Disease relevance of Pre-Eclampsia

• The incidence of preeclampsia was lower in the aspirin group (69 of 1485 women [4.6 percent]) than in the placebo group (94 of 1500 women [6.3 percent]) (relative risk, 0.7; 95 percent confidence interval, 0.6 to 1.0; P = 0.05), whereas the incidence of gestational hypertension was 6.7 and 5.9 percent, respectively [1].
• Risk factors for preeclampsia, abruptio placentae, and adverse neonatal outcomes among women with chronic hypertension. National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units [2].
• Pulmonary edema after ritodrine therapy in a patient with preeclampsia [3].
• We suggest that AT(1)-B(2) heterodimers contribute to angiotensin II hypersensitivity in preeclampsia [4].
• BACKGROUND.--Pregnancy-induced hypertension (PIH), defined as either isolated hypertension after the 20th week of gestation or hypertension with proteinuria (preeclampsia), occurs in 5% to 15% of pregnancies and is associated with maternal and neonatal morbidity [5].

Psychiatry related information on Pre-Eclampsia

• Low-dose aspirin to prevent preeclampsia in women at high risk. National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units [6].
• The study also determined whether genetic variability in the gene encoding for microsomal epoxide hydrolase (EPHX) contributes to individual differences in susceptibility to the development of preeclampsia [7].

High impact information on Pre-Eclampsia

• RESULTS: Calcium supplementation did not significantly reduce the incidence or severity of preeclampsia or delay its onset [8].
• We therefore propose that an increase in the sensitivity of platelet calcium to arginine vasopressin can be used as an early predictor of subsequent preeclampsia [9].
• Although the mean creatinine clearance was reduced in the women with preeclampsia, the range of values overlapped with those in the other groups [10].
• Increased AT(1) receptor heterodimers in preeclampsia mediate enhanced angiotensin II responsiveness [4].
• Moreover, we identify preeclampsia as the first disorder associated with altered G-protein-coupled receptor heterodimerization [4].

Chemical compound and disease context of Pre-Eclampsia

• Future interventions should make correcting prostacyclin deficiency a major part of the strategy to balance the abnormal vasoconstrictor-vasodilator ratio present in preeclampsia [11].
• Prostacyclin and thromboxane and the development of preeclampsia [12].
• CONCLUSIONS: Our results indicate that endothelial function is impaired in women with previous preeclampsia and is not explained by established maternal risk factors but is reversed by antioxidant ascorbic acid administration [13].
• Because most trials using aspirin to reduce TxA2 production have failed to prevent preeclampsia, it is critical to determine whether eicosanoid changes occur before the onset of clinical disease or are secondary to clinical manifestations of preeclampsia [11].
• BACKGROUND: Women who took the synthetic estrogen diethylstilbestrol during pregnancy exhibit an elevated risk of breast cancer, whereas those who suffered from preeclampsia, which is associated with low circulating pregnancy estrogens, exhibit a reduced risk [14].
• Cord serum theobromine concentrations were negatively associated with preeclampsia (aOR = 0.31; CI = 0.11-0.87 for highest compared with lowest quartile) [15].

Biological context of Pre-Eclampsia

• Platelet intracellular calcium responses to arginine vasopressin during the first trimester were a sensitive predictor of the subsequent development of preeclampsia (P less than 0.00009) [9].
• CONCLUSIONS: Calcium supplementation during pregnancy leads to an important reduction in systolic and diastolic blood pressure and preeclampsia [16].
• Hence the decrease in fetal prostacyclin production in pre-eclampsia is not related to gestational age; furthermore, it is also seen in other chronic placental insufficiency states [17].
• Genetic susceptibility to pre-eclampsia is associated with HLA DR4; it may be conferred by fetomaternal sharing of a single recessive HLA-linked gene [18].
• We prospectively measured the complement activation products Ba, Bb, SC5b-9, and C4d, as well as the conventional complement determinants C3, C4, and CH50, during pregnancy in 14 patients with SLE and 10 women with preeclampsia [19].

Anatomical context of Pre-Eclampsia

• In preeclampsia, differentiating/invading cytotrophoblasts fail to express properly many of these molecules, including integrin, cadherin, and Ig superfamily members [20].
• Prostacyclin activity in amniotic fluid in pre-eclampsia [21].
• Recent data point to an involvement of GCM proteins in different pathological contexts, such as preeclampsia, hyper- or hypoparathyroidism, and parathyroid gland tumors [22].
• In cases when cytotrophoblast differentiation was compromised (in placentas from women with preeclampsia, or in cells grown under hypoxic conditions in culture), Id-2 expression was maintained [23].
• We measured the in vitro effects of 2% plasma from women with preeclampsia, compared with 2% plasma from normotensive pregnant women, on cultured endothelial cell nitrite production and nitric oxide synthase activity [24].

Gene context of Pre-Eclampsia

• Combinations of maternal KIR and fetal HLA-C genes influence the risk of preeclampsia and reproductive success [25].
• Here, we confirm that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt1 that fall after delivery [26].
• Heparin-binding EGF-like growth factor (HBEGF), which is expressed in the placenta during normal pregnancy, is down regulated in pre-eclampsia, a human pregnancy disorder associated with poor trophoblast differentiation and survival [27].
• The soluble VEGFR1 is overexpressed in placenta in preeclampsia patients [28].
• Preeclampsia is associated with impaired regulation of the placental nitric oxide-cyclic guanosine monophosphate pathway by corticotropin-releasing hormone (CRH) and CRH-related peptides [29].

Analytical, diagnostic and therapeutic context of Pre-Eclampsia

• In contrast, levels of the angiotensin II receptor were elevated in preeclampsia and reduced in IUGR subjects, as shown by RT-PCR and Western blotting analysis [30].
• In preeclampsia, the protein C inhibitor level was higher than in normal pregnancy; it was also higher in normal pregnancy when compared to the control group [31].
• DNA samples collected as part of a large population-based case-control study were genotyped to examine the associations of five prothrombotic gene polymorphisms with pre-eclampsia (PE) and gestational hypertension (GH) [32].
• The results indicate that competitive immunoassays detect the total amount of circulating VEGF, which enables observations regarding the increase in VEGF in pregnancy and preeclampsia to be made [33].
• Cord venous EP was higher in infants delivered by elective cesarean section from women with severe preeclampsia (115; 75-177 mU/ml, p less than 0.001) than in control infants (23; 18-27); in the whole group EP correlated with pH (r = -0.493, p less than 0.001) [34].

References