97 research outputs found

    Preterm birth and reduced birthweight in first and second teenage pregnancies: a register-based cohort study

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    <p>Abstract</p> <p>Background</p> <p>Higher risks of preterm birth and small for gestational age babies have been reported in teenagers. The aim of this study was to investigate the relationship between first and second teenage pregnancies and preterm birth, birthweight and small for gestational age (SGA).</p> <p>Methods</p> <p>All women aged 14 to 29 yrs who gave birth to live singletons in the North Western Region of England between January 1st 2004 and December 31st 2006 were identified. Women were classified in three groups; 14-17 yrs, 18-19 yrs and 20-29 yrs (reference group). The outcome measures were preterm birth, very preterm birth, birthweight, SGA (< 5<sup>th </sup>percentile), very SGA (VSGA< 3<sup>rd </sup>percentile). We compared these outcome measures in teenagers' first and second pregnancies with those of mothers aged 20 to 29 yrs.</p> <p>Results</p> <p>The risk of preterm birth was increased in first (OR = 1.21, [95% CI: 1.01-1.45]) and second (OR = 1.93, [95% CI: 1.38-2.69]) time mothers aged 14-17 yrs compared to the reference group. Birthweight was reduced in the first (mean difference = -24 g; [95% CI: -40, -7]) and second (mean difference = -80 g; [95% CI: -115, -46]) time mothers aged 14-17 yrs compared to the reference group. There was some evidence of a protective effect against VSGA in 14-17 yr old first time mothers (OR = 0.79, [95% CI: 0.63-0.99]).</p> <p>Conclusions</p> <p>Teenage mothers are at increased risk of preterm birth compared to adult mothers and this risk is further increased in second time teen pregnancies. This study highlights the importance of ensuring pregnant teenagers have appropriate antenatal care. A first pregnancy may be the first and only time a pregnant teenager interacts with health services and this opportunity for health education and the promotion of contraception should not be overlooked.</p

    Hypoglycemia and the Origin of Hypoxia-Induced Reduction in Human Fetal Growth

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    The most well known reproductive consequence of residence at high altitude (HA >2700 m) is reduction in fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA.Doppler and ultrasound were used to measure maternal uterine and fetal umbilical blood flows in 69 and 58 residents of 400 vs 3600 m. Arterial and venous blood samples from mother and fetus were collected at elective cesarean delivery and analyzed for glucose, lactate and insulin. Maternal delivery and fetal uptakes for oxygen and glucose were calculated.The maternal arterial – venous glucose concentration difference was greater at HA. However, umbilical venous and arterial glucose concentrations were markedly decreased, resulting in lower glucose delivery at 3600 m. Fetal glucose consumption was reduced by >28%, but strongly correlated with glucose delivery, highlighting the relevance of glucose concentration to fetal uptake. At altitude, fetal lactate levels were increased, insulin concentrations decreased, and the expression of GLUT1 glucose transporter protein in the placental basal membrane was reduced.Our results support that preferential anaerobic consumption of glucose by the placenta at high altitude spares oxygen for fetal use, but limits glucose availability for fetal growth. Thus reduced fetal growth at high altitude is associated with fetal hypoglycemia, hypoinsulinemia and a trend towards lactacidemia. Our data support that placentally-mediated reduction in glucose transport is an initiating factor for reduced fetal growth under conditions of chronic hypoxemia

    Early influences on cardiovascular and renal development

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    The hypothesis that a developmental component plays a role in subsequent disease initially arose from epidemiological studies relating birth size to both risk factors for cardiovascular disease and actual cardiovascular disease prevalence in later life. The findings that small size at birth is associated with an increased risk of cardiovascular disease have led to concerns about the effect size and the causality of the associations. However, recent studies have overcome most methodological flaws and suggested small effect sizes for these associations for the individual, but an potential important effect size on a population level. Various mechanisms underlying these associations have been hypothesized, including fetal undernutrition, genetic susceptibility and postnatal accelerated growth. The specific adverse exposures in fetal and early postnatal life leading to cardiovascular disease in adult life are not yet fully understood. Current studies suggest that both environmental and genetic factors in various periods of life may underlie the complex associations of fetal growth retardation and low birth weight with cardiovascular disease in later life. To estimate the population effect size and to identify the underlying mechanisms, well-designed epidemiological studies are needed. This review is focused on specific adverse fetal exposures, cardiovascular adaptations and perspectives for new studies. Copyrigh

    Early influences on cardiovascular and renal development

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