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 325 records · Page 18Linked to original sources
PubMed2002

Transforming growth factor-beta 1 does not relate to hypertension in pre-eclampsia.

1. Pre-eclampsia is a human disease of pregnancy characterized by high blood pressure, proteinuria and end-organ damage, if severe. Pre-eclampsia is thought to be related to changes in early placental development, with the formation of a shallower than normal placental bed. 2. Transforming growth factor (TGF)-beta1 is a multifunctional fibrogenic growth factor involved in immune regulation that is elevated in some populations with a high risk of hypertensive end-organ disease related to increases in endothelin release. Transforming growth factor-beta1 is also an important factor in placental implantation. Alterations in TGF-beta1 may be related to abnormal placental development in early pregnancy and, thus, are a candidate for the development of hypertension in pre-eclampsia. 3. The aim of the present study was to examine the placental distribution and serum concentration of TGF-beta1 in patients with pre-eclampsia compared with normal pregnancy. 4. Patients with pre-eclampsia (n = 12) were compared with patients with normal pregnancy (n = 14). Transforming growth factor-beta1 was determined by TGF-beta1 Max ELISA (Promega, Madsion, WI, USA) after serum dilution (1/150) and acid activation. Placental distribution was determined by immunostaining with TGF-beta1 (Santa Cruz, Santa Cruz, CA, USA; 20 ng/mL) and the villi and decidual trophoblast were scored for intensity and extent of staining. 5. Patients with pre-eclampsia had a mean gestational age of 36 weeks, whereas those with a normal pregnancy had a mean gestational age of 39.0 +/- 0.4 weeks. There was no difference in TGF-beta1 concentration between the two groups (mean (+/-SEM) 27.1 +/- 1.0 vs 26.4 +/- 0.7 pg/mL for normal pregnancy and pre-eclampsia, respectively; P = 0.73, Mann-Whitney U-test). There was no correlation between systolic or diastolic blood pressure and TGF-beta1 concentration (regression analysis P = 0.4 and 0.2). Immunostaining was absent in the villous trophoblast cells and endovascular and extravillous trophoblast of term placentas. 6. Although TGF-beta1 is present in trophoblast cells in early pregnancy during placental development, TGF-beta1 concentrations were not increased in the placenta at term in pre-eclampsia and there was no correlation between blood pressure and serum TGF-beta1, suggesting that TGF-beta1 does not play a role in the development of late gestation pre-eclampsia and hypertension.

Adult↗
PubMed2005

Could antioxidant supplementation prevent pre-eclampsia?

Pre-eclampsia is a disorder characterised by pregnancy-induced hypertension and new-onset proteinuria occurring in the second half of pregnancy. Worldwide, approximately 2-3% of all pregnant women develop pre-eclampsia. The condition is a major cause of maternal and fetal morbidity and mortality. Abnormal placentation is an important predisposing factor for pre-eclampsia, while endothelial activation appears to be central to the pathophysiological changes, possibly indicative of a two-stage disorder characterised by reduced placental perfusion and a maternal syndrome. There is increasing evidence that pre-eclampsia is associated with both increased oxidative stress and reduced antioxidant defences, which has led to the hypothesis that oxidative stress may play an important role in the pathogenesis of pre-eclampsia, perhaps acting as the link in a two-stage model of pre-eclampsia. In support of this hypothesis a small, but important, preliminary study has shown a highly significant (P=0.02) reduction in the incidence of pre-eclampsia in women at risk who were taking a supplement of vitamins C and E from mid-pregnancy. Furthermore, these findings support the hypothesis that oxidative stress is at least partly responsible for the endothelial dysfunction of pre-eclampsia. Several larger multicentre trials are currently underway to evaluate the efficacy, safety and cost benefits of antioxidant supplementation during pregnancy for the prevention of pre-eclampsia in both low- and high-risk women, including women with diabetes. The results of these trials are awaited with interest.

Antioxidants↗
PubMed2003

The relationship between insulin and insulin-like growth factor binding protein-1 is modified by pre-eclampsia.

Insulin is the main negative regulator of insulin-like growth factor binding protein-1 (IGFBP-1) in the non-pregnant state. Although changes in insulin resistance and circulating level of IGFBP-1 occur in pre-eclampsia, little is known about the relationship between insulin and IGFBP-1 in pregnancies complicated by the disease. In this study, we have investigated whether the relationship between insulin and IGFBP-1 is modified by pre-eclampsia. Maternal levels of insulin and IGFBP-1 were measured, at 4-weekly intervals between 16 and 36 weeks' gestation, in plasma samples obtained from ten normal pregnant controls and ten women who developed pre-eclampsia. The controls were chosen to be similar in maternal age and booking body mass index to the pre-eclampsia group. Insulin levels increased in both the normal controls and the women who developed pre-eclampsia. The levels in pre-eclampsia were significantly greater than those in normal pregnancy at 32 and 36 weeks' gestation (p = 0.02 and 0.005, respectively). IGFBP-1 levels were unchanged in normal pregnancy and rose in pre-eclampsia. In normal pregnancy, insulin levels were inversely related to IGFBP-1 levels throughout. In women developing pre-eclampsia, the relationship between insulin and IGFBP-1 was negative at 16 weeks and positive from 24 weeks. These data suggest that whereas the inverse relationship between insulin and IGFBP-1 is maintained during normal pregnancy, this relationship is reversed in women who develop pre-eclampsia.

Adult↗
PubMed2003

Influence of pre-eclampsia on fetal growth.

OBJECTIVE: We examined the effect of pre-eclampsia on fetal growth in a cohort of pregnant women delivering singleton infants. METHODS: Analyses were restricted to 155 women with pre-eclampsia and 5570 normotensive women. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) after adjusting for confounders. We estimated ORs for very low birth weight (VLBW; < 1500 g), low birth weight (LBW; < 2500 g), and small for gestational age (SGA; weight < or = 10th centile by each gestational age, race, sex and parity strata) in relation to maternal pre-eclampsia status. RESULTS: After adjusting for maternal age, race, smoking, Medicaid status and gestational age, the OR for VLBW was 30.7 (95% CI 7.0-134.9). Pre-eclampsia was associated with a 3.8-fold increased risk of LBW (95% CI 1.9-7.5). Women with pre-eclampsia were 3.6 times more likely to deliver an SGA newborn as compared with normotensive women (95% CI 2.3-5.7). Advanced maternal age, African-American race, parity or smoking status did not modify the associations of pre-eclampsia with LBW and SGA. CONCLUSIONS: Our results are consistent with other reports that have documented a strong relationship between pre-eclampsia and restricted fetal growth. Further, our results expand the literature by documenting a particularly strong association between pre-eclampsia and VLBW. However, our findings regarding the relationship between pre-eclampsia and fetal growth may be confounded by unmeasured factors including maternal weight prior to pregnancy and pregnancy weight gain.

Adult↗
PubMed2003

Neonates born to pre-eclamptic mothers have a higher percentage of natural killer cells (CD3-/CD56+16+) in umbilical cord blood than those without pre-eclampsia.

OBJECTIVE: Maternal endothelial dysfunction and intravascular inflammation have been implicated in the mechanisms of disease responsible for the clinical syndrome of pre-eclampsia. Recently, the activation of the innate limb of the immune response (neutrophils and monocytes) in the fetal circulation has been reported in neonates born to mothers with pre-eclampsia. Natural killer (NK) cells are identified morphologically as a subpopulation of lymphocytes, but functionally as one component of the innate immune system. NK cells participate in the control of viral or bacterial infection, regulation of hematopoiesis, production of cytokines and cytotoxicity of neoplastic cells. Accumulating evidence suggests that the innate system is required for mounting an adequate adaptive response. NK cells, originally defined as effector cells of the innate immune system, may also play a role as regulatory cells for the adaptive immune system. This study was designed to determine the proportion of the NK cell subset of lymphocytes in umbilical cord blood of neonates born to mothers with and without pre-eclampsia. METHODS: A cross-sectional study including neonates of mothers with (n = 48) and those without pre-eclampsia (control group) (n = 72) was conducted. Pre-eclampsia was diagnosed in the presence of hypertension and proteinuria. The control group consisted of neonates (premature and term) with no evidence of acute inflammation within the extraplacental membranes (chorioamnionitis). Umbilical cord blood was collected at the time of delivery, and assayed using monoclonal antibodies for selective cluster differentiation (CD) antigens in order to determine the proportion of NK cells as a percentage of total lymphocytes. The immunophenotypic characteristic was determined using flow cytometry, and NK cells were identified by positivity of CD16 and CD56 without CD3 (CD3-/CD56+16+). Log transformation of the percentage of NK cells was performed. Parametric statistics were used for analysis. Multiple regression analysis was utilized to examine the contribution of potentially confounding factors on the proportion of NK cells. A p value of < 0.05 was considered statistically significant. RESULTS: Neonates born to mothers with pre-eclampsia had a significantly higher percentage of NK cells (CD3-/CD56+16+) than those in the control group (pre-eclampsia, mean +/- SD 17 +/- 9% vs. control, mean +/- SD 12 +/- 7.5%; p = 0.001). Multiple regression analysis suggested that umbilical cord blood pH of < 7.2, labor with vaginal delivery and maternal pre-eclampsia were associated with an increased percentage of NK cells in umbilical cord blood. CONCLUSIONS: Pre-eclampsia is associated with a higher NK cell (CD3-/CD56+16+) subset of lymphocytes in umbilical cord blood than in the control group. This difference cannot be explained by fetal acidosis or the presence of labor.

CD3 Complex↗
PubMed2002

Eclampsia in Sweden.

OBJECTIVE: Assess the actual rate of eclampsia in Sweden, describe the clinical picture of the disease and the maternal and perinatal outcomes. METHODS: Analysis of data regarding incidence of eclampsia registered in the Swedish Medical Birth Register 1991-1992. The records of all the cases with the diagnosis of eclampsia in Sweden during 1991-1992 were retrospectively evaluated regarding maternal and fetal outcomes. RESULTS: The incidence of eclampsia after case review was 3.3/10,000 births. There was no maternal mortality. Severe maternal complications occurred in 30%. Recurrent fits were reported in 41%. Antenatal eclampsia was usually either not preceded by symptoms or signs of preeclampsia or by just a very short period of prodromal symptoms. Among intrapartum and postnatal cases of eclampsia, preeclampsia or high blood pressure was more frequently noted when convulsions occurred. Perinatal mortality rate was 4/80 (4.7%). Of the infants, 13% were small for gestational age. CONCLUSION: Compared with earlier studies, the incidence of eclampsia has increased significantly. It is questionable whether the incidence of eclampsia could be reduced by earlier diagnosis and treatment of preeclampsia. The risk of severe complications and recurrent fits was substantial, which underlines the importance of adequate treatment of eclampsia.

Adult↗
PubMed1999

Eclampsia: a 13-year experience at a United States tertiary care center.

Eclampsia, the occurrence of a grand mal seizure in the setting of hypertension in pregnancy, remains a major women's health issue and an important cause of maternal and fetal morbidity in the United States. We reviewed the incidence, management, and outcome of cases of eclampsia during a 13-year period at a major maternity hospital. We confirmed 33 cases of eclampsia seen during that period and have evaluated risk factors in this population. Medical records were reviewed to obtain demographic and clinical data. Characteristics of the eclamptic women were compared with those of the general obstetric population during the same time period. The overall incidence of eclampsia at this tertiary care center was 0.028%. The majority of eclamptic women (75%) had four or more prenatal visits. Young age (< or = 20 years) and first pregnancy remained important risk factors for eclampsia. Although many women with eclampsia had preceding hypertension or elevated urine protein levels or both, some experienced eclampsia as their first disease manifestation. Although the occurrence of eclampsia was low, eclampsia continues to complicate pregnancy in this large U.S. obstetric population.

Adult↗
PubMed1994

Late postpartum eclampsia revisited.

OBJECTIVE: To describe the clinical and neurologic findings in patients with late postpartum eclampsia (convulsions beginning more than 48 hours, but less than 4 weeks, after delivery). METHODS: This study evaluated all patients with the diagnosis of late postpartum eclampsia managed at our institution between August 1977 and July 1992. RESULTS: There were 54 cases of late postpartum eclampsia among a total of 334 cases of eclampsia during the study period. Late postpartum eclampsia constituted 56% of total postpartum eclampsia and 16% of all cases of eclampsia. Convulsions began from postpartum days 3-23 (mean 6). Thirty women (56%) had been identified as preeclamptic before their convulsions. A history of either severe headache or visual disturbances before convulsion was elicited in 83% of the patients. During the study period, eight women not included in the study group had late postpartum seizures attributed to other causes. CONCLUSIONS: Severe headache or visual disturbance frequently antedates late postpartum eclampsia. Only eight of 62 patients with late postpartum seizures had identifiable etiologies other than eclampsia.

Adult↗
PubMed1994

Endothelial cell activation by tumour necrosis factor-alpha (TNF-alpha) and the development of pre-eclampsia.

Pre-eclampsia may develop as a result of an endothelial activation. Tumour necrosis factor-alpha (TNF-alpha) activates endothelial cells which release soluble E-selectin, a putative circulating marker specific for endothelial damage. A retrospective longitudinal study of maternal blood samples, collected at different gestational ages in pregnancy, was undertaken to determine whether the development of pre-eclampsia is associated with TNF-alpha-mediated endothelial activation. This study included 19 women who developed pre-eclampsia and 22 women whose pregnancy outcome was normal. Ten women had blood samples taken before pre-eclampsia was clinically detected and, in all these, TNF-alpha was below the immunoassay limit of detection (< 80 pg/ml). Five had further samples taken after pre-eclampsia was clinically diagnosed and, initially, TNF-alpha was still below the lower limit of detection in all five pregnancies, but rose later in three (80, 156 and 250 pg/ml). In nine other patients with diagnosed pre-eclampsia, TNF-alpha was detected in only two (80 and 650 pg/ml). TNF-alpha was identified in only one of the 22 normal pregnancies (80 pg/ml), this being at term. There was no statistical difference in soluble E-selectin levels between normal and pre-eclamptic pregnancies, neither before nor after pre-eclampsia was diagnosed. Hence, blood TNF-alpha levels measured by immunoassay can be elevated in approximately 36% of cases of established pre-eclampsia, but this rise occurs only after the syndrome is detected clinically. Blood concentrations of TNF-alpha and soluble E-selectin are not related to severity of the disorder. These findings suggest that circulating TNF-alpha does not contribute to the initiation of endothelial cell activation that may be associated with the development of pre-eclampsia, but may rise as a consequence of the pathological processes of this disorder.

Cell Adhesion Molecules↗
PubMed2006

Pre-eclampsia: contribution of maternal constitutional factors and the consequences for cardiovascular health.

1. Pre-eclampsia is a serious complication of pregnancy that is potentially life threatening for both the mother and baby. It encompasses a number of abnormalities that may be present in other clinical conditions. 2. A placenta is essential for the development of pre-eclampsia and can be important in the pathogenesis of pre-eclampsia. Normal pregnancy is associated with remodelling of the maternal spiral arteries, which deliver blood to the placental villous space. Remodelling involves invasion by placental cytotrophoblasts that cause the maternal spiral arteries to lose their smooth muscle and become capacitance vessels; this process, known as placentation, is complete by 20 weeks of pregnancy. Poor placentation is associated with small-for-gestational-age fetuses and some cases of pre-eclampsia. It is thought that poor placentation can result in a hypoxic placenta that releases 'toxic substances' into the maternal circulation, contributing to the maternal syndrome. A number of candidate 'toxic substances' have been proposed, but none is universally raised in pre-eclampsia. 3. Although the placenta is necessary for the development of pre-eclampsia, the extent to which placental abnormalities contribute to the condition varies. It is becoming apparent that maternal constitutional factors may also be important in this syndrome. Underlying hypertension, diabetes and obesity strongly predispose to pre-eclampsia. However, a continuum of risk may exist for blood pressure, bodyweight, glucose and lipids, which, in combination with each other and some degree of placental abnormalities, may lead to the development of pre-eclampsia. 4. The present review will focus on the maternal constitutional factors that define the metabolic syndrome and examine their contribution to pre-eclampsia and the long-term consequences for cardiovascular health.

Biomarkers↗
PubMed1976

Carbohydrate metabolism in pre-eclampsia.

Intravenous glucose tolerance tests were performed on 30 primigravidae with pre-eclampsia and 15 normal primigravidae in late pregnancy. The groups were matched for age, height and weight and had no stigmata of potential diabetes. Plasma glucose, plasma immunoreactive insulin and plasma placental lactogen (HPL) levels were measured before (fasting) and at timed intervals after the glucose challenge; the glucose response was expressed as the increment index. The patients with severe pre-eclampsia had significantly lower fasting plasma glucose levels than those with mild pre-eclampsia and normal pregnancies. The mean increment index in both the severe and mild pre-eclamptic groups was significantly lower than that of the normal pregnant group. Fasting HPL levels were significantly lower in patients with severe pre-eclampsia than in those who had mild pre-eclampsia or a normal pregnancy. Both the fasting plasma insulin and insulin response following glucose injection were lower in patients with severe pre-eclampsia than in those with mild pre-eclampsia or a normal pregnancy. The differences however were not statistically significant. The results of this study suggest that carbohydrate metabolism in severe pre-eclampsia is altered to an extent similar to that in patients with chemical gestational diabetes, and this alteration may be due to maternal beta-cell anoxia caused by the vascular changes in pre-eclampsia.

Adolescent↗
PubMed1985

Pre-eclampsia in second pregnancy.

A total population of pregnant women from Aberdeen City District 1967-1978 has been studied. There were 29 851 pregnancies and 6637 women had a first recorded pregnancy between 1967 and 1978 and had two or more pregnancy events. As expected the incidence of pre-eclampsia in a second pregnancy was less than that in a first pregnancy, but it was dependent on the outcome of the first pregnancy. If the first pregnancy was complicated by proteinuric pre-eclampsia than the incidence of the condition in the second pregnancy was similar to that in a first pregnancy, but women who were normotensive in the first pregnancy had a reduced incidence of the condition in the second pregnancy. The incidence of proteinuric pre-eclampsia after early abortion (less than 13 weeks), either spontaneous or induced was similar to the population incidence in a first pregnancy, but after a late spontaneous abortion the risk of proteinuric pre-eclampsia was significantly reduced. Change of civil status of the offspring from first to second pregnancy did not affect the incidence of pre-eclampsia in a second pregnancy. There was an effect of birthweight in that women who had proteinuric pre-eclampsia in conjunction with a low-birthweight baby (less than 2500 g) in their first pregnancy had double the incidence of proteinuric pre-eclampsia in their second pregnancy. Only a pregnancy of 37 weeks or more is likely to offer protection or 'immunity' to pre-eclampsia in a second pregnancy and even then the effect is moderated by the development of pre-eclampsia in the first pregnancy.

Abortion, Spontaneous↗
PubMed1996

Insulin-like growth factor-binding protein 1 and insulin-like growth factor-binding protein 3 in pre-eclampsia.

OBJECTIVE: To investigate circulating levels of insulin-like growth factor-binding protein 1 (IGFBP-1) and IGFBP-3 in the mother and the fetus in pregnancies complicated by pre-eclampsia, and the relationship between serum levels of IGFBPs and fetal birthweight. DESIGN: A prospective study over an 18 month period. SETTING: A tertiary care academic medical centre. PARTICIPANTS: Sixty-six pregnant women with pre-eclampsia (35 cases of mild/moderate pre-eclampsia and 31 cases of severe pre-eclampsia) and 78 nonpre-eclamptic pregnant women of matched gestational weeks and maternal ages. MAIN OUTCOME MEASURES: Serum concentrations of IGFBP-1 and IGFBP-3 at the time of delivery. RESULTS: In pre-eclampsia associated with intrauterine growth retardation (IUGR), maternal and cord serum IGFBP-1 levels at the time of delivery were elevated. By contrast, circulating IGFBP-3 levels in both the mother and the fetus were lower in pre-eclampsia with IUGR than in nonpre-eclamptic pregnancy. However, there was no difference in serum IGFBP-1 and IGFBP-3 levels between pre-eclampsia without IUGR and nonpre-eclamptic pregnancy in both the mother and the fetus. CONCLUSIONS: In pre-eclampsia, elevated concentrations of circulating IGFBP-1 and decreased serum IGFBP-3 levels were observed in both the mother and the fetus. However, these changes may simply reflect low birthweight in pre-eclampsia.

Adolescent↗
PubMed1997

Increased levels of intercellular adhesion molecules and vascular cell adhesion molecules in pre-eclampsia.

OBJECTIVE: To investigate the correlation between soluble forms of the intercellular adhesion molecule (sICAM-1) and vascular cell adhesion molecule (sVCAM-1) and the severity of pre-eclampsia or its possible consequences for fetal growth. DESIGN: Prospective observational study. SETTING: Institute of Medical Genetics, University of Oslo, Department of Medical Genetics and Haematological Research Laboratory, Ullevål University Hospital; and the Department of Obstetrics and Gynaecology, The National Hospital, Oslo, Norway. PARTICIPANTS: Seventy-six women with normotensive pregnancies and 157 women with pre-eclampsia divided into three subgroups: mild, severe and pre-eclampsia with fetal growth retardation. METHODS: ELISA-measurements of plasma sICAM-1 and sVCAM-1 were performed in a group of healthy pregnant normotensive women and three groups of women with varying degrees of pre-eclampsia. RESULTS: sICAM-1 concentrations were higher in the pre-eclampsia group compared with the control group, but this difference was not statistically significant. Plasma concentrations of sVCAM-1 were significantly greater (P < 0.0001) in all pre-eclampsia subgroups (835.34, 855.25 and 964.05 ng/mL) compared with the control group (667.62 ng/mL). Within the pre-eclampsia group, plasma concentration of sVCAM-1 was significantly higher in the subgroup exhibiting fetal growth retardation (P = 0.03) compared with mild pre-eclampsia. CONCLUSION: The observed increases in plasma concentrations of sVCAM-1 suggest that measurements of this adhesion molecule may be useful in monitoring pregnancies with respect to the development of pre-eclampsia or fetal growth retardation.

Adult↗
PubMed1998

Association of circulating endothelium and noradrenaline with increased calcium-channel binding sites in the placental bed in pre-eclampsia.

OBJECTIVE: To evaluate factors contributing to both placental hypoperfusion and maternal vasoconstriction in pre-eclampsia. DESIGN: Single centre, comparative study of calcium-channel density and affinity in the placental bed of pregnant women with normotension and pre-eclampsia. SETTING: Teaching hospital. PARTICIPANTS: Twenty-two primigravidae in the third trimester of pregnancy: 10 with pre-eclampsia and 12 normotensive. METHODS: Plasma levels of endothelin-1 (by RIA) and noradrenaline (by HPLC-ED) were measured. Both pharmacological characterisation and anatomical localisation of dihydropyridine-sensitive binding sites (using radioligand-binding studies and autorradiographic techniques) were determined with 3H-isradipine in placental bed tissues to determine both the density (Bmax) and the affinity (Kd) of receptor sites. RESULTS: Higher plasma levels of endothelin-1 and noradrenalin were found in women with pre-eclampsia compared with normotensive women. Placental bed tissues bound 3H-isradipine in a saturable, reversible time and temperature-dependent manner with very low Kd values. Study of the 3H-isradipine specificity binding included the use of several dihydropyridine displacers. In the group with pre-eclampsia the Scatchard analysis of the results showed a significant increase (P < 0.001) both in the affinity [Kd = 0.23 nmol (0.04) vs 0.45 nmol (0.03), pre-eclampsia vs normotensive] and in the density of calcium-channel binding sites [Bmax = 77.70 fmol/mg (1.30) vs 64.30 fmol/mg (1 80) tissue, pre-eclampsia vs normotensive]. Autoradiography confirmed that in the placental bed tissue of those with pre-eclampsia there was a much higher silver grain density in the arteries walls, compared with normotensive women. CONCLUSIONS: In pre-eclampsia there is an increase in the maternal circulation of two strong vasoconstrictor factors (endothelin-1 and noradrenalin) and a sharp increase both in the density and the affinity of calcium-channel binding sites in placental bed central area. The latter may strongly contribute to the perpetuation of the uteroplacental hypoperfusion either by itself or by amplifying the local actions of circulating factors, such as endothelin-1 and noradrenalin.

Adult↗
PubMed1999

Twin mothers, pregnancy hypertension and pre-eclampsia.

OBJECTIVE: To estimate the maternal genetic contribution to the hypertensive diseases of pregnancy. DESIGN: A cohort study of female twins with information on hypertensive diseases of pregnancy obtained by questionnaire screening, and verification of diagnosis from hospital or general practitioner records. SETTING: A volunteer twin registry in the UK with recruitment through the media without reference to pregnancies or disease status. POPULATION: Adult female, same-sex twin pairs who completed a pregnancy history questionnaire and consented to record inspection. MAIN OUTCOME MEASURE: Self-reported and hospital-validated diagnosis of non-proteinuric pregnancy hypertension and of pregnancy hypertension with proteinuria (pre-eclampsia). RESULTS: Self-reported pre-eclampsia had a heritability of 0.221 and non-proteinuric hypertension of 0. 198. However, none of the pairs who were self-reported as concordant for pre-eclampsia were confirmed from hospital records. Using hospital records, the heritability of pre-eclampsia was 0 and 0.375 for non-proteinuric hypertension. Using a model treating pre-eclampsia as a separate disease from non-proteinuric hypertension, and assuming that the next pair identified was both monozygotic and concordant for pre-eclampsia, the estimated heritability of pre-eclampsia remained 0 (95% CI 0-0.49). Using a threshold model in which non-proteinuric hypertension is treated as a mild form of pre-eclampsia, heritability is estimated at 0.247 (95% CI 0.23-0.454). CONCLUSION: Neither non-proteinuric hypertension nor pre-eclampsia are inherited in simple Mendelian fashion. The genetic contribution to multi-factorial inheritance is smaller than hitherto believed.

Adolescent↗
PubMed2005

Assessment of risk for the development of pre-eclampsia by maternal characteristics and uterine artery Doppler.

OBJECTIVE: To develop a method for the estimation of patient-specific risk for the development of pre-eclampsia by combining maternal history and uterine artery Doppler. DESIGN: Prospective multicentre observational study. SETTING: Antenatal clinics in seven hospitals in the UK and three overseas centres. POPULATION: Unselected women with singleton pregnancies attending for routine antenatal care. METHODS: Doppler studies of the uterine arteries were performed using colour flow mapping and pulsed wave Doppler at 23 weeks of gestation. The mean pulsatility index (PI) of the two uterine arteries was calculated. Doppler and maternal history variables were combined to develop a model for risk assessment. The incidence of pre-eclampsia was used to derive the prior risk for this complication. The posterior risk was derived by multiplying the prior odds with likelihood ratios (LRs) derived from independent risk factors identified from the maternal history, and the LR estimated from the heights of the frequency distributions of mean PI in affected and unaffected pregnancies. MAIN OUTCOME MEASURE: Pre-eclampsia. RESULTS: There were 17,480 women recruited to the study, in which 17,319 (99.1%) of these Doppler examination of both uterine arteries were completed, and outcome data were available in 16,806 (97.0%). Pre-eclampsia occurred in 369 (2.20%) cases. Significant independent prediction of pre-eclampsia was provided by mean PI, ethnic origin, body mass index (BMI), parity, cigarette smoking, history of hypertension and family or personal history of pre-eclampsia. Models were derived allowing calculation of patient-specific risk for development of pre-eclampsia. For a false-positive rate of 25%, the detection rate of pre-eclampsia by screening using maternal history was 45.3%, with uterine artery Doppler it was 63.1% and with combined assessment it was 67.5%. CONCLUSIONS: Combining risk factors in the mother's history with Doppler of the uterine arteries allows calculation of patient-specific risk for the development of pre-eclampsia.

Arteries↗
PubMed2004

Periodontal disease as a risk factor for pre-eclampsia: a case control study.

OBJECTIVE: To investigate the association between periodontal disease and pre-eclampsia, while controlling known risk factors for pre-eclampsia. METHODS: A matched case-control study was carried out on 41 pre-eclamptic women and 41 normotensive, healthy, pregnant, control women. The pre-eclamptic women and controls were individually matched for age, gravidity, parity, smoking and prenatal care. The number of teeth and the number of restorations and decay on all tooth surfaces, and clinical periodontal parameters, excluding third molars were determined within 48 h before delivery. The relation of independent variables to pre-eclampsia was assessed using conditional multiple logistic regression analysis on subject-based data. RESULTS: There were no statistically significant differences in mean percentages of sites with plaque between groups. The mean probing depth (PD) and mean clinical attachment level (CAL) for pre-eclamptic patients were significantly greater compared to those of normotensive patients (P < 0.01). The percentage of sites exhibiting bleeding on probing (BOP) (P < 0.05), the number of sites with PD >/= 4 mm and with CAL >/= 3 mm was significantly higher among pre-eclamptic patients than those with normotensive patients (P < 0.01). Conditional multiple logistic regression analysis indicated that periodontal disease and triglycerides level were significantly associated with pre-eclampsia. Other independent variables (maternal body weight and serum total cholesterol level) did not appear to be associated with pre-eclampsia. Conditional multiple logistic regression results showed that pre-eclamptic patients were 3.47 (95% CI = 1.07-11.95) times more likely to have periodontal disease than normotensive patients. CONCLUSION: The present study shows that maternal periodontal disease during pregnancy is associated with an increased risk for the development of pre-eclampsia. The higher incidence of periodontal disease parameters in pre-eclamptic group would suggest a possible role for periodontal disease in the development of pre-eclampsia. The nature both of periodontitis and pre-eclampsia is multifactorial, and caution should be exercised when implicating periodontal disease in causation of pre-eclampsia.

Adult↗