Cerebrovascular Hemodynamics in Pregnant Women With Mild Chronic Hypertension

2004 ◽  
Vol 103 (2) ◽  
pp. 294-298 ◽  
Author(s):  
Shlomit Riskin-Mashiah ◽  
Michael A. Belfort
Keyword(s):  
Pregnant Women ◽  
Chronic Hypertension ◽  
Cerebrovascular Hemodynamics

Does genetically-defined ancestry predict booking blood pressure in pregnant women with chronic hypertension?

2019 ◽  
Vol 17 ◽  
pp. S11
Author(s):  
Frances Conti-Ramsden ◽  
Raquel Iniesta ◽  
Phil Chowienczyk ◽  
Lucy C. Chappell
Keyword(s):  
Blood Pressure ◽  
Pregnant Women ◽  
Chronic Hypertension

scholarly journals The Association of Familial Hypertension and Risk of Gestational Hypertension and Preeclampsia

2021 ◽  
Vol 18 (13) ◽  
pp. 7045
Author(s):  
Małgorzata Lewandowska
Keyword(s):  
Risk Factor ◽  
Pregnant Women ◽  
Odds Ratio ◽  
Independent Risk Factor ◽  
Gestational Hypertension ◽  
First Trimester ◽  
Chronic Hypertension ◽  
Modifiable Factors ◽  
The Family ◽  
Maternal Hypertension

It has not been established how history of hypertension in the father or mother of pregnant women, combined with obesity or smoking, affects the risk of main forms of pregnancy-induced hypertension. A cohort of 912 pregnant women, recruited in the first trimester, was assessed; 113 (12.4%) women developed gestational hypertension (GH), 24 (2.6%) developed preeclampsia (PE) and 775 women remained normotensive (a control group). Multiple logistic regression was used to calculate adjusted odds ratios (AOR) (and 95% confidence intervals) of GH and PE for chronic hypertension in the father or mother of pregnant women. Some differences were discovered. (1) Paternal hypertension (vs. absence of hypertension in the family) was an independent risk factor for GH (AOR-a = 1.98 (1.2–3.28), p = 0.008). This odds ratio increased in pregnant women who smoked in the first trimester (AOR-a = 4.71 (1.01–21.96); p = 0.048) or smoked before pregnancy (AOR-a = 3.15 (1.16–8.54); p = 0.024), or had pre-pregnancy overweight (AOR-a = 2.67 (1.02–7.02); p = 0.046). (2) Maternal hypertension (vs. absence of hypertension in the family) was an independent risk factor for preeclampsia (PE) (AOR-a = 3.26 (1.3–8.16); p = 0.012). This odds ratio increased in the obese women (AOR-a = 6.51 (1.05–40.25); p = 0.044) and (paradoxically) in women who had never smoked (AOR-a = 5.31 (1.91–14.8); p = 0.001). Conclusions: Chronic hypertension in the father or mother affected the risk of preeclampsia and gestational hypertension in different ways. Modifiable factors (overweight/obesity and smoking) may exacerbate the relationships in question, however, paradoxically, beneficial effects of smoking for preeclampsia risk are also possible. Importantly, paternal and maternal hypertension were not independent risk factors for GH/PE in a subgroup of women with normal body mass index (BMI).

The Significance of Antiphospholipid Antibodies in Pregnant Women with Chronic Hypertension

2004 ◽  
Vol 21 (5) ◽  
pp. 275-279 ◽  
Author(s):  
Gerda G Zeeman ◽  
James M Alexander ◽  
Donald D McIntire ◽  
Kenneth J Leveno
Keyword(s):  
Pregnant Women ◽  
Antiphospholipid Antibodies ◽  
Chronic Hypertension

scholarly journals Relationship Parity and Contraception with Mild Preeclampsia at Puskesmas Jagir

2016 ◽  
Vol 4 (1) ◽  
pp. 100
Author(s):  
Rizky Pradana Setiawan
Keyword(s):  
Diabetes Mellitus ◽  
Body Weight ◽  
Family History ◽  
Pregnant Women ◽  
Calcium Supplementation ◽  
Chronic Hypertension ◽  
Family History Of Diabetes ◽  
Maternal Characteristics ◽  
History Of ◽  
Mild Preeclampsia

Mild preeclampsia is the frequent disease experienced by pregnant women in Puskesmas Jagir in 2011-2014. The number of mild preeclampsia in Puskesmas Jagir keep increase significantly. The purpose of this study is to analyze the association between the characteristics, family history and calcium supplementation in pregnant women with mild preeclampsia at Puskesmas Jagir Surabaya. The type of research is non-reactive research with case control design. Subjects was taken from the population using simple random sampling. The variables studied were age, body weight changes, parity, family history of preeclampsia, contraception, family history of diabetes mellitus, family history of chronic hypertension, and calcium supplementation. The statistical test was Chi-square test with α = 0.05, odds Ratio is calculated by value with 95% confidence interval (CI 95%). Variables associated with mild preeclampsia is a maternal characteristics such as parity (p = 0.001, OR 0.17) and contraception (p = 0.019, OR = 5.636). Variables that are not associated with mild preeclampsia is a maternal characteristics such as the form of changes in body weight during pregnancy, age, and family history of diabetes mellitus in the form of family history and family history of hypertension and calcium supplementation. There is a association between parity and contraception with mild preeclampsia.Keywords: mild preeclampsia, parity, contraception 

scholarly journals Genetic Association of ERAP1 and ERAP2 With Eclampsia and Preeclampsia in Northeastern Brazilian Women

2021 ◽  
Author(s):  
LEONARDO CAPISTRANO FERREIRA ◽  
CARLOS EDUARDO MAIA GOMES ◽  
PRIYA DUGGAL ◽  
INGRID DE PAULA HOLANDA ◽  
AMANDA SAMARA DE LIMA ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Genetic Variants ◽  
Antigen Processing ◽  
P Value ◽  
Chronic Hypertension ◽  
Ang Ii ◽  
Small Peptides ◽  
Increased Risk ◽  
Genotype C ◽  
Risk Of Preeclampsia

Abstract The clinical spectrum of hypertensive disorders of pregnancy (HDP) is determined by the interplay between environmental and genetic factors, most of which remains unknown. ERAP1, ERAP2 and LNPEP genes code for multifunctional aminopeptidases involved with antigen processing and degradation of small peptides such as angiotensin II (Ang II), vasopressin and oxytocin. We aimed to test for associations between genetic variants in aminopeptidases and HDP. A total of 1282 pregnant women (normotensive controls, n=693; preeclampsia, n=342; chronic hypertension with superimposed preeclampsia, n=61; eclampsia, n=74; and HELLP syndrome, n=112) were genotyped for variants in LNPEP (rs27300, rs38034, rs2303138), ERAP1 (rs27044, rs30187) and ERAP2 (rs2549796 rs2927609 rs11135484). We also evaluated the effect of ERAP1 rs30187 on plasma Ang II levels in an additional cohort of 65 pregnant women. The genotype C/C, in ERAP1 rs30187 variant (c.1583T>C, p.Lys528Arg), was associated with increased risk of eclampsia (OR=1.85, p=0.019) whereas ERAP2 haplotype rs2549796(C)-rs2927609(C)-rs11135484(G) was associated with preeclampsia (OR=1.96, corrected p-value=0.01). Ang II plasma levels did not differ across rs30187 genotypic groups (p=0.895). In conclusion, ERAP1 gene is associated with eclampsia whereas ERAP2 is associated with preeclampsia, although the mechanism by which genetic variants in ERAPs influence the risk of preeclampsia and eclampsia remain to be elucidated.

scholarly journals Association between insulin resistance and preeclampsia in obese non-diabetic women receiving metformin

2017 ◽  
Vol 10 (4) ◽  
pp. 170-173 ◽  
Author(s):  
Jyoti Balani ◽  
Steve Hyer ◽  
Argyro Syngelaki ◽  
Ranjit Akolekar ◽  
Kypros H Nicolaides ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Pregnant Women ◽  
Significant Contribution ◽  
Randomised Trial ◽  
Secondary Analysis ◽  
Chronic Hypertension ◽  
Model Assessment ◽  
Gestational Weight ◽  
Metformin Group ◽  
History Of

Objectives To examine whether the reduced incidence of preeclampsia in non-diabetic obese pregnant women treated with metformin is mediated by changes in insulin resistance. Methods This was a secondary analysis of obese pregnant women in a randomised trial (MOP trial). Fasting plasma glucose and insulin were measured in 384 of the 400 women who participated in the MOP trial. Homeostasis model assessment of insulin resistance (HOMA-IR) was compared in the metformin and placebo groups and in those that developed preeclampsia versus those that did not develop preeclampsia. Results At 28 weeks, median HOMA-IR was significantly lower in the metformin group. Logistic regression analysis demonstrated that there was a significant contribution in the prediction of preeclampsia from maternal history of chronic hypertension and gestational weight gain, but not HOMA-IR either at randomisation ( p = 0.514) or at 28 weeks ( p = 0.643). Conclusions Reduced incidence of preeclampsia in non-diabetic obese pregnant women treated with metformin is unlikely to be due to changes in insulin resistance.

Abstract P322: Vasopressin Release is Enhanced Before the Development of Preeclampsia in Humans Despite Exaggerated Suppression of Plasma Osmolality

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Mark K Santillan ◽  
Sabrina M Scroggins ◽  
Alyssa T Ray ◽  
Phillip C Witcher ◽  
Jeremy A Sandgren ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Gestational Age ◽  
Clinical Symptoms ◽  
Freezing Point ◽  
Tissue Bank ◽  
Plasma Osmolality ◽  
Fetal Tissue ◽  
Chronic Hypertension ◽  
Vasopressin Release ◽  
Osmotic Stimuli

Plasma osmolality (Osm) suppression is of critical importance to maintain appropriate blood volume to perfuse the uterus during pregnancy. Osm is reduced starting at the fifth week of gestation via increased arginine vasopressin (AVP) secretion. This increased secretion is maintained via a decrease in the AVP/osmotic release threshold. We previously demonstrated that pregnant women who develop preeclampsia (PreE) exhibit exaggerated AVP secretion as early as the 6th week of gestation via measurement of copeptin, the stable C-terminal fragment of AVP. It is unclear whether AVP secretion is elevated before the onset of PreE due to osmotic or non-osmotic stimuli. We tested the hypothesis that elevated AVP secretion before PreE may be associated with elevated Osm (a strong stimulant of AVP secretion). Plasma and clinical data from pregnant women were obtained from the University of Iowa Maternal-Fetal Tissue Bank (IRB#200910784). Osm was measured using the freezing-point suppression technique. Osm was assessed in non-pregnant women (n=109), pregnant women who later developed PreE (n=12 for 7-12 weeks, n=9 for 16-24 weeks), and maternal and gestational age matched controls (n=25 for 6-13 weeks, n=15 for 14-27 weeks). As expected, Osm was decreased in control pregnancies (non-pregnant 291±1 vs pregnant 286±1 mOsm/kg, p<0.05). Contrary to our hypothesis, the Osm decrease was exaggerated in women who would later develop PreE (1st trimester: PreE 279±4 vs control 287±3, and 2 nd trimester: PreE 277±4 vs control 285±3 mOsm/kg; effect of PreE p<0.05, gestational age p=NS, interaction p=NS) even after controlling for age, BMI, diabetes, chronic hypertension, history of preeclampsia, and gravida (model p<0.05). Despite suppressed Osm, plasma copeptin was elevated in the PreE group at all timepoints (p<0.05). These data support the conclusion that long before the development of clinical symptoms of PreE, the rate of secretion of AVP is inappropriately increased despite maintenance of normal osmotic-regulating actions of AVP. This effect must be the result of increased non-osmotic stimuli for AVP, and a suppression of the AVP/osmotic release threshold beyond that observed in control pregnancies.

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