Presence Of Maternal Hypertension Research Articles

Childhood school outcomes for infants born to women with hypertensive disorders during pregnancy.

To investigate the childhood school outcomes for infants born to women with hypertensive disorders during pregnancy. A retrospective population-based cohort study linking perinatal data from 2003 to 2013 to developmental scores at preparatory school and educational scores at school grades 3, 5, and 7 in Victoria, Australia. Exposures of interest were the presence of hypertensive disorders during pregnancy and iatrogenic delivery for preeclampsia. Multivariable logistic regression and generalised estimating equation models were employed. In total, 682,386 births ≥32weeks' gestation were linked to 175,665 child developmental results and 412,834 with at least one educational result. Compared to infants born to women without a hypertensive disorder, infants born to women with a hypertensive disorder had no increased risk of poorer developmental outcomes at school entry but a significantly increased risk of poorer educational outcomes across grades 3, 5, and 7. Compared to infants born to women without preeclampsia, infants born to women iatrogenically delivered for preeclampsia had no increased risk of poorer developmental outcomes (aOR=1.12, 95% CI: 0.98-1.28) but a significantly increased risk of poorer educational outcomes at grades 3 (aOR=1.23, 95% CI: 1.09-1.38), 5 (aOR=1.27, 95% CI: 1.13-1.43), and 7 (aOR=1.24, 95% CI: 1.09-1.43). The presence of maternal hypertension in pregnancy, particularly where preeclampsia was the indication for iatrogenic delivery, is associated with impaired school educational outcomes.

Prenatal, perinatal and postnatal events associated with hypomineralized second primary molar: a systematic review with meta-analysis.

The etiology of hypomineralized second primary molar (HSPM) appears to be multifactorial but remains uncertain. Thus, the objective was to systematically review studies that investigated adverse health conditions in the prenatal, perinatal and postnatal periods associated with HSPM. The search was carried out in five databases and in gray literature. The risk of bias of observational studies was analyzed according to the Newcastle-Ottawa scale. A total of 1878 studies were identified. Fourteen were eligible, and seven were included in the meta-analysis. Maternal smoking (OR = 2.88; 95%CI: 1.62-5.15) and presence of maternal hypertension (OR = 2.91; 95%CI: 1.35-6.28) were significantly associated with higher odds of HSPM. In the perinatal period, factors associated with HSPM were low birth weight (OR = 1.50; 95%CI: 1.15-1.96), prematurity (OR = 1.93; 95%CI: 1.37-2.71), delivery complications (OR = 2.42; 95%CI: 1.52-3.83) and need for an incubator (OR = 1.65; 95%CI: 1.01-2.70). Not breastfeeding (OR = 1.26; 95%CI: 1.01-1.58), use of antibiotics by the child (OR = 1.24; 95%CI: 1.04-1.48), fever (OR = 1.37; 95%CI: 1.10-1.72) and asthma (OR = 1.91; 95%CI: 1.16-3.13) were the postnatal factors associated with HSPM. Maternal smoking, maternal hypertension, low birth weight, prematurity, delivery complications, need for incubation, not breastfeeding, antibiotic use, fever and childhood asthma were associated with HSPM. Well-designed prospective cohort studies are needed. Clinical relevance Understanding the etiological factors can be guiding aspects for individual clinical approaches, as well as guiding the design of preventive interventions for HSPM.

Role of the Atg9a gene in intrauterine growth and survival of fetal mice

Autophagy is activated by environment unfavorable for survival and requires Atg9a protein. Mice heterozygous for p57Kip2, devoid of the imprinted paternal allele (p57Kip2+/−), are known to develop hypertension during pregnancy. To determine whether fetal Atg9a is involved in the intrauterine survival and growth of fetal mice, this study was performed on Atg9a heterozygous (Atg9a+/−) pregnant mice with and without p57Kip2+/−. The pregnant mice heterozygous for both knockout alleles of Atg9a and p57Kip2 (Atg9a+/−/p57Kip2+/−), but not those heterozygous for Atg9a alone, developed hypertension during pregnancy. Placental expression of Atg9a mRNA was significantly decreased in the Atg9a−/− mice compared to Atg9a+/− or Atg9a+/+ mice. The Atg9a−/− fetal mice exhibited significantly retarded growth and were more likely to die in utero compared to Atg9a+/+ and Atg9a+/− fetal mice. Growth retardation was observed in the presence of maternal hypertension in Atg9a−/− fetal mice. These results suggest that Atg9a−/− fetal mice from pregnant dams heterozygous for both knockout alleles of Atg9a and p57Kip2 are more susceptible to hypertensive stress than fetuses with intact autophagic machinery.

Fetal Development: Voice Processing in Normotensive and Hypertensive Pregnancies

Recent observation of maternal voice recognition provides evidence of rudimentary memory and learning in healthy term fetuses. However, such higher order auditory processing has not been examined in the presence of maternal hypertension, which is associated with reduced and/or impaired uteroplacental blood flow. In this study, voice processing was examined in 40 fetuses (gestational ages of 33 to 41 weeks) of hypertensive and normotensive women. Fetuses received 2 min of no sound, 2 min of a tape-recorded story read by their mothers or by a female stranger, and 2 min of no sound while fetal heart rate was recorded. Results demonstrated that fetuses in the normotensive group had heart rate accelerations during the playing of their mother's voice, whereas the response occurred in the hypertensive group following maternal voice offset. Across all fetuses, a greater fetal heart rate change was observed when the amniotic fluid index was above compared to below the median (i.e., 150 mm), indicating that amniotic fluid volume may be an independent moderator of fetal auditory sensitivity. It was concluded that differential fetal responding to the mother's voice in pregnancies complicated by maternal hypertension may reflect functional elevation of sensorineural threshold or a delay in auditory system maturation, signifying functional differences during fetal life or subtle differences in the development of the central nervous system.

Prevalence of some risk factors in children with epilepsy compared to their controls

The goal of this case-control study was to identify the significance of certain risk factors for epilepsy in Turkey. A total of 805 cases, aged 1-16 years, followed-up for epilepsy at the Pediatric Neurology Department and a control group consisting of 846 age-matched cases without epilepsy were included in the study. The risk factors examined were gender, neurological impairment, febrile convulsion, head trauma, central nervous system infections, parental consanguinity, family history of epilepsy, prenatal and natal risk and newborn jaundice. Data regarding the investigated epilepsy risk factors were obtained through a questionnaire via personal interviews and the medical records and were assessed using univariate and multivariate analysis. Univariate analysis showed an increased risk for epilepsy with a history of atypical febrile seizure (21.97-fold), severe and moderate head injury (27.76- and 7.09-fold respectively), CNS infection (4.76-fold), history of epilepsy in first-, second- or third-degree relatives (6.42-, 3.09- and 2.66-fold, respectively), presence of maternal hypertension (4.31-fold), an apgar score < or =6 at any time (7.78-fold) and neonatal jaundice (3.12-fold). Abnormal neurological signs increased the epilepsy risk 5.92 times in univariate analysis and 30.26 times in multivariate analysis. The most important risk factors for epilepsy in this study were neurological impairment, history of atypical febrile seizures, severe head injury and a low apgar score. Other important risk factors were moderate head trauma and a history of epilepsy in the family.

Circadian rhythm of maternal blood pressure and fetal growth

This study aimed at examining any relation between the circadian variation in blood pressure (BP) in human pregnancy and fetal growth. A prospective study included 52 pregnant women monitored during the third trimester of pregnancy. There were 33 uncomplicated pregnancies with normal fetal growth (Group 1) and 19 pregnancies complicated by intrauterine growth retardation (IUGR), confirmed at birth (Group 2). Ten women (five in each group) had pregnancy-induced hypertension. All women were hospitalized and followed a similar daily routine. BP was recorded with an automatic wearable device. Measurements were obtained every 20 min for 24 ± 1 h. BP profiles were analyzed by conventional statistical methods and by cosinor, involving the least squares fit of cosine curves with an anticipated period (24 h) to the data. BP parameters, fetal outcome, demographic and obstetric characteristics were compared between the two groups. Logistic regression and multivariate analyses were used to assess factors putatively associated with fetal outcome. The circadian amplitude of diastolic BP was found to be larger in normotensive women with IUGR. As gauged by odds ratios (OR), the circadian amplitude of diastolic BP (OR = 1.7, 95% CI: 1.1–2.8; P = 0.03) and hematocrit (OR = 1.4, 95% CI: 1.0–1.9; P = 0.04) were the only variables positively and independently associated with IUGR. In the presence of maternal hypertension, the circadian amplitude of systolic BP was negatively associated with IUGR (OR = 0.7, 95% CI: 0.5–1.0; P = 0.03). A larger circadian variation in diastolic BP, rather than a difference in the mean value of systolic or diastolic BP, was found to be statistically significantly associated with IUGR. This study adds another condition in which the circadian BP amplitude constitutes a harbinger of elevated risk, apart from an association with a shortened lifespan in the absence or presence of malignant hypertension and with an increased risk of stroke and nephropathy reported earlier.

Prognostic Significance of Early Elevated Serum Uric Acid Concentrations in Low Birthweight Infants 1149

Uric acid (UA) concentrations can be elevated after ischemia-reperfusion injury and high levels in the first day of life have been associated with intracranial pathology in low birthweight infants (Pediatr Res 1996; 39: 238A). To determine the prognostic significance of high serum UA concentrations in the first 24 hours after birth, the records of 154 inborn infants who weighed 7.5 mg/dl and by univariate analysis was significantly related to gestational age, peak serum creatinine, serum HCO3 and base deficit, the presence of pregnancy-induced hypertension (PIH), intrauterine growth retardation and how long after birth the sample was obtained. By multiple logistic regression, peak creatinine concentrations, base deficit and time of sample were risk factors for high serum UA concentrations. There were no significant differences in UA concentrations between those with any IVH or PVL(n = 41, UA=5.35 ± 0.32 mg/dl) and those with none (n=97, UA=5.88± 0.22 mg/dl, p > 0.05), nor did UA concentrations differ between the survivors vs the 21 who died (5.73 ± 0.19 vs 5.45 ± 0.43 mg/dl, p > 0.05). Elevated UA concentrations were not found in those with more severe intracranial pathology (Grades III and IV IVH and/or PVL) nor in the group defined as bad outcome (died or had IVH/PVL). Of the 132 infants eligible for follow-up, 79 (60%) were seen at a median age of 11 months(range 5-29 mo). The 20 infants with neurodevelopmental or neuromotor abnormalities had a first day UA concentration of 5.38 ± 0.38 compared with 6.03± 0.33 for those with a normal exam (p > 0.05). Elevated serum UA concentrations in the first 24 hr of life do not relate to intracranial pathology, death or abnormal neurological outcome. Since the concentrations are higher in the presence of maternal hypertension, serum creatinine and how long after birth the sample is obtained, it is possible that any detection of elevated serum UA from ischemia-reperfusion injury in the infant is obscured by transplacental passage of UA from the mother (serum UA is higher in mothers with PIH) and from a longer half-life for UA in the infant's circulation during the first day of life.

The very low birthweight infant: maternal complications leading to preterm birth, placental lesions, and intrauterine growth.

The placental lesions of the very low birthweight (VLBW) infant were investigated in relation to clinical complications leading to preterm birth and evidence of growth impairment. The 249 singleton gestations yielding infants less than 1500 g were grouped according to the clinical complications leading to preterm birth as premature membrane rupture (116/249, 47%) preterm labor (55/249, 22%), pregnancy-induced hypertension (PIH, 54/249, 22%), and normotensive abruption (ABR, 24/249, 10%). Specifically excluded from this data set were cases with greater than 2 weeks discordance, fetal congenital anomalies, placenta previa, and maternal medical or gestational diseases such as chronic hypertension and diabetes mellitus, and intrauterine growth retardation (IUGR) as a primary indication for delivery. Placental weight and lesions including decidual vasculopathy and related villous lesions, chronic villitis/intervillositis, and decidual plasmacytosis were considered as variables in analyses in which raw birthweight was the dependent variable and gestational age a confounder. Of the 195 VLBW, 79 (41%) infants from normotensive mothers had lesions of decidual vasculopathy or chronic inflammation. In the VLBW infants from hypertensive mothers, growth restriction was related to markers of decidual vasculopathy. In the absence of maternal hypertension the growth restriction was independently associated with chronic villitis. Decidual vasculopathy (characteristic of PIH) and chronic intrauterine inflammation underlie the complications of many normotensive VLBW infants. The placental lesions in VLBW-IUGR depend on the presence or absence of maternal hypertension. In the absence of maternal hypertension, VLBW-IUGR is associated with chronic inflammation and is independent of decidual vasculopathy. In the presence of maternal hypertension, VLBW-IUGR is directly related to decidual vasculopathy.

The development of abnormal heart rate patterns after absent end-diastolic velocity in umbilical artery: Analysis of risk factors

Our objectives were to evaluate the time interval elapsing between the occurrence of absent end-diastolic velocity in the umbilical artery and either the development abnormal fetal heart rate patterns or delivery and to establish the maternal and fetal factors that may affect this interval. Thirty-seven fetuses free of structural and chromosomal abnormalities in which the development of absent end-diastolic velocity in umbilical artery was evidenced by serial Doppler recordings were studied. At the first occurrence the following factors were considered: gestational age, presence of hypertension or preeclampsia, amniotic fluid index, severity of growth retardation, and 10 different Doppler indices calculated from extracardiac and intracardiac vascular districts. Actuarial statistical methods were applied, with the occurrence of antepartum late heart rate deceleration as the censoring variable. The interval between the first occurrence of absent end-diastolic velocity in umbilical artery and delivery ranged from 1 to 26 days. Indications for delivery were the development of antepartum late heart rate decelerations in 23 fetuses (62.1%) and different maternal or fetal complications in the remaining 14 fetuses. Multivariate analysis revealed that gestational age and the presence of hypertension and pulsations in umbilical vein were the dominant factors in determining the length of this time interval. The duration of the time interval between the occurrence of absent end-diastolic velocity in umbilical artery and abnormal heart rate pattern differs considerably among fetuses, and it is mainly determined by gestational age and presence of maternal hypertension and pulsations in umbilical vein.