Recurrence of Preeclampsia in Northern Tanzania: A Registry-based Cohort Study.

Preeclampsia occurs in about 4 per cent of pregnancies worldwide, and may have particularly serious consequences for women in Africa. Studies in western countries have shown that women with preeclampsia in one pregnancy have a substantially increased risk of preeclampsia in subsequent pregnancies. We estimate the recurrence risks of preeclampsia in data from Northern Tanzania. A prospective cohort study was designed using 19,811 women who delivered singleton infants at a hospital in Northern Tanzania between 2000 and 2008. A total of 3,909 women were recorded with subsequent deliveries in the hospital with follow up through 2010. Adjusted recurrence risks of preeclampsia were computed using regression models. The absolute recurrence risk of preeclampsia was 25%, which was 9.2-fold (95% CI: 6.4 - 13.2) compared with the risk for women without prior preeclampsia. When there were signs that the preeclampsia in a previous pregnancy had been serious either because the baby was delivered preterm or had died in the perinatal period, the recurrence risk of preeclampsia was even higher. Women who had preeclampsia had increased risk of a series of adverse pregnancy outcomes in future pregnancies. These include perinatal death (RR= 4.3), a baby with low birth weight (RR= 3.5), or a preterm birth (RR= 2.5). These risks were only partly explained by recurrence of preeclampsia. Preeclampsia in one pregnancy is a strong predictor for preeclampsia and other adverse pregnancy outcomes in subsequent pregnancies in Tanzania. Women with previous preeclampsia may benefit from close follow-up during their pregnancies

The Comparison of Creatinine and Cystatin C Value in Preeclampsia Severity and Neonatal Outcome

Objectives: to compare the levels of creatinine and cystatin C with the severity of preeclampsia, and assess neonatal outcomes.Materials and Methods: Creatinine, cystatin C, and neonatal outcomes were assesed in 17 normotensive samples, 17 samples of mild preeclampsia and 17 samples of severe preeclampsia. Analysis of data with statistical tests of ANOVA and t test differences between 2 proportions.Results: The mean levels of creatinine in the normotensive group, mild preeclampsia, severe preeclampsia are 0.56 mg/dL, 0.67 mg/ dL, and 0.75 mg/dL, p=0.138; While on cystatin C are 0.82 mg/L, 1.03 mg/L and 1.32 mg/L, p=0.000. The adverse neonatal out-come wasn't found in the normotensive group. In mild pre-eclampsia obtained 1 preterm birth and 1 intrauterine fetal death (IUFD), whereas in severe preeclampsia obtained 3 babies born preterm, 1 IUFD, and 1 intrauterine growth restriction (IUGR).Conclusion: levels of cystatin C was increased significantly in line with increased severity of preeclampsia, whereas creatinine was not increased significantly. Cystatin C is better than crea-tinine as a marker of renal dysfunction in preeclampsia patients. There was an increase in adverse neonatal outcomes in the group of preeclampsia

Serum thyroid hormone levels in preeclampsia women in Gorgan

Etiology of preeclampsia is clearly unknown. The aim of this study was to assess thyroid hormone levels in mild and severe preeclampsia women and compare them with healthy pregnant women. This study was done on 50 healthy pregnant and 50 preeclampsia women in the third trimester in the Sayyad Shirazi educational Hospital, Gynecology Department of Golestan University of Medical Sciences, Iran, 2014. There were significant differences in T4 level among mild preeclampsia and healthy pregnant women. There were also significant differences in T4 and T3 levels between severe, mild preeclampsia women and healthy pregnant women. We observed a significant positive correlation between systolic and diastolic blood pressure and thyroid hormones. Serum T3 and T4 levels were significantly increased with development of preeclampsia. There is association between thyroid hormone abnormalities and hypertension. The difference of our study with other findings could be related to different geographical areas, races and diets. Variation of thyroid functioning later in life may develop in preeclampsia women. Thus, it suggests that thyroid function test may necessary to screen preeclampsia women during pregnancy and after parturition. © 2015, Asian Network for Scientific Information. All rights reserved

CADENCE’S DEFENSE MECHANISM IN RECOVERING HER LOST MEMORY IN WE WERE LIARS BY E. LOCKHART

LA PREECLAMPSIA DIFERENCIAS EPIDEMIOLÓGICAS ENTRE PREECLAMPSIA DE INICIO TEMPRANO (PRECOZ) CON PREECLAMPSIA DE INICIO TARDÍO DIFERENCIAS CLÍNICAS ENTRE PIP Y PIT INVASIÓN TROFOBLÁSTICA DEFICIENTE, LA HIPOPERFUSIÓN PLACENTARIA ANÁLISIS DE ANTECEDENTES INVESTIGATIVOS PLANTEAMIENTO OPERACIONAL CRONOGRAMA DEL TRABAJ

A Practical Understanding of Preeclampsia for a Nurse in a Third World Setting

Preeclampsia is a disease of pregnancy that affects approximately 3-5% of women with child. It is one of the primary causes of mortality in mothers and babies across the globe. The exact cause, pathogenesis, or disease progression is unknown. Therefore, there is no definition of which patients are at risk for developing preeclampsia and what can work as a preventative measure. In high socioeconomic settings where there is good healthcare, standard treatment is established to manage the symptoms and decrease the progression of preeclampsia to eclampsia. However, in more rural, third-world settings of developing countries, caring for patients with preeclampsia is not a straightforward matter. Due to decreased access to health care, low economic status, and lack of education, preeclampsia is often seen yet seldom treated among this population. The discussion below addresses several possible pathophysiological processes of preeclampsia, as well as potential risk factors. The standard treatments of care are then discussed, followed by the evaluation of studies regarding alternative treatments for preeclampsia. The importance of screening pregnant women in developing nations is included. The discussion is concluded by a summary of what caring for preeclampsia in a third-world setting might look like for a missionary nurse

HLA gene expression is altered in whole blood and placenta from women who later developed preeclampsia

Preeclampsia is a multi-system disease that significantly contributes to maternal and fetal morbidity and mortality. In this study, we used a non-biased microarray approach to identify dysregulated genes in maternal whole blood samples which may be associated with the development of preeclampsia. Whole blood samples were obtained at 28 weeks of gestation from 5 women who later developed preeclampsia (cases) and 10 matched women with normotensive pregnancies (controls). Placenta samples were obtained from an independent cohort of 19 women with preeclampsia matched with 19 women with normotensive pregnancies. We studied gene expression profiles using Illumina microarray in blood and validated changes in gene expression in whole blood and placenta tissue by qPCR. We found a transcriptional profile differentiating cases from controls; 236 genes were significantly dysregulated in blood from women who developed preeclampsia. Functional annotation of microarray results indicated that most of the genes found to be dysregulated were involved in inflammatory pathways. Whilst general trends were preserved, only HLA-A was validated in whole blood samples from cases using qPCR (2.30 ± 0.9 fold change) whereas in placental tissue HLA-DRB1 expression was found to be significantly increased in samples from women with preeclampsia (5.88 ± 2.24 fold change). We have identified that HLA-A is up-regulated in the circulation of women who went on to develop preeclampsia. In placenta of women with preeclampsia we identified that HLA-DRB1 is up-regulated. Our data provide further evidence for involvement of the HLA gene family in the pathogenesis of preeclampsia

In preeclampsia, maternal third trimester subcutaneous adipocyte lipolysis is more resistant to suppression by insulin than in healthy pregnancy

Obesity increases preeclampsia risk, and maternal dyslipidemia may result from exaggerated adipocyte lipolysis. We compared adipocyte function in preeclampsia with healthy pregnancy to establish whether there is increased lipolysis. Subcutaneous and visceral adipose tissue biopsies were collected at caesarean section from healthy (n=31) and preeclampsia (n=13) mothers. Lipolysis in response to isoproterenol (200 nmol/L) and insulin (10 nmol/L) was assessed. In healthy pregnancy, subcutaneous adipocytes had higher diameter than visceral adipocytes (<i>P</i><0.001). Subcutaneous and visceral adipocyte mean diameter in preeclampsia was similar to that in healthy pregnant controls, but cell distribution was shifted toward smaller cell diameter in preeclampsia. Total lipolysis rates under all conditions were lower in healthy visceral than subcutaneous adipocytes but did not differ after normalization for cell diameter. Visceral adipocyte insulin sensitivity was lower than subcutaneous in healthy pregnancy and inversely correlated with plasma triglyceride (<i>r</i>=−0.50; <i>P</i>=0.004). Visceral adipose tissue had lower <i>ADRB3, LPL,</i> and leptin and higher insulin receptor messenger RNA expression than subcutaneous adipose tissue. There was no difference in subcutaneous adipocyte lipolysis rates between preeclampsia and healthy controls, but subcutaneous adipocytes had lower sensitivity to insulin in preeclampsia, independent of cell diameter (<i>P</i><0.05). In preeclampsia, visceral adipose tissue had higher <i>LPL</i> messenger RNA expression than subcutaneous. In conclusion, in healthy pregnancy, the larger total mass of subcutaneous adipose tissue may release more fatty acids into the circulation than visceral adipose tissue. Reduced insulin suppression of subcutaneous adipocyte lipolysis may increase the burden of plasma fatty acids that the mother has to process in preeclampsia

A lesson for cancer research : placental microarray gene analysis in preeclampsia

Tumor progression and pregnancy share many common features, such as immune tolerance and invasion. The invasion of trophoblasts in the placenta into the uterine wall is essential for fetal development, and is thus precisely regulated. Its deregulation has been implicated in preeclampsia, a leading cause for maternal and perinatal mortality and morbidity. Pathogenesis of preeclampsia remains to be defined. Microarray-based gene profiling has been widely used for identifying genes responsible for preeclampsia. In this review, we have summarized the recent data from the microarray studies with preeclamptic placentas. Despite the complex of gene signatures, suggestive of the heterogeneity of preeclampsia, these studies identified a number of differentially expressed genes associated with preeclampsia. Interestingly, most of them have been reported to be tightly involved in tumor progression. We have discussed these interesting genes and analyzed their potential molecular functions in preeclampsia, compared with their roles in malignancy development. Further investigations are warranted to explore the involvement in molecular network of each identified gene, which may provide not only novel strategies for prevention and therapy for preeclampsia but also a better understanding of cancer cells. The trophoblastic cells, with their capacity for proliferation and differentiation, apoptosis and survival, migration, angiogenesis and immune modulation by exploiting similar molecular pathways, make them a compelling model for cancer research

Haptoglobin Phenotype, Preeclampsia Risk and the Efficacy of Vitamin C and E Supplementation to Prevent Preeclampsia in a Racially Diverse Population

Haptoglobin's (Hp) antioxidant and pro-angiogenic properties differ between the 1-1, 2-1, and 2-2 phenotypes. Hp phenotype affects cardiovascular disease risk and treatment response to antioxidant vitamins in some non-pregnant populations. We previously demonstrated that preeclampsia risk was doubled in white Hp 2-1 women, compared to Hp 1-1 women. Our objectives were to determine whether we could reproduce this finding in a larger cohort, and to determine whether Hp phenotype influences lack of efficacy of antioxidant vitamins in preventing preeclampsia and serious complications of pregnancy-associated hypertension (PAH). This is a secondary analysis of a randomized controlled trial in which 10,154 low-risk women received daily vitamin C and E, or placebo, from 9-16 weeks gestation until delivery. Hp phenotype was determined in the study prediction cohort (n = 2,393) and a case-control cohort (703 cases, 1,406 controls). The primary outcome was severe PAH, or mild or severe PAH with elevated liver enzymes, elevated serum creatinine, thrombocytopenia, eclampsia, fetal growth restriction, medically indicated preterm birth or perinatal death. Preeclampsia was a secondary outcome. Odds ratios were estimated by logistic regression. Sampling weights were used to reduce bias from an overrepresentation of women with preeclampsia or the primary outcome. There was no relationship between Hp phenotype and the primary outcome or preeclampsia in Hispanic, white/other or black women. Vitamin supplementation did not reduce the risk of the primary outcome or preeclampsia in women of any phenotype. Supplementation increased preeclampsia risk (odds ratio 3.30; 95% confidence interval 1.61-6.82, p<0.01) in Hispanic Hp 2-2 women. Hp phenotype does not influence preeclampsia risk, or identify a subset of women who may benefit from vitamin C and E supplementation to prevent preeclampsia