Pregnancy-induced Hypertension Preeclampsia Research Articles

Placental pathology associated with maternal age and maternal obesity in singleton pregnancy

Objective Maternal age, maternal obesity and neonatal sex dimorphism are known to affect pregnancy and neonatal outcome. However, the effects of these factors on specific placental pathology are less well-documented. Study design Clinical information, placental pathology and neonatal data from singleton delivery were collected at our hospital in March 2020 to October 2021 and correlation studies were performed. Results A total 3,119 singleton placentas were examined between March 2020 and October 2021 in conjunction with clinical information and neonatal birth data. Advanced maternal age (>35) was significantly associated with a variety of pregnancy complications and placental pathology including preeclampsia/pregnancy induced hypertension (Pre/PIH), gestational diabetes mellitus (GDM2), intrauterine growth restriction (IUGR), and increased maternal body mass index (BMI) at delivery. Maternal obesity (BMI >30 at the time of delivery) was significantly associated with a variety of clinical features and placental pathology including PRE/PIH, GDM2 and decidual vasculopathy (mural arterial hypertrophy). No specific placental pathology was associated with neonatal sex except for more maternal inflammatory response (MIR, chronic deciduitis) in neonates of male sex. Conclusion Maternal age and maternal obesity were associated with not only clinical complications of pregnancy and neonatal birth weight but also specific placental pathology. Understanding the effects of maternal and environmental factors will help improve pregnancy outcome.

Serum uric acid levels in pregnancy induced hypertension preeclampsia

Preeclampsia is a pregnancy specific syndrome which involves an increase of arterial blood pressure, accompanied by proteinuria, oedma or even both. This investigation was intended to compare the serum uric acid level in preeclamptic and normal pregnant women and its correlation with some important maternal and fetal results. The subjects were partitioned into two groups, Group I: control subjects normal pregnant women and Group II: pregnancy induced hypertensive women. Each groups consisted of 30 pregnant women of Uttar Pradesh (India). The blood sample was collected and analyzed for biochemical parameters, blood urea, serum uric acid, serum creatinine and total protein. The result data were dissected by using SPSS. The systolic (SBP) and diastolic blood pressure (DBP) and serum uric acid were significantly (P Keywords: Preeclampsia, Uric acid, Early-onset preeclampsia, Late-onset preeclampsia.

Effect of raised serum uric acid level on perinatal and maternal outcome in cases of pregnancy-induced hypertension

The aim of this study was to find out the effects of raised serum uric acid level on perinatal and maternal outcome in cases of pregnancy-induced hypertension. One hundred pregnant women with gestational period beyond 28 weeks with pregnancy-induced hypertension-preeclampsia and eclampsia were included in this study and divided into two groups. Group A (n=65) patients with a serum uric acid level >6 mg/dL was compared to Group B (n=35) patients with a uric acid level <6 gm/dL. It revealed that high uric acid level in patients with pregnancy-induced hypertension was a risk factor for several maternal complications like postpartum hemorrhage (Group A, 12 cases; Group B, 7 cases), postpartum eclampsia (Group A, 7 cases; Group B, 3 cases), abruptio placentae (Group A, 6 cases; Group B, 2 cases), HELLP syndrome (Group A, 2 cases; Group B, no case) and pulmonary edema (Group A, 3 cases; Group B, no case). In case of perinatal outcome, the birth weight, intrauterine growth retardation, intrauterine death, stillbirth and neonatal death rate were worse in Group A 1.9 kg, 46, 19, 7 and 8 cases in comparison to Group B, where those were 2.1, 13, 6, 2, and 2 cases respectively. In conclusion, high uric acid in blood in patient with hypertensive disorders in pregnancy is a risk factor for several maternal complications.

Cerebral palsy and perinatal mortality after pregnancy‐induced hypertension across the gestational age spectrum: observations of a reconstructed total population cohort

Pregnancy-induced hypertension/pre-eclampsia (PIH/PE) is associated with cerebral palsy (CP) in term births but if sufficiently severe to necessitate preterm delivery predicts a lower risk of CP than observed in gestational peers. We investigated whether this apparent 'protection' was attributable to inappropriately chosen comparison groups and/or an increased risk of perinatal death. Perinatal information was collected from medical records of children with CP, individually matched neonatal survivors without CP, and representative samples of perinatal deaths of Western Australian birth cohorts from 1980 to 1995. Compared with these data, the sensitivity of statutorily collected PIH/PE data was assessed for each outcome group. Using these sensitivities, the estimated risks of death and CP in births to all women with and without PIH/PE were compared. Sensitivity of statutory PIH/PE data decreased with increasingly poor outcome. Reconstructed cohorts showed that PIH/PE increased the risks both of CP and of perinatal death in births at lower gestations except in births <27 weeks, where the risk of perinatal death only increased greatly. PIH/PE does not protect against poor outcome at any gestational age. Previously reported protective effects originate from inappropriate control for gestational age and not from higher gestation-specific perinatal mortality.

Lack of association between maternal periodontal status and adverse pregnancy outcomes: a multicentric epidemiologic study

Objective(s): The aim of this study was to explore the relationship between periodontal health and pregnancy outcomes in a large cohort of Italian postpartum women. Methods: 750 postpartum women were enrolled in a case–control study within 5 days from delivery at three Italian obstetric clinics. Cases were defined as those mothers who delivered an infant weighing under 2500 g (LBW) and/or had premature delivery and/or delivered small for gestational age newborns (SGA) and/or experienced preeclampsia/pregnancy induced hypertension (PE/PIH) or preterm premature rupture of membranes (pPROM) during pregnancy. All women received comprehensive oral and dental examination. Associations between adverse pregnancy outcome and exposures of interest were evaluated by the use of multivariate logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results: There was no significant difference between cases and controls with respect to country of birth, age, place of residence, educational achievement, smoking, and periodontal status. By definition, infant birth weight [2,750 g (IQR = 2,300–3,200 g) and 3,275, (IQR = 3,010–3,538 g) p < 0.001, respectively] and gestational age at delivery [259 days (IQR = 245–273) and 273 days (IQR = 266–280), p < 0.01, respectively] were significantly lower in cases than in controls. In multivariate analyses, a borderline association was found between poor obstetric outcomes and current smokers (OR: 1.5; 95% CI: 0.1–2.5). Finally, after adjusting for smoking status neither country of birth, nor age or place of residence or education or periodontitis were associated with a significantly increased risk of adverse pregnancy outcome. Conclusion(s): Our data failed to demonstrate the association between periodontitis and an adverse pregnancy outcome such as preterm birth, low birth weight, preeclampsia, intrauterine growth restriction, and premature rupture of membranes.

LEPR c.668A&gt;G polymorphism in a cohort of Sri Lankan women with pre-eclampsia / pregnancy induced hypertension: a case control study

BackgroundLeptin is known to be elevated in pre-eclampsia/ pregnancy induced hypertension (PE/PIH). However the reports on the association of leptin receptor (LEPR) c.668A>G polymorphism with PE/PIH are inconsistent.FindingsLEPR c.668A>G polymorphism was studied in a cohort of women with PE/PIH (N = 61) and normotensive pregnancies (N = 40) by polymerase chain reaction / restriction fragment length polymorphism. Genotype and allele frequencies were in Hardy-Weinberg equilibrium within both groups (Chi square test). Allele and genotype frequencies were not significantly different between PE/PIH and normotensive pregnancies (Chi square test). Leptin levels (Kruskal Wallis analysis of variance) and leptin/body mass index (one way analysis of variance) were not significantly different between genotypes within each group. However, leptin (Mann Whitney U test) and leptin normalised to body mass index (unpaired t test) were significantly higher in PE/PIH women homozygous and heterozygous for the G668 allele than in respective normotensives.ConclusionsWhether the leptin receptor c.668A>G polymorphism increases the risk of developing PE/PIH in Sri Lankan women remains inconclusive in view of the smaller sample studied. However leptin levels in PE/PIH appeared to be modulated by this polymorphism.

Clinical observation of low molecular weight heparin combined with magnesium sulfate treatment on patients with pregnancy-induced hypertension

Objective To observe the clinical effect and safety of low molecular weight heparin in treatment of pregnancy-induced hypertension. Methods 40 patients included were randomly divided into two groups. 20 patients of treatment group were treated with low molecular weight heparin combined with magnesium sulfate. 20 patients of control group were treated with magnesium sulfate. Results The blood pressure and D-dimer of treatment group were significantly lower than control group ( P ＜ 0. 05 ). The platelet count, prothrombin time and bleeding of two groups were not significant different ( P ＞ 0. 05 ). Conclusion Low molecular weight heparin used in the treatment of severe pre-eclampsia pregnancy-induced hypertension are effeclive,safe and reliable, worthy of popularization. Key words: Pregnancy-induced hypertension; Low molecular weight heparin; Magnesium sulfate

Placental vascular lesion differences in pregnancy-induced hypertension and normotensive fetal growth restriction

Pregnancy-induced hypertension/preeclampsia (PIH) and fetal growth restriction (FGR) share a common placental origin. The pathologic classification that divides placental lesions to maternal or fetal origin was compared between these disorders. Placentas from pregnancies that were complicated by PIH, normotensive FGR, or by both (combined) were analyzed, and lesions were classified as those consistent with maternal under-perfusion and with fetal thromboocclusive disease. Maternal vascular lesions were more common in the PIH group and combined group (61% and 59%, respectively), compared with the FGR group (16.2%; P < .001), and villous lesions were more common in the combined group, compared with the FGR and PIH groups (79.5%, 53.5%, and 46.9%, respectively; P = .004). Fetal villous changes were observed in 16.2% in the FGR group, compared with 3.1% in the PIH group (P = .03), and chronic villitis was 15.2% in the FGR group vs 1.6% in the PIH group (P = .004). Placental lesions correspond with different clinical presentations.

The clinical significance of absence of end-diastolic velocities of the umbilical artery detected in the severely preterm fetus

Objective: To determine whether there is a gestational age cutoff at the time of diagnosis of AEDV of the umbilical artery Doppler waveform that is associated with nearly zero perinatal survival. Methods: Over an 8-year period we identified and compared the outcomes of pregnancies in which AEDV of the umbilical artery Doppler waveform was detected between 19–24 and 25–28 weeks of gestation. All fetuses had normal structure and karyotypes. Small for gestational age (SGA) was defined as less than the 10th percentile for gestational age based on Brenner’s curve. Values are reported in median (range). Results: There were no survivors among the 27 cases identified at 19–24 weeks of gestation: 5 terminations for severe-SGA fetus (birth weight 336 [130–430] grams), 3 terminations for severe preeclampsia and SGA fetus, 12 fetal deaths, 7 neonatal deaths, and 10 cases (46%) of pregnancy-induced hypertension/preeclampsia (PIH/PE). All 8 cases detected at 25–28 weeks of gestation resulted in neonatal survival at discharge ( P <0.0001), and there were 2 cases (25%) of PIH/PE ( P = 0.54). Conclusion: In this study, AEDV of the umbilical artery Doppler waveform identified at less than 25 weeks of gestation is associated with a 100% perinatal mortality rate and a high rate of PIH/PE. This information should be incorporated into the counseling and management of women in this clinical setting.

Platelet-activating factor-acetylhydrolase activity in normotensive and hypertensive pregnancies

The purpose of our study was to evaluate the hypothesis that pregnancy is associated with decreased platelet-activating factor-acetylhydrolase activity in women with normotension, but not in women with hypertension. We evaluated plasma platelet-activating factor-acetylhydrolase activity in normal nonpregnant women (n = 10), normal pregnant women (n = 24), pregnant women with pregnancy-induced hypertension-preeclampsia (n = 7), and a group of men with normotension (n = 10). Platelet-activating factor-acetylhydrolase activity was lower at 32 weeks of gestation during normal pregnancies compared with nonpregnant controls (p < 0.001); however, in women with pregnancy-induced hypertension-preeclampsia, platelet-activating factor-acetylhydrolase activity was not decreased. Platelet-activating factor-acetylhydrolase activity in men was higher than in all women (p < 0.01). Pregnant women with normotension may be refractory to pressor agents such as angiotensin II in part because of the decrease in plasma platelet-activating factor-acetylhydrolase activity, which results in an increase in platelet-activating factor. In contrast, enzyme activity is not decreased in pregnant women with hypertension, who have increased sensitivity to various pressor agents.

The relation of angiotensin-converting enzyme to the pregnancy-induced hypertension-preeclampsia syndrome

Angiotensin-converting enzyme, the polypeptide that converts angiotensin I to angiotensin II, was measured in the serum of 114 pregnant women who had normal blood pressure, pregnancy-induced hypertension-preeclampsia, and chronic hypertension with or without pregnancy-induced hypertension. Angiotensin-converting enzyme levels were unrelated to weeks of gestation. The angiotensin-converting enzyme levels were similar in normotensive women (21 .l f 6.9 units/ml), women with chronic hypertension without pregnancy-induced hypertension (23.1 -t 2.7 units/ml), and patients with pregnancyinduced hypertension where magnesium sulfate (22.6 & 6.7 units/ml) had been administered prior to angiotensin-converting enzyme assay, but these values were significantly less than those in patients with pregnancy-induced hypertension with no magnesium sulfate (29.1 f 6.5 units/ml) therapy and in women with chronic hypertension with superimposed pregnancy-induced hypertension (30.7 -e 4.4 units/ml) (p < 0.005). Maternal venous and umbilical venous and arterial angiotensin-converting enzyme levels were as follows: The maternal venous level was less than the cord venous level and greater than the cord arterial value. Neither neonatal size nor twin gestation influenced the angiotensin-converting enzyme levels. Patients with diabetes mellitus had variable angiotensin-converting enzyme values regardless of the status of the blood pressure. The physiologic theories of blood pressure control in pregnant women are discussed in relation to the renin-angiotensin, bradykinin, and prostaglandin systems, (AM J OBSTET GYNECOL~ 986; 154:792-800.)

The relation of angiotensin-converting enzyme to the pregnancy-induced hypertension-preeclampsia syndrome

Angiotensin-converting enzyme, the polypeptide that converts angiotensin I to angiotensin II, was measured in the serum of 114 pregnant women who had normal blood pressure, pregnancy-induced hypertension-preeclampsia, and chronic hypertension with or without pregnancy-induced hypertension. Angiotensin-converting enzyme levels were unrelated to weeks of gestation. The angiotensin-converting enzyme levels were similar in normotensive women (21.1 ± 6.9 units/ml), women with chronic hypertension without pregnancy-induced hypertension (23.1 ± 2.7 units/ml), and patients with pregnancy-induced hypertension where magnesium sulfate (22.6 ± 8.7 units/ml) had been administered prior to angiotensin-converting enzyme assay, but these values were significantly less than those in patients with pregnancy-induced hypertension with no magnesium sulfate (29.1 ± 6.5 units/ml) therapy and in women with chronic hypertension with superimposed pregnancy-induced hypertension (30.7 ± 4.4 units/ml) (p < 0.005). Maternal venous and umbilical venous and arterial angiotensin-converting enzyme levels were as follows: The maternal venous level was less than the cord venous level and greater than the cord arterial value. Neither neonatal size nor twin gestation influenced the angiotensin-converting enzyme levels. Patients with diabetes mellitus had variable angiotensin-converting enzyme values regardless of the status of the blood pressure. The physiologic theories of blood pressure control in pregnant women are discussed in relation to the renin-angiotensin, bradykinin, and prostaglandin systems.