Fetal growth rate and adverse perinatal events.
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OBJECTIVE: To study fetal weight gain and its association with adverse perinatal events in a serially scanned high-risk population. SUBJECTS AND METHODS: A total of 200 pregnant women considered at increased risk of uteroplacental insufficiency had a total of 1140 scans in the third trimester, with a median of six scans in each pregnancy. The average fetal growth rate was retrospectively calculated for the last 6 weeks to birth, and expressed as daily weight gain in grams per day. Adverse pregnancy outcome was defined as operative delivery for fetal distress, acidotic umbilical artery pH (< 7.15), or admission to the neonatal intensive care unit (NICU). RESULTS: Fetuses with normal outcome in this high-risk pregnancy population had an average antenatal growth rate of 24.2 g/day. Compared to pregnancies with normal outcome, the growth rate was slower in those that required operative delivery for fetal distress (20.9 g/day, p < 0.05) and those that required admission to the NICU (20.3 g/day, p < 0.05). The growth rate in pregnancies resulting in acidotic umbilical artery pH also seemed lower, but this did not reach statistical significance. CONCLUSIONS: Impaired fetal weight gain prior to birth is associated with adverse perinatal events suggestive of growth failure. (+info)
Maternal placental abnormality and the risk of sudden infant death syndrome.
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To determine whether placental abnormality (placental abruption or placental previa) during pregnancy predisposes an infant to a high risk of sudden infant death syndrome (SIDS), the authors conducted a population-based case-control study using 1989-1991 California linked birth and death certificate data. They identified 2,107 SIDS cases, 96% of whom were diagnosed through autopsy. Ten controls were randomly selected for each case from the same linked birth-death certificate data, matched to the case on year of birth. About 1.4% of mothers of cases and 0.7% of mothers of controls had either placental abruption or placenta previa during the index pregnancy. After adjustment for potential confounders, placental abnormality during pregnancy was associated with a twofold increase in the risk of SIDS in offspring (odds ratio = 2.1, 95% confidence interval 1.3-3.1). The individual effects of placental abruption and placenta previa on the risk of SIDS did not differ significantly. An impaired fetal development due to placental abnormality may predispose an infant to a high risk of SIDS. (+info)
Glucose metabolism and beta-cell mass in adult offspring of rats protein and/or energy restricted during the last week of pregnancy.
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An association between low birth weight and later impaired glucose tolerance was recently demonstrated in several human populations. Although fetal malnutrition is probably involved, the biological bases of such a relationship are not yet clear, and animal studies on the matter are scarce. The present study was aimed to identify, in adult (8-wk) female offspring, the effects of reduced protein and/or energy intake strictly limited to the last week of pregnancy. Thus we have tested three protocols of gestational malnutrition: a low-protein isocaloric diet (5 instead of 15%), with pair feeding to the mothers receiving the control diet; a restricted diet (50% of the control diet); and a low-protein restricted diet (50% of low-protein diet). Only the low-protein diet protocols, independent of total energy intake, led to a lower birth weight. The adult offspring female rats in the three deprived groups exhibited no decrease in body weight and no major impairment in glucose tolerance, glucose utilization, or glucose production (basal state and hyperinsulinemic clamp studies). However, pancreatic insulin content and beta-cell mass were significantly decreased in the low-protein isocaloric diet group compared with the two energy-restricted groups. Such impairment of beta-cell mass development induced by protein deficiency limited to the last part of intrauterine life could represent a situation predisposing to impaired glucose tolerance. (+info)
Altered arterial concentrations of placental hormones during maximal placental growth in a model of placental insufficiency.
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Pregnant ewes were exposed chronically to thermoneutral (TN; 20+/-2 degrees C, 30% relative humidity; n=8) or hyperthermic (HT; 40+/-2 degrees C 12 h/day, 35+/-2 degrees C 12 h/day, 30% relative humidity, n=6) environments between days 37 and 93 of pregnancy. Ewes were killed following 56 days of exposure to either environment (days in treatment (dit)), corresponding to 93+/-1 day post coitus (dpc). Maternal core body temperatures (CBT) in HT ewes were significantly elevated above the TN ewes (HT; 39.86+/-0.1 degrees C vs TN; 39.20+/-0.1 degrees C; P<0.001). Both groups of animals displayed circadian CBT, though HT ewes had elevated amplitudes (HT; 0.181+/-0.002 degrees C vs TN; 0.091+/-0.002 degrees C; P<0.001) and increased phase shift constants (HT; 2100 h vs TN; 1800 h; P<0.001). Ewes exposed to chronic heat stress had significantly reduced progesterone and ovine placental lactogen (oPL) concentrations from 72 and 62 dpc respectively (P<0.05), corresponding to approximately 30 dit. However, when compared with the TN ewes, HT cotyledonary tissue oPL mRNA and protein concentrations were not significantly different (P>0.1). Prolactin concentrations rose immediately upon entry into the HT environment, reaching concentrations approximately four times that of TN ewes, a level maintained throughout the study (HT; 216.31+/-32.82 vs TN; 54. 40+/-10.0; P<0.0001). Despite similar feed intakes and euglycemia in both groups of ewes, HT fetal body weights were significantly reduced when compared with TN fetuses (HT; 514.6+/-48.7 vs TN; 703. 4+/-44.8; P<0.05), while placental weights (HT; 363.6+/-63.3 vs TN; 571.2+/-95.9) were not significantly affected by 56 days of heat exposure. Furthermore, the relationship between body weight and fetal length, the ponderal index, was significantly reduced in HT fetuses (HT; 3.01+/-0.13 vs TN; 3.57+/-0.18; P<0.05). HT fetal liver weights were also significantly reduced (HT; 27.31+/-4.73 vs TN; 45.16+/-6.16; P<0.05) and as a result, the brain/liver weight ratio was increased. This study demonstrates that chronic heat exposure lowers circulating placental hormone concentrations. The observation that PL mRNA and protein contents are similar across the two treatments, suggests that reduced hormone concentrations are the result of impaired trophoblast cell development, specifically trophoblast migration. Furthermore, the impact of heat exposure during maximal placental growth is great enough to restrict early fetal development, even before the fetal maximal growth phase (100 dpc-term). These data highlight that intrauterine growth retardation (IUGR) may result primarily from placental trophoblast cell dysfunction, and secondarily from later reduced placental size. (+info)
Placental blood flow measured by simultaneous multigate spectral Doppler imaging in pregnancies complicated by placental vascular abnormalities.
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OBJECTIVE: To evaluate the role of placental blood flow measurements by simultaneous multigate spectral Doppler imaging in pregnancies complicated by intrauterine growth restriction (IUGR), and for early detection of placental vascular abnormalities in high- and low-risk pregnancies. METHODS: To assess the sensitivity and specificity of abnormal placental blood flow in detecting IUGR, we followed 22 women whose pregnancies were complicated by IUGR at 28-34 weeks' gestation, and compared the findings with those obtained in 22 matched controls. We defined placental blood flow impedance as abnormal when 10% of placental pulsatility index (PI) measurements were greater than, or equal to, the mean umbilical artery PI (placental PI/umbilical PI > or = 1). To determine the predictive value of abnormal placental blood flow measurement for identifying developing uteroplacental insufficiency, we examined an unselected group of 100 low- and high-risk patients at 20-22 weeks' gestation. We correlated the Doppler findings with the development of pre-eclampsia, IUGR, placental abruption, oligohydramnios and the presence of persistent late decelerations during labor. RESULTS: Placental blood flow determination was more sensitive than umbilical artery blood flow in detecting abnormal umbilical-placental flow impedances as manifested by the presence of IUGR. Of the 100 mixed high- and low-risk patients examined at 20-22 weeks, 32 had abnormal placental blood flow. Of these, 19 (59.4%) subsequently developed pathologies associated with placental vascular disease. Of the 68 patients with normal placental blood flow, only six (8.8%) developed such pathologies. The sensitivity was 76% (19/25), with positive predictive value 59.4% (19/32); the specificity was 82.7% (62/75), with negative predictive value 91.2% (62/68). CONCLUSIONS: Abnormal intraplacental blood flow at 28-34 weeks' gestation is strongly associated with IUGR. In addition, it has moderate positive and negative predictive values for identifying subsequent development of uteroplacental vascular abnormalities. (+info)
Effects of placental insufficiency on the ovine fetal renin-angiotensin system.
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We postulated that chronic placental insufficiency would be associated with reduced expression of renal renin and angiotensinogen genes in the fetal sheep. Placental development was restricted in ewes by removing the majority of caruncles prior to mating (placentally restricted (PR) group). The weights of PR fetuses were significantly reduced (P < 0.05, 2.98 +/- 0.33 kg) compared to control fetuses (4.20 +/- 0.30 kg). Kidney weights were also significantly reduced in the PR fetuses (P < 0.05, 8.4 +/- 0.9 g) compared with control fetuses (12.2 +/- 1.3 g). The ratios of renal renin/-actin mRNA levels were significantly reduced in PR fetuses (P < 0.001, 0.35 +/- 0.02) when compared to control animals (0.98 +/- 0.13). The renal angiotensinogen mRNA/18S rRNA ratio was significantly lower (P < 0.05, 0.28 +/- 0.13) in PR fetuses compared with control fetuses (0.72 +/- 0.10), while hepatic angiotensinogen was unaffected. There was a positive correlation between renal renin mRNA and renal angiotensinogen mRNA levels (r = 0.65, P < 0.05, n = 12). It is unlikely that these changes in renal angiotensinogen and renin mRNA were due to the small increment in plasma cortisol levels (< 5 nmol l-1). There was, however, a positive correlation between arterial PO2 and renal renin mRNA (r2 = 0.77, P < 0.01). Plasma renin levels were not different between the two groups. Thus, restriction of nutrient and oxygen supply throughout fetal life was associated with suppression of renal renin and renal angiotensinogen gene expression, with no effect on hepatic angiotensinogen mRNA levels. This specific suppression of fetal renal renin and angiotensinogen expression could alter the activity of the intrarenal RAS and so affect growth and development of the kidney. (+info)
A prospective management study of slow-release aspirin in the palliation of uteroplacental insufficiency predicted by uterine artery Doppler at 20 weeks.
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OBJECTIVE: To investigate the effect of low-dose, slow-release aspirin in reducing the incidence and/or severity of pregnancy complications in women identified as high risk of developing problems associated with uteroplacental insufficiency, namely pre-eclampsia or delivering a small-for-gestational age (SGA) baby. DESIGN: A prospective, randomized management study. One thousand and twenty-two women of mixed parity underwent color flow/pulsed Doppler (CFPD) imaging of the uterine arteries at the time of the 17-23 week (mean 19.9) anomaly scan. Women who were screen positive were randomized to a control or treatment group. The treatment group was given 100-mg slow-release aspirin (Disprin CV) daily and followed up at regular intervals. Women in the routine group received routine antenatal care. Main outcome measures were pre-eclampsia and SGA < 3rd centile. Secondary outcome measures were: SGA < 10th centile, pre-eclampsia requiring delivery before 34 weeks, placental abruption, an Apgar score < 7 at 5 min, admission to neonatal intensive care unit or a pregnancy that resulted in a stillbirth or neonatal death. Odds ratios (OR) with 95% confidence intervals (CI) were calculated for severe and any complications. RESULTS: Two hundred and sixteen women were screen positive according to the defined criteria. One hundred and three women were assigned to the treatment group and 113 to the control group. The difference in the incidence of pre-eclampsia and SGA < 3rd centile between the control and treatment groups did not reach statistical significance. There was a statistically significant reduction in any (OR 0.41 (CI 0.35-0.45), P < 0.01) and severe pregnancy complications (OR 0.43 (CI 0.21-0.84), P < 0.05) in the treatment group compared with the controls. CONCLUSIONS: The administration of slow-release aspirin to women identified as high risk, using color Doppler imaging of the uterine arteries at 20 weeks' gestation, did not significantly alter the incidence of pre-eclampsia or delivery of a SGA baby. It did, however, improve the outcome by reducing the overall incidence of complications associated with uteroplacental insufficiency. (+info)
Coronary heart disease after prenatal exposure to the Dutch famine, 1944-45.
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OBJECTIVE: To assess the effect of prenatal exposure to maternal malnutrition on coronary heart disease in people born around the time of the Dutch famine, 1944-45. DESIGN: Historical cohort study. SETTING: Community study. PATIENTS: Singletons born alive between November 1943 and February 1947 for whom detailed birth records were available. DESIGN: The prevalence of coronary heart disease was compared between those exposed to famine in late gestation (n = 120), in mid-gestation (n = 108), or in early gestation (n = 68), and those born in the year before the famine or those conceived in the year after the famine (non-exposed subjects, n = 440). MAIN OUTCOME MEASURES: Prevalence of coronary heart disease, defined as the presence of angina pectoris according to the Rose questionnaire, Q waves on the ECG, or a history of coronary revascularisation. RESULTS: The prevalence of coronary heart disease was higher in those exposed in early gestation than in non-exposed people (8.8% v 3.2%; odds ratio adjusted for sex 3.0, 95% confidence interval (CI) 1.1 to 8.1). The prevalence was not increased in those exposed in mid gestation (0.9%) or late gestation (2.5%). People with coronary heart disease tended to have lower birth weights (3215 g v 3352 g, p = 0.13), and smaller head circumferences at birth (32.2 cm v 32.8 cm, p = 0.05), but the effect of exposure to famine in early gestation was independent of birth weight (adjusted odds ratio 3.2, 95% CI 1.2 to 8.8). CONCLUSIONS: Although the numbers are very small, this is the first evidence suggesting that maternal malnutrition during early gestation contributes to the occurrence of coronary heart disease in the offspring. (+info)