalence of 4%) are considered as screen positive and the serum test is applied to the remaining women, then around 42% of pre-eclamptic pregnancies would be detected at a 6.5% false-positive rate. Pre-eclampsia screening performance using the Quadruple test markers was materially better than that using the Triple test markers. CONCLUSION: Adding screening for pre-eclampsia to an existing Down syndrome screening programme using the Quadruple test markers is simple and worthwhile. It will detect over 40% of pregnancies with pre-eclampsia at an acceptable false-positive rate (about 6%) and with minimal additional costs.

Biomarkers↗
PubMed2002

The role of hyperglycosylated hCG in trophoblast invasion and the prediction of subsequent pre-eclampsia.

OBJECTIVE: Hyperglycosylated hCG (HhCG) is the predominant form of chorionic gonadotrophin in states characterized by aggressive trophoblast invasion such as early pregnancy or choriocarcinoma. Pre-eclampsia may be the result of failed or inadequate trophoblast invasion. We investigated whether low levels of maternal urine HhCG levels would predict subsequent pre-eclampsia. STUDY DESIGN: Mid-trimester urine (14-21 weeks) was collected and frozen from non-hypertensive women undergoing genetic amniocentesis. Inclusion criteria were: normal singleton pregnancies without a prior history of pre-eclampsia, hypertension, diabetes or other vascular disorders. The specimens were subsequently thawed, and HhCG levels standardized to urine creatinine were measured. Maternal charts were reviewed after delivery to determine the development of pre-eclampsia. There were a total of 568 study subjects. RESULTS: Pre-eclampsia developed in 26 (4.6%) women. There was a significant correlation between low urine HhCG and subsequent pre-eclampsia (Mantel-Haenszel test of linear association: Chi-square 10.52, p=0.001). The mean HhCG level (ng/mg creatinine) was significantly greater in normals than in those destined to develop pre-eclampsia: 42.7 versus 20.3, p=0.002 (Mann-Whitney U-test). There was a progressive increase in the risk of subsequent pre-eclampsia as HhCG levels fell: HhCG < or =0.9 MoM RR (95% CI)=1.51 (1.15-1.98) compared with < or =0.1 MoM 10.42 (2.0-54.3). CONCLUSION: Low maternal mid-trimester urine HhCG predicted subsequent pre-eclampsia. This appears to support the view that pre-eclampsia results at least in part from poor trophoblast invasion. Thus, HhCG may play a role in trophoblast invasion and measurement of this in urine identifies women at high risk for developing pre-eclampsia.

Amniocentesis↗
PubMed1995

Pre-eclampsia: physiology and immunological aspects.

Pre-eclampsia is a frequent, unpredictable syndrome which is dangerous for both mother and foetus. The concept of placental ischemia has gained wide acceptance among the numerous theories put forward to explain the illness. The setting up of preeclampsia seems to be scheduled in two steps: (1) an absolute or relative placental ischemia due to vascular diseases or hypertrophic placenta, or most often secondary to implantation defect, particularly anomaly with the invasive trophoblast; (2) a diffuse endothelial disease. The connection between these two steps is incompletely disclosed. The authors demonstrate that the maternal immune system which is strongly stressed during all the stages of normal gestation is implicated in pre-eclampsia. Its role is probably not univocal. Foeto-trophoblastic antigens could be poorly recognised. This defect of recognition could lead to the abnormalities of trophoblastic invasion observed in pre-eclampsia. Pre-eclampsia does not seem to be accompanied by an immunological rejection of the foetus. Some genetically predisposed patients do not have a sufficiently competent immune system to neutralise one or more of the toxic products released by the ischemic placenta. Certain types of pre-eclampsia could be auto-immune, with the auto-antibodies directed against certain types of phospholipids or trophoblastic constituents. A disequilibrium between oxidation and anti-oxidation mechanisms involving neutrophils could lead to aggression of the endothelium which is observed in pre-eclampsia. Pre-eclampsia could represent a form of immuno-dystrophy, with the excessive production of adverse cytokines locally, directed against the trophoblast. Without directly implicating the immune system as the trigger of pre-eclampsia, it seems that its role is unclear. In some cases it develops protective mechanisms which, when overwhelmed or inadequate, allows pre-eclampsia to occur. In other cases it can form part of the cascade of aggressions leading to the abnormalities encountered. The integration of these abnormalities in the pathophysiological models, could help improve the classification of pre-eclampsia. This attempt will lead to a more adapted preventive and therapeutic management of pre-eclampsia.

Autoimmune Diseases↗
PubMed2006

Hypoadiponectinemia and circulating angiogenic factors in overweight patients complicated with pre-eclampsia.

OBJECTIVE: Obesity is a risk factor for pre-eclampsia, and adiponectin is an important adipocyte-derived hormone that might protect the endothelium. Recent reports have underlined importance of circulating angiogenic factors for pathophysiology of pre-eclampsia. Here we examined whether adiponectin in conjunction with angiogenic factors plays some roles in the pathophysiology of pre-eclampsia. STUDY DESIGN: We measured serum concentrations of adiponectin and angiogenic factors, vascular endothelial growth factor, placental growth factor, and the soluble vascular endothelial growth factor receptors, soluble fms-like tyrosine Kinase 1 (sFlt-1) and soluble fetal liver kinase 1 (sFlk-1), in women with pre-eclampsia and healthy pregnant women. We also investigated the differences of these factors in overweight and normal-weight patients with pre-eclampsia. RESULTS: Significant correlations were found among the circulating adiponectin and angiogenic factors placental growth factor (R = 0.772, P = .0012) and sFlt-1 (R = 0.787, P = .0005); while, no correlation was found between adiponectin and sFlk-1 (R = 0.3, P = .3434) in patients with pre-eclampsia. Overweight patients with pre-eclampsia showed significantly lower adiponectin levels and a mild imbalance of circulating angiogenic factors, compared with normal-weight patients with pre-eclampsia. CONCLUSION: Overweight women with pre-eclampsia appeared to have lower levels of adiponectin and sFlt1 and higher levels of placental growth factor than women with pre-eclampsia who were of normal weight. These results suggest that hypoadiponectinemia might be involved in the pathophysiology of overweight patients with pre-eclampsia.

Adiponectin↗