Early pregnancy soluble E-selectin concentrations and risk of preeclampsia.
ABSTRACT Circulating biomarkers of endothelial dysfunction and inflammation are elevated in late pregnancy in women with preeclampsia. We examined plasma levels of inflammatory cytokines and adhesion molecules in early pregnancy, to assess their ability to predict preeclampsia.
In a prospective longitudinal study, 2600 women with singleton pregnancies and no history of hypertension were recruited at their antenatal hospital (booking) visit at gestational week 12-16. Of these, 49 (1.9%) developed preeclampsia, whereas 74 women matched for age and BMI with uncomplicated pregnancies were selected as controls. A subset of women with risk factors for preeclampsia were sampled again at gestational weeks 16 and 28 (11 cases, 39 controls) and postnatally (six cases, 36 controls).
From multiplex analysis, soluble E-selectin concentrations were higher at 12-16 weeks in women who subsequently developed preeclampsia (15.1 ± 4.9 versus 12.9 ± 4.5 ng/ml, P = 0.02). At gestational week 28, E-selectin concentrations were again higher in women who went on to develop preeclampsia compared with controls (14.4 ± 5.6 versus 10.7 ± 3.5 ng/ml, P = 0.010), whereas levels were not different between the two groups in postpartum samples.
Changes in soluble E-selectin concentration in early pregnancy may reflect underlying pathophysiological processes, potentially providing mechanistic insights into preeclampsia.
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ABSTRACT: The aim of the prospective study was to compare standard parameters as Doppler ultrasound and 24-h blood pressure measurement with possible maternal serological markers regarding their prognostic value in predicting hypertensive diseases in pregnancy. Twenty-four-hour blood pressure measurement was performed before and after 32+0 gestational week in 57 pregnant women with either chronic hypertension ( n=13), preeclampsia ( n=21), pregnancy-induced hypertension (PIH; n=12) or normotension ( n=11). Blood samples were taken and the concentrations of soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), activin A and inhibin A were determined as well as serum uric acid, creatinine, total serum protein and serum albumin. Doppler ultrasound of the uterine arteries was examined before 32+0 gestational week in the same patients. For the statistical evaluation Kruskal-Wallis-Test and Mann-Whitney-U-Test were performed. Differences in the predictive value were evaluated by receiver-operating characteristics. VCAM-1 was significantly elevated in women developing hypertensive diseases as compared to normotensive women (preeclampsia: p<0.001; PIH: p<0.05; chronic hypertension: p<0.001). In early pregnancy activin A and inhibin A were significantly higher in preeclamptic patients than in the other groups (activin A: normotension: p<0.005; PIH: p<0.001; chronic hypertension: p<0.005) (inhibin A: normotension: p<0.005; PIH: p<0.001; chronic hypertension: p<0.01), thus suggesting them to be specific markers for the development of preeclampsia. Mean arterial pressure was significantly elevated in preeclampsia ( p<0.001) and chronic hypertension ( p<0.005) as compared to normotensives. Twenty-four-hour blood pressure monitoring with determination of mean arterial pressure and measurement of VCAM-1, activin A and inhibin A as serum parameters can be suggested as useful tests in the specific prediction of different types of hypertensive diseases in pregnancy.Archives of Gynecology and Obstetrics 10/2004; 270(2):110-5. · 1.33 Impact Factor
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ABSTRACT: We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated.Hypertension 02/2007; 49(1):90-5. · 6.87 Impact Factor
Article: Th1/Th2 balance in preeclampsia.[show abstract] [hide abstract]
ABSTRACT: The syndrome of preeclampsia has previously been ascribed to generalized maternal endothelial dysfunction, poor placentation and excessive maternal inflammatory response. Recent reports suggest that preeclampsia is associated with a Th1 predominant profile and may be considered as a failure of the tolerance system allowing the second physiological trophoblastic invasion. In this review, we discuss that Th1 predominant immunity is closely related to inflammation, endothelial dysfunction and poor placentation.Journal of Reproductive Immunology 09/2003; 59(2):161-73. · 2.34 Impact Factor