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Reproduction (Cambridge, England).... 2001In pigs, as in other species, fetal growth retardation is associated with reduced birth weight and increased risk of fetal and neonatal death. As there are few... (Review)
Review
In pigs, as in other species, fetal growth retardation is associated with reduced birth weight and increased risk of fetal and neonatal death. As there are few opportunities after birth to remedy the detrimental effects of low birth weight, it is important to understand both the intrinsic and extrinsic factors associated with inadequate fetal growth and to determine when growth retarded fetuses deviate from the growth trajectory of their normal sized littermates. Inadequately grown pig fetuses can be identified statistically as early as day 30 of the 114 days of gestation, indicating that limited uterine space is not a primary determinant of fetal growth. Comparisons of the smallest fetus within a litter with a normal sized sibling reveal that inadequately grown fetuses have altered endocrine status and lower circulating concentrations of many essential amino acids. In addition, the placenta supplying the smallest fetus is disproportionately small and has a reduced capacity to transport amino acids. Understanding the timing and the causes of fetal growth retardation in pigs may help us to devise appropriate strategies to reduce the incidence and hence the detrimental postnatal consequences of runting.
Topics: Adrenal Glands; Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Birth Weight; Female; Fetal Growth Retardation; Fetal Weight; Genotype; Gestational Age; Litter Size; Male; Muscles; Pregnancy; Sex Factors; Swine; Thyroid Hormones; Uterus
PubMed: 11980193
DOI: No ID Found -
Long-term physiological and economic consequences of growth retardation in children and adolescents.The Proceedings of the Nutrition Society May 2000The application of a lifespan perspective in human biology in recent years has shown that a number of early environmental factors influencing human growth and... (Review)
Review
The application of a lifespan perspective in human biology in recent years has shown that a number of early environmental factors influencing human growth and development have long-term biological or psycho-social consequences. Human growth is characterized by prolonged infancy, an extended childhood phase and high rates of growth during the adolescent growth spurt. It is unlikely that these characteristics would have evolved without having advantages, and curtailments have the potential for disadvantage. The present paper examines the evidence for long-term physiological and economic consequences of growth retardation in children and adolescents. The emphasis is the biological and economic imperatives of survival, subsistence, reproduction and production rather than aspects of metabolic competence. Many of the consequences of growth retardation are determined by the direct effect on body size, but many other consequences arise from the conditions that cause the growth retardation. Catch up of retarded growth can occur, but does not usually do so because of the continued presence of the retarding agents. Basal metabolism and physical work capacity are usually commensurate with the size of the individual; mechanical efficiency of physical work is unchanged, but falls in activity levels may occur along with a reduction in the pace of activity. Growth retardation in childhood is associated with a higher disease and mortality risk in adulthood, with decreased productivity and employment and promotion prospects. Studies are showing that relative deprivation and the accumulation of socially patterned exposures are important in some societies. Height and growth retardation have proved invaluable in reflecting these factors, but the next generation of studies may require more discriminating indices.
Topics: Adolescent; Adult; Body Composition; Body Height; Body Weight; Child; Child Nutrition Disorders; Child, Preschool; Environment; Female; Growth Disorders; Humans; Male; Nutrition Disorders; Physical Exertion; Reproduction; Socioeconomic Factors
PubMed: 10946793
DOI: 10.1017/s0029665100000276 -
Seminars in Perinatology Jun 2008Abnormal fetal growth is associated with preterm birth, stillbirth, neonatal death, respiratory distress syndrome, and necrotizing enterocolitis. An optimal fetal growth... (Review)
Review
Abnormal fetal growth is associated with preterm birth, stillbirth, neonatal death, respiratory distress syndrome, and necrotizing enterocolitis. An optimal fetal growth standard would be one that most correctly identifies the fetus at risk for poor perinatal outcome. A growth standard that is created using population-specific data is more applicable than generalized growth curves since there is evidence that optimal neonatal outcome is achieved at different birth weights in different populations. The development of fetal growth standards based exclusively on neonatal birth weights is flawed as fetal growth restriction is associated with preterm delivery. Likewise, employing clinically derived ultrasound standards for term gestations would include a population that is more likely to have abnormal growth. Novel approaches to defining normal intrauterine growth combine birth weights at term and fetal growth patterns in-utero to create growth curves useful in defining the normal intrauterine growth experience. This review examines the performance of a variety of the growth characterizing standards that have been employed to define abnormal growth and examines their performance in the prediction of adverse perinatal outcome.
Topics: Anthropometry; Birth Weight; Female; Fetal Development; Fetal Growth Retardation; Fetal Weight; Gestational Age; Growth; Humans; Infant Mortality; Infant, Newborn; Infant, Premature; Male; Models, Biological; Pregnancy; Pregnancy Outcome; Reference Values; Risk Assessment
PubMed: 18482613
DOI: 10.1053/j.semperi.2007.11.001 -
Hormone Research 2006There is considerable evidence to show that babies born prematurely have poor postnatal growth, and the more premature the baby, the greater the impairment is likely to... (Review)
Review
There is considerable evidence to show that babies born prematurely have poor postnatal growth, and the more premature the baby, the greater the impairment is likely to be and the longer it will persist. Nutrition has been shown to play an important part in this, but adequate nutrition is difficult, if not impossible, to achieve in these infants. In the most immature infants, growth retardation may continue for many months and catch-up may be delayed and incomplete. Evidence from long-term studies suggests that preterm infants will be shorter and lighter than term controls and that reduced stature and head size may be linked with lower intelligence. Although there is evidence linking better growth to better neurodevelopmental outcome, with reports suggesting that this can be achieved with dietary manipulation, there are also data that suggest that there could be a link between increased postnatal growth and increased morbidity and mortality in later childhood and adult life. Here, we provide an overview of current understanding of growth impairment in infants born prematurely and the effects in later life.
Topics: Body Size; Fetal Development; Humans; Infant, Newborn; Infant, Premature; Regression Analysis
PubMed: 16612118
DOI: 10.1159/000091510 -
Soins. Pediatrie, Puericulture 2022Assessing weight and height development is a key element of pediatric follow-up. Growth retardation, even in isolation, may be the first symptom of a chronic disease...
Assessing weight and height development is a key element of pediatric follow-up. Growth retardation, even in isolation, may be the first symptom of a chronic disease and should therefore always be investigated. Many chronic diseases can be responsible and in most cases, diagnosis and management of the disease will minimize the impact on statural growth. The reconstruction of growth curves on the health record is essential to obtain a vision of the growth kinetics of the child and to orient the diagnosis. The study of the evolution of the ratio between weight and height is an essential point in the diagnostic process.
Topics: Body Height; Child; Humans
PubMed: 35995530
DOI: 10.1016/j.spp.2022.06.003 -
The Journal of Pediatrics Jan 1997To evaluate in preterm infants the role of intrauterine growth retardation and infant body proportionality on subsequent childhood growth. (Clinical Trial)
Clinical Trial Comparative Study Randomized Controlled Trial
OBJECTIVE
To evaluate in preterm infants the role of intrauterine growth retardation and infant body proportionality on subsequent childhood growth.
METHODS
Preterm infants (818) prospectively enrolled in the Infant Health and Development Program were studied from birth to 36 months of corrected age. Weights and lengths were recorded at eight intervals. Growth parameters were compared in preterm infants with differing body symmetry at birth, defined by length-for-age and weight-for-age. Infants with both low length-for-age and low weight-for-age at birth were categorized as symmetrically growth retarded, and infants with normal length-for-age and low weight-for-age were categorized as asymmetrically growth retarded.
RESULTS
Infants born with low length-for-age demonstrated increased growth velocity until 8 months of corrected age (p <0.001). However, infants born with low weight-for-age demonstrated decreased weight-gain velocity compared with preterm infants with appropriate weight for gestational age (AGA) until 40 weeks of corrected age (p <0.001). Heights and weights of infants with either symmetric or asymmetric intrauterine growth retardation remained significantly retarded compared with AGA preterm patients and the National Child Health Survey (NCHS) reference population (p <0.001). Infants born short but with normal weight did not significantly differ from AGA preterm infants in either weight or length at 36 months of corrected age. Preterm infants with both symmetric and asymmetric growth retardation demonstrated limited catch-up growth in weight until age 4 months and then paralleled the AGA preterm patients and the NCHS reference population. Very low birth weight (< or = 1250 gm), gestational age, and a broad-based day-care intervention did not influence growth outcome after control for the presence of intrauterine growth retardation.
CONCLUSIONS
Preterm infants with both symmetric and asymmetric intrauterine growth retardation demonstrate limited catch-up growth. Intrauterine growth deficits persist into early childhood.
Topics: Body Height; Female; Fetal Growth Retardation; Humans; Infant, Newborn; Infant, Premature; Infant, Small for Gestational Age; Male; Prospective Studies; Weight Gain
PubMed: 9003857
DOI: 10.1016/s0022-3476(97)70316-0 -
Early Human Development Jul 1991In an experimental model of fetal growth retardation which involves the reduction of placental mass in ewes, we have investigated the effects of intrauterine deprivation... (Comparative Study)
Comparative Study
In an experimental model of fetal growth retardation which involves the reduction of placental mass in ewes, we have investigated the effects of intrauterine deprivation on aspects of structural development of the trachea and lungs of fetal sheep (140 days gestation). We have also measured the volume of luminal liquid aspirated from the lungs and the phospholipid content of this liquid as an index of pulmonary surfactant production. The effects of growth retardation are evident in the trachea where the structural development of the mucosal and submucosal layers has been affected. Abnormal aspects of development include the frequent lack of a ciliated border on epithelial cells in the mucosal layer and the reduction in the extent of the folds usually characteristic of this layer in near term fetal sheep. Although the fetal lungs are smaller in growth retardation (P less than 0.01) they are appropriate for fetal weight and their structural development does not appear to have been retarded. In contrast, lung liquid volume is significantly reduced in relation to lung weight in growth retarded fetuses and the concentration of phospholipids in lung liquids is also reduced (P less than 0.01).
Topics: Animals; Exudates and Transudates; Fetal Growth Retardation; Lung; Male; Organ Size; Phospholipids; Pulmonary Surfactants; Sheep; Trachea
PubMed: 1914984
DOI: 10.1016/0378-3782(91)90039-6 -
Clinics in Perinatology Mar 1986Normal fetal growth is a logarithmic process, marked by rapid mitosis at its early stages and by cellular hypertrophy and the accumulation of fat, glycogen, and... (Review)
Review
Normal fetal growth is a logarithmic process, marked by rapid mitosis at its early stages and by cellular hypertrophy and the accumulation of fat, glycogen, and connective tissue later in gestation. Growth-retarding influences can alter cell number, with a symmetric pattern of IUGR resulting if they occur early. Later insults, the result of uteroplacental compromise, affect cell size and may cause an asymmetric growth retardation. Fetuses with asymmetric growth retardation are at particular risk for intrauterine fetal demise and fetal distress in labor. The assessment of fetal growth is complicated by a lack of clear definition for what constitutes normality. Fetal growth curves should be derived from uncomplicated pregnancies. Separate curves should be available on the basis of multiple gestation and sex, maternal parity, and ethnic-racial grouping. Correction factors for maternal height and prepregnancy weight as well as sibling size at birth would be useful. Birth weight-derived data are suspect for preterm gestations; sonographic fetal weight curves may improve accuracy. Without sensitive epidemiologic growth assessment, other modalities (clinical, biochemical, and sonographic) will have limited usefulness. The assessment of fetal growth may include clinical means but care must be taken to garner a meticulous history and to record precisely serial fundal height. Many biochemical methods have been proposed for the detection of IUGR but they have a limited role as screening tests. Ultrasound remains the best method for the diagnosis, characterization, and follow-up of IUGR. Ultrasonography allows for the precise estimation of fetal weight. The calculation of HC:AC ratios allows for characterization of the pattern of IUGR. Evaluation of amniotic fluid volume and placental grading as well as the search for congenital anomalies are helpful exercises. Doppler flow studies of uterine and fetal blood flow may provide an understanding of the cause and severity of the growth-retarding process. Finally, careful antenatal surveillance and judicious timing of delivery are required following the identification of IUGR. Delivery should be planned in concert with the neonatologist.
Topics: Biometry; Birth Weight; Embryonic and Fetal Development; Female; Fetal Growth Retardation; Gestational Age; Humans; Male; Pregnancy; Smoking; Ultrasonography; Uterus
PubMed: 3514051
DOI: No ID Found -
Kidney International Sep 2010Rapamycin, a potent immunosuppressant used in renal transplantation, has been reported to impair longitudinal growth in experimental studies. Rapamycin is both...
Rapamycin, a potent immunosuppressant used in renal transplantation, has been reported to impair longitudinal growth in experimental studies. Rapamycin is both antiproliferative and antiangiogenic; therefore, it has the potential to disrupt vascular endothelial growth factor (VEGF) action in the growth plate and to interfere with insulin-like growth factor I (IGF-I) signaling. To further investigate the mechanisms of rapamycin action on longitudinal growth, we gave the 4-week-old rats rapamycin daily for two weeks. Compared with a vehicle-treated group, rapamycin-treated animals were severely growth retarded and had marked alterations in the growth plate. Vascular invasion was disturbed in the rapamycin group, there was a significant reduction in osteoclast cells near the chondro-osseus junction, and there was lower VEGF protein and mRNA expression in the terminal chondrocytes of the growth cartilage. Compared with the control group, the rapamycin group had higher levels of circulating IGF-I as well as the mRNAs for IGF-I and of the receptors of IGF-I and growth hormone in the liver but not in the growth cartilage. Thus our findings explain the adverse effect of rapamycin on growth plate dynamics. This should be taken into account when the drug is administered to children.
Topics: Animals; Animals, Newborn; Chondrocytes; Growth; Growth Plate; Immunosuppressive Agents; Insulin-Like Growth Factor I; Neovascularization, Physiologic; Osteoclasts; RNA, Messenger; Rats; Receptor, IGF Type 1; Sirolimus; Vascular Endothelial Growth Factor A
PubMed: 20555322
DOI: 10.1038/ki.2010.173 -
The Journal of Allergy and Clinical... Mar 1977Growth in height, bone age, and sexual maturation have been studied in asthmatic boys 2 to 20 yr of age. The mean pattern of growth in height has been analyzed...
Growth in height, bone age, and sexual maturation have been studied in asthmatic boys 2 to 20 yr of age. The mean pattern of growth in height has been analyzed mixed-longitudinally in 531 patients (1,754 measures) and seemed to be determined by a delay in physiologic maturation. The asthmatic boys' growth in height showed no retardation during infancy, a small but consistent retardation during childhood, a more pronounced delay at adolescence, and a catch-up growth toward adulthood. The mean adolescent growth spurt is delayed by about 1.3 yr. Bone age has been analyzed mixed-longitudinally in a subsample of 370 patients (660 observations) and showed a slight retardation at all ages between 6 and 13 yr. Development of pubic hair of 91 subjects analyzed cross-sectionally was definitely retarded when compared to adequate reference data. Evidence was given that factors secondary to the asthmatic syndrome are involved in the retardation of growth and development.
Topics: Adolescent; Adult; Age Determination by Skeleton; Asthma; Bacterial Infections; Belgium; Body Height; Child; Child, Preschool; Growth; Growth Disorders; Humans; Male; Puberty; Sampling Studies; Stress, Physiological
PubMed: 190283
DOI: 10.1016/0091-6749(77)90150-6