Subsequent Development Of Pregnancy-induced Hypertension Research Articles

Systolic blood pressure and fatty acid-binding protein 4 predict pregnancy-induced hypertension in overweight nulliparous women

IntroductionThe insulin-sensitivity regulator adipocyte fatty acid-binding protein 4 (FABP4) integrates metabolic and inflammatory responses. We hypothesize that there is relationship between FABP4 and factors related to metabolic syndrome in pregnancy-induced hypertension (PIH). MethodsIn this prospective observational study, among the 72 relatively overweight (BMI ≥24 kg/m2) nulliparous women, 14 developed non-proteinuric PIH and 12 developed proteinuric PIH (preeclampsia), whereas 46 had normotensive pregnancies. Insulin sensitivity was assessed via the whole-body insulin sensitivity index (ISI) and the homeostatic model of assessment – insulin resistance (HOMA-IR) at 24 weeks of gestation. Maternal serum levels of FABP4, high-sensitive C-reactive protein (hs-CRP), total testosterone, and non-protein-bound calculated free testosterone (cfT) were determined at 24 and 32 weeks. ResultsMeasures of ISI, HOMA-IR, hs-CRP, testosterone and lipids did not differ at 24 and/or at 32 weeks in women who were subsequently hypertensive. SBP was higher at all time points and FABP4 levels tended to be higher at 24 and 32 weeks in patients compared to controls. In logistic regression analysis, baseline FABP4 (OR [95% CI] 1.069 [1.020–1.121], P = 0.006) and SBP after 10 min standing (OR [95% CI] 1.087 [1.029–1.149], P = 0.003) were associated with the development of PIH. FABP4 levels at 24 weeks did not correlate with insulin sensitivity. Neither was correlation seen between FABP4 levels at 24 and 32 weeks, vs. those of hs-CRP and testosterone. Discussion and conclusionsSerum FABP4 concentration and SBP after 10 min standing in an orthostatic test at 24 weeks are associated with subsequent development of PIH.

Elevated serum angiopoietin-like protein 6 in women with subsequent pregnancy-induced hypertension: a preliminary study

Objective: Association of maternal angiopoietin-like protein 6 (Angptl6) levels with subsequent development of pregnancy-induced hypertension (PIH). Methods: At 24 and 32 weeks of gestation in 47 relatively overweight (BMI ≥ 24 kg/m2), nulliparous pregnant women serum concentrations of Angptl6 were quantified prospectively. Insulin sensitivity and lipids were measured at 24 weeks. Results: Angptl6 levels at 24 weeks, but not at 32 weeks, were significantly higher in women with subsequent PIH. Metabolic factors at 24 weeks did not correlate with Angptl6 levels. Conclusion: This preliminary study suggests that in the second trimester, Angptl6 levels are higher in women with subsequent PIH.

Second-trimester maternal β-human chorionic gonadotropin level associated with subsequent development of pregnancy-induced hypertension

Objective To determine whether maternal β-human chorionic gonadotropin(β-hCG) level in second-trimester may be associated with subsequent development of pregnancy-induced hypertension(PIH). Methods Seven hundred and sixty-two women in mid-trimester were to have maternal urine β-hCG standardized concentrations and maternal serum β-hCG measurements. Their case histories were recorded and reviewed from mid-trimester to delivery. The relation was observed between maternal urine, serum markers and subsequent development of PIH. Results Among 762 women, 504 cases were normal pregnancies, 42 cases had PIH, 94 cases had premature rupture of membrane (PROM), 69 cases had preterm delivery (PD), 53 other cases were excluded by various reasons. The levels of maternal urine, serum β-hCG in PIH were (61.75±9.78) IU/L and (304.56±54.17) ng/mg respectively, which were higher significantly than normal pregnancy group ([20.65±7.61] IU/L and [146.34±47.81] ng/mg, P<0.05). When maternal serum, urine β-hCG levels ≥2 MOM (multiple of mean), the incidences of developing PIH were increased significantly as compared with those of β-hCG <2 MOM women. The incidence of PIH increased from 5.1% in pregnancies with urine β-hCG ≥2 MOM to 11.7% in cases with urine β-hCG ≥4 MOM. Conclusion The elevation of maternal mid-trimester urine, serum β-hCG levels is not only an early signal for dysfunction of placenta but also a dangerous signal for development of PIH. Second-trimester maternal urine β-hCG measurement proves to be superior to serum marker in clinical prediction.

Plasma levels of microparticles at 24 weeks of gestation do not predict subsequent pregnancy complications

To discern whether plasma levels of microparticles (MPs) measured at 24 weeks of gestation predict late complications of pregnancy. Secondary analysis of samples obtained prospectively. Large academic medical center. Two hundred sixty-two healthy women selected from 642 nulliparous women with singleton pregnancies. Sampling for blood cell MPs and thrombophilias at 24 weeks of gestation and measurements of blood flow resistance in uterine, placental, and umbilical arteries at 24 and 31 to 33 weeks of gestation. Relationship between levels of MPs and late pregnancy complications, thrombophilias, and blood flow resistance. Flow cytometry only detected MPs derived from endothelial cells (CD31(+)) and platelet (CD41(+)). No statistically significant correlation was found between levels of CD31(+) or CD41(+) MPs and subsequent occurrence of pregnancy-induced hypertension, preeclampsia, intrauterine growth restriction, or small for gestational age infants. Nor was there a statistically significant correlation with blood flow resistance parameters at 24 weeks of gestation (except for the left uterine artery) or at 31 to 33 weeks of gestation. Levels of these MPs in thrombophilic and nonthrombophilic women were similar. Levels of circulating MPs at 24 weeks of gestation had no predictive value for subsequent development of pregnancy-induced hypertension, preeclampsia, intrauterine growth restriction, or small for gestational age infants.

Determination of Insulin Resistance Using the Homeostatic Model Assessment (HOMA) and its Relation With the Risk of Developing Pregnancy-Induced Hypertension

To assess whether increased insulin resistance determined by homeostatic model assessment (HOMA) early in pregnancy is associated with the subsequent development of pregnancy-induced hypertension (PIH) in Colombian women with known risk factors. We conducted a nested case control study in a prospective cohort of 572 normotensive pregnant women, with gestational age < or = 30 weeks, recruited in Bucaramanga and Floridablanca, Colombia. Fasting plasma glucose and insulin concentrations were determined at enrollment, and HOMA index was calculated. Log-transformed HOMA (log-HOMA) was used in the statistical analysis. Thirty nine PIH cases (18 preeclampsia [PE], 21 gestational hypertension [GH]) were compared to 78 controls, matched by body mass index, gestational and maternal age at enrollment. Women who subsequently developed PIH had higher levels of log-HOMA at enrollment (-0.13 +/- 0.54 v 0.21 +/- 0.60; P = .002), which was significantly associated with the development of PIH (odds ratio 3.13, 95% confidence interval 1.41-6.94; P = .005). Higher log-HOMA was found in women who subsequently developed PE (0.28 +/- 0.58; P = .003), and in those who presented with GH (0.15 +/- 0.62; P = .026). Women who subsequently develop PIH have a higher degree of insulin resistance determined by log-HOMA early in pregnancy, before the onset of clinical manifestations of the disease. The HOMA seems to be a useful method to evaluate women at risk of developing PIH. More studies are required to confirm its usefulness as a screening tool to identify pregnant women at risk of developing PIH.

Midpregnancy serum C-peptide concentration and subsequent pregnancy-induced hypertension.

To test the hypothesis that elevated midpregnancy serum insulin (IRI) and C-peptide (CP) concentrations are associated with later development of pregnancy-induced hypertension (PIH), independent of prepregnancy obesity and midpregnancy blood pressure. In this prospective study, a cohort of normotensive women, ages > or = years performed a 50-g glucose challenge test at 24-30 weeks' gestational age. Blood samples were collected after an overnight fast and 1 h after glucose ingestion. Serum IRI and CP concentrations were measured in each sample. Maternal height, blood pressure and proteinuria were measured at the time of glucose challenge testing and after 36 weeks' gestational age. Of 320 subjects enrolled 44 women (13.8%) had subsequent PIH. Crude odds ratios (ORs) for devevelopment of PIH associated with each 1 U rise in log fasting IRI, log lasting CP. and glucosed-induced increase in CP (expressed as log [postprandial CP/fasting CP]) were 2.0 (95% CI 1.3-3.3), 1.8 (CI 1.2-2.7), and 2.3 (CI 1.1-4.9) respectively. After controlling for prepregnancy BMI, gestational age, and midpregnancy mean arterial pressure, adjusted ORs corresponding to log fastig IRI and CP for the development of PIH were 1.3 (95% CI 0.7-2.3) and 1.7 (CI 1.1-2.7) respectively, and, afterq adjustment for fasting CP, the adjusted OR of the glucose-induced rise in log CP was 3.7 (CI 1.5-9.3). Mid-pregnancy tasting and postoral glucose CP levels are associated with subsequent development of PIH, independent of maternal obesity and midpregnancy baseline blood pressure. These findings many reflect an amplified beta3-cell response to glycemic stimulus, similar to that found in states of insulin resistance, that appears to be independently associated with PIH.

Second-trimester plasma homocysteine levels and pregnancy-induced hypertension, preeclampsia, and intrauterine growth restriction

Objective: The purpose of this study was to determine whether second-trimester plasma homocysteine levels are elevated among women whose pregnancies are subsequently complicated by pregnancy-induced hypertension, preeclampsia, or intrauterine growth restriction. Study Design: Women with normal but relatively low plasma zinc levels were randomly assigned to receive zinc supplementation or placebo from 19 weeks’ gestation until delivery. Plasma homocysteine concentration and plasma and erythrocyte folate levels were determined for all available stored samples (zinc group, 231/294; placebo group, 206/286) at 26 and 37 weeks’ gestation. Among all women with available samples, pregnancy-induced hypertension (n = 12) or preeclampsia (n = 4) developed in 16 women, and 22 pregnancies were complicated by intrauterine growth restriction. Results: Mean homocysteine levels in women with pregnancy-induced hypertension and preeclampsia were similar to those of control subjects at 26 weeks’ gestation but were significantly higher at 37 weeks’ gestation. Homocysteine levels were similar between women with pregnancies complicated by intrauterine growth restriction and control subjects at both time points. Conclusion: Second-trimester plasma homocysteine concentrations do not predict the subsequent development of pregnancy-induced hypertension, preeclampsia, and intrauterine growth restriction. (Am J Obstet Gynecol 2000;183:805-9.)

Erratum: Relationship of insulin resistance and hyperinsulinemia to blood pressure during pregnancy

The purpose of our study was to examine the relationship between insulin resistance and blood pressure during pregnancy and to determine to what extent insulin resistance is related to the subsequent development of pregnancy-induced hypertension. The study population consisted of 292 women who had serum insulin, glucose and insulin-glucose ratios determined at 26–28 weeks gestation in a fasting state and 1 hr after a 50-g oral glucose challenge. These were compared with blood pressures at 26–28 weeks gestation and in the late third trimester. A statistically significant correlation exists overall between (1) blood pressure at 26–28 weeks gestation and both fasting insulin and insulin-glucose ratios, as well as (2) systolic blood pressure at term and fasting insulin levels. However, when controlled for confounding variables including body mass index, race and age, no statistically significant relationship remained. The metabolic variables in patients with pregnancy-induced hypertension were not statistically different from the normotensive patients. In conclusion, this study demonstrates that insulin resistance and hyperinsulinemia are not major determinants of blood pressure during pregnancy. J. Matern.–Fetal Med. 6:174–179, 1997. © 1997 Wiley-Liss, Inc.

Relationship of insulin resistance and hyperinsulinemia to blood pressure during pregnancy.

The purpose of our study was to examine the relationship between insulin resistance and blood pressure during pregnancy and to determine to what extent insulin resistance is related to the subsequent development of pregnancy-induced hypertension. The study population consisted of 292 women who had serum insulin, glucose and insulin-glucose ratios determined at 26-28 weeks gestation in a fasting state and 1 hr after a 50-g oral glucose challenge. These were compared with blood pressures at 26-28 weeks gestation and in the late third trimester. A statistically significant correlation exists overall between (1) blood pressure at 26-28 weeks gestation and both fasting insulin and insulin-glucose ratios, as well as (2) systolic blood pressure at term and fasting insulin levels. However, when controlled for confounding variables including body mass index, race and age, no statistically significant relationship remained. The metabolic variables in patients with pregnancy-induced hypertension were not statistically different from the normotensive patients. In conclusion, this study demonstrates that insulin resistance and hyperinsulinemia are not major determinants of blood pressure during pregnancy.

Relationship of insulin resistance and hyperinsulinemia to blood pressure during pregnancy

The purpose of our study was to examine the relationship between insulin resistance and blood pressure during pregnancy and to determine to what extent insulin resistance is related to the subsequent development of pregnancy-induced hypertension. The study population consisted of 292 women who had serum insulin, glucose and insulin-glucose ratios determined at 26–28 weeks gestation in a fasting state and 1 hr after a 50-g oral glucose challenge. These were compared with blood pressures at 26–28 weeks gestation and in the late third trimester. A statistically significant correlation exists overall between (1) blood pressure at 26–28 weeks gestation and both fasting insulin and insulin-glucose ratios, as well as (2) systolic blood pressure at term and fasting insulin levels. However, when controlled for confounding variables including body mass index, race and age, no statistically significant relationship remained. The metabolic variables in patients with pregnancy-induced hypertension were not statistically different from the normotensive patients. In conclusion, this study demonstrates that insulin resistance and hyperinsulinemia are not major determinants of blood pressure during pregnancy. J. Matern.-Fetal Med. 6:174–179, 1997. © 1997 Wiley-Liss, Inc.

The use of the hand-grip test for predicting pregnancy-induced hypertension

To assess the potential of the hand-grip exercise test as a screening test for pregnancy-induced hypertension a prospective non-interventional study was carried out in a teaching hospital antenatal clinic. The hand-grip test was performed on 200 nulliparous, normotensive subjects at 28–32 weeks gestation. The main outcome measurement was the subsequent development of pregnancy-induced hypertension or pre-eclampsia. The sensitivity of the technique in predicting pregnancy-induced hypertension was 53% and the specificity was 94%. The sensitivity of the test in predicting pre-eclampsia was 80% and the specificity was 92%. The time-consuming nature of the hand-grip test probably restricts use of the technique to research studies where selection of a high-risk group is required.

Factors Associated with Pregnancy-Induced Hypertension

This article reports the results of a correlational study that explored the association between the three factors of pregravid weight, prenatal weight gain at 28 weeks and maternal age, and the subsequent development of pregnancy-induced hypertension (PIH). A significant relationship between low maternal age and PIH development was found. Further data analysis showed that PIH occurred significantly more often when the second trimester mean arterial pressure (MAP) did not drop to a level lower than the first trimester MAP. Clinically, emphasis should be placed on early detection of women at high risk for PIH development. Analysis of the MAP changes could prove to be a low-cost, effective and low-risk predictive test for PIH development.