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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevailing concept of etiologic heterogeneity for the diabetes mellitus syndrome is one of multiple genetic factors interacting with a variety of environmental influences. Variation in expression of the disorder, particularly the need for insulin, does not correlate with known etiologic distinctions. There is much evidence for genetic heterogeneity, as well as phenotypic variation when etiology can be presumed to be identical. The vascular manifestations of diabetes include microangiopathy unique to diabetes and larger vessel disease that differs from that of normal aging only by its prematurity. There is as much evidence for heterogeneity of the vascular expression as there is for glucose intolerance. Approximately 25% of persons with insulin-dependent diabetes may never develop the microvascular disease. The pathogenesis of vascular disease in diabetes may involve a number of abnormalities of plasma, circulating cells, and vascular tissue. Were absolute control of glycemia possible, some of the contributing factors involved in vasculopathy would possibly be alleviated. In the absence of automated physiologic insulin replacement the potential deleterious effect of our current methods of treatment might be reduced by specific inhibition of excess catecholamine, growth hormone and/or glucagon responses.
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PMID:Nature and nurture in the expression of diabetes mellitus and its vascular manifestations. 33 1

Intra-uterine growth retardation (IUGR) comprises a heterogeneous population of infants due to the variety of causes and degrees of severity. Among the risk factors, smoking, maternal weight gain, age and disease state as well as socioeconomical, nutritional and environmental factors would be susceptible to preventive measures while others such as ethnic origin, parity and genetic potential lie beyond the scope of medical management. Still other factors remain unknown since as many as 30% of the small-for-gestational age births are labelled idiopathic. Factors predicting post-natal growth rate and catch-up growth are poorly understood. Prematurity and very low birthweight are risk factors leading to delayed growth. Maternal alcoholism may be responsible for neurosensorial handicaps and certain authors suggest this population is more susceptible to delayed growth. Inversely, the severity of hormone disorders at birth and sex apparently have no predictive value. Preliminary studies report the effects of growth hormone therapy in children with short stature secondary to intra-uterine growth retardation and indicate significant results in these patients with a normal secretion of endogenous growth hormone. At 1.2-1.4 IU/kg/week of hGH (3 times the dose given in cases of GH insufficiency) height increases by one standard deviation during the first two years of treatment without excessive bone maturation. The exact dose required and the optimal age for initiating treatment as well as long-term effects remain to be ascertained.
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PMID:[Retardation of intrauterine growth. Prognosis and therapeutic perspectives]. 793 42

The transition from fetus to neonate involves three phases: late gestation, parturition and the processes needed to establish independent homoeostatic regulation after separation from the placenta. These phases are regulated by a series of fetal and placental endocrine events. Glucocorticoids have an important role in the preparation for birth, including involvement in lung and cardiac development, and the maturation of enzymes in a variety of pathways. Fetal cortisol production is, in turn, also under hormonal control. Parturition is a complex process, which is still poorly understood in humans. The final steps are largely dependent on the effect of prostaglandin F2 alpha on the myometrium associated with increased oxytocin activity. The transition to birth is accompanied by changes in respiration, circulation, glucose homoeostasis, and the onset of independent oral feeding and thermoregulation. Several examples of endocrine components of the transition from fetal to neonatal life are reviewed here: the role of prostanoids, the onset of thermogenesis, and changes in the thyroid hormone and growth hormone axes. The effects of hormone levels on prematurity and growth retardation are also discussed.
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PMID:The transition from fetus to neonate--an endocrine perspective. 1010 45

Characteristics probably associated with the fetal hormonal milieu have recently been shown to increase (birth size indicators, prematurity, neonatal jaundice) or decrease (pregnancy toxaemia) breast cancer risk in the female offspring. However, it is unknown whether differences in pregnancy hormone levels may contribute to the marked geographical variation in breast cancer incidence. We have compared, in a highly standardized manner, pregnancy hormone levels in a population with high incidence and one with low incidence of breast cancer. Three hundred and four pregnant Caucasian women in Boston and 334 pregnant Chinese women in Shanghai were enrolled from March 1994 to October 1995. Levels of oestradiol, oestriol, prolactin, progesterone, human growth hormone, albumin and sex hormone-binding globulin were measured in maternal blood at weeks 16 and 27 of gestation and compared between the two study sites using non-parametric Wilcoxon's rank-sum test. Demographical, anthropometrical and pregnancy characteristics were ascertained through interview, and relevant variables concerning delivery and the newborn were abstracted from medical records and paediatric charts. During the first visit, median serum levels of all studied hormones were statistically significant, and in most instances substantially, higher among Chinese women, who have a low incidence of breast cancer, compared with American women, who have a high incidence of breast cancer. An analogous pattern was evident during the second visit, although the relative differences tended to be smaller. Further research is needed to identify lifestyle or other exogenous determinants of pregnancy hormone levels, as well as possible mechanisms by which they may influence carcinogenic processes in the breast and possibly other organs.
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PMID:Maternal pregnancy hormone levels in an area with a high incidence (Boston, USA) and in an area with a low incidence (Shanghai, China) of breast cancer. 1102 43

Recent published data show that at hospital discharge, most infants born at <30 weeks of gestation would not achieve the median birth weight of the reference fetus at the same postconceptional age, and many would be less than the 10th centile. Estimating from the current recommendations of calorie and protein intakes, these infants accrue large deficits in intakes of protein and calorie during the first weeks of life. Postnatal growth retardation over a prolonged period of time is related to neurodevelopmental delays. While a total energy intake of 120 kcal/kg/day has generally been considered adequate, protein requirement in low gestation infants remains a matter for debate. Increasing the dietary protein:calorie ratio has previously been proposed as a strategy to enhance growth and to achieve a body composition similar to that of the reference fetus. Previous study data reveal that serum insulin-like growth factor I (IGF-I) concentration is positively correlated with protein intake, and nitrogen retention, in turn, is positively correlated with serum IGF-I concentration. Remarkably, elevated serum growth hormone but low serum IGF-I concentrations have been reported in low gestation infants and in infants with intrauterine growth retardation, suggesting IGF-I being a nutritionally regulated hormonal factor in the postnatal growth retardation. As neurodevelopment in extreme prematurity is likely affected by multiple factors, we hypothesize that a combined strategy of the previously proposed hormonal supplement with hydrocortisone and tri-iodothyronine together with increased dietary protein intake (progressively increasing from 1.5 g/kg/day intravenously administered amino acids immediately after birth, then 3.6 g/100 kcal at approximately 125 kcal/kg/day when enterally fed till the infant reaches a body weight of >or=1.8 kg and at >or=50th centile weight of the reference fetus at the same postconceptional age) would likely be synergistic and more effective in improving neurodevelopmental outcome.
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PMID:Nutritionally regulated hormonal factors in prolonged postnatal growth retardation and its associated adverse neurodevelopmental outcome in extreme prematurity. 1289 Sep 31

The aims of this study were: (1) to determine whether premature and small-for-gestational-age (SGA) children have alterations to the insulin-like growth factor (IGF)-IGF binding protein axis and (2) to evaluate growth in premature children. Three groups of children were evaluated: (i) premature children of </= 32 weeks gestation, which included appropriate-for-gestational-age (AGA) and small-for-gestational-age (SGA) subgroups; (ii) term children of >36 weeks gestation, which included AGA and SGA subgroups; and (iii) children born at term and AGA with normal childhood heights and weights. Fasting plasma IGF-I, insulin-like growth factor binding protein-3 (IGFBP-3), and IGF-II (all expressed as microgm/L) were drawn on available subjects. To examine the influence of SGA on the IGF-IGFBP axis, term SGA subjects were compared with term AGA subjects. To examine the influence of prematurity on the IGF-IGFBP axis, preterm SGA subjects were compared with term SGA subjects and preterm AGA subjects were compared with the normal-stature AGA controls. This ensured that groups of very similar stature and nutritional statuses were compared. Auxological data were available for 24 premature children, and biochemical data were available for 77 children, including the premature children. Across the height standard deviation score (SDS) range, premature children did not reach mid-parental height (MPH) SDS and were approximately 0.6 standard deviations (SDs) below the MPH SD (P < 0.0001). Plasma IGF-I and IGFBP-3 levels were higher in term SGA subjects compared with term AGA subjects (P < 0.001, respectively). Conversely, IGF-I and IGFBP-3 values were lower in the premature SGA subgroup compared with the premature AGA subgroup (P < 0.001 for both), and both were also lower in the premature AGA subgroup compared with the normal-statured AGA subgroup (P < 0.001 for both). IGF-II values were higher in the preterm group than in the term group (P < 0.001). In conclusion, very low birth weight (VLBW) children, regardless of whether they were AGA or SGA, have low plasma IGF-I and IGFBP-3 levels in mid-childhood, suggesting partial growth hormone (GH) resistance. Conversely, term SGA children have elevated plasma IGF-I and IGFBP-3 levels. When combined, premature birth plays a more dominant role than SGA on the IGF-IGF binding protein axis.
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PMID:The endocrine consequences for very low birth weight premature infants. 1513 95

Human adolescent pregnancy is characterized by poor pregnancy outcome; the risks of spontaneous miscarriage, prematurity, and low birth weight are particularly acute in girls who are still growing at the time of conception. Studies using a highly controlled sheep paradigm demonstrate that, in growing adolescents who are overnourished throughout pregnancy, growth of the placenta is impaired, resulting in a decrease in lamb birth weight relative to control-fed adolescents of equivalent age. Rapid maternal growth is also associated with increased spontaneous abortion rates in late gestation and a reduction in gestation length. Nutritionally sensitive hormones of the maternal somatotrophic axis may orchestrate nutrient partitioning in this paradigm and the particular role of growth hormone is discussed. At midgestation, the placentae of rapidly growing dams exhibit less proliferation in the fetal trophectoderm and reduced placental mRNA expression of a range of angiogenic factors. These changes occur before differences in placental size are apparent but may impact on subsequent vascularity. By late pregnancy, placental mass in the rapidly growing versus the control dams is reduced by approximately 45%; the fetuses display asymmetric growth restriction and are hypoxic and hypoglycemic. These growth-restricted pregnancies are associated with major reductions in absolute uterine and umbilical blood flows, leading to attenuated fetal oxygen, glucose, and amino acid uptakes. Placental glucose transport capacity is markedly reduced in the rapidly growing dams but is normal when expressed on a weight-specific placental basis. Thus, it is the small size of the placenta per se rather than alterations in its nutrient metabolism or transfer capacity that is the major limitation to fetal growth in the growing adolescent sheep. Information obtained from this highly controlled paradigm is clearly relevant to the clinical management of human adolescent pregnancies. In addition, the paradigm provides a robust model of placental growth restriction that replicates many of the key features of human intrauterine growth restriction per se.
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PMID:Nutritionally mediated placental growth restriction in the growing adolescent: consequences for the fetus. 1520 Dec 3

The evidence for outcome following fetal growth restriction (FGR) has previously been inferred from studies, based on babies who were born small for gestational age (SGA). Great care is required when evaluating studies in this area due to a number of potential confounders. It does appear, however, that FGR is associated with an increased risk of poor neurological outcome. This includes an increased risk of cerebral palsy in babies greater than 32 weeks' gestation. Below 32 weeks, the effects of prematurity appear to negate the effects of FGR. FGR is also associated with cognitive deficit and behaviour problems. Babies with poor prenatal head growth appear to have a worse cognitive outcome. However, the role of 'fetal brain sparing' remains unclear, as impaired cognitive outcome is still evident in babies with appropriate head growth. Recent studies, which have identified FGR more accurately using fetal growth standards, have found an increased incidence of major intracranial injury and other adverse neonatal outcomes, which had previously been thought to occur less frequently in FGR babies. FGR is also associated with poor postnatal growth. The majority of children with FGR demonstrate catch-up growth in the first 2 years of life. Children who fail to demonstrate catch-up growth have a high risk of long-term growth problems. There is evidence of impaired growth hormone activity in some children with FGR who have persistent poor growth in the postnatal period.
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PMID:Paediatric consequences of fetal growth restriction. 1569 77

Newborns with intrauterine hypotrophy are at particular risk group of neonates. Diagnosis based on an adequate estimated gestational age, compared with accurate anthropometric measurements after birth. Among children born with low birth weight (< 2500 g) stands in one particular group--those small for gestational age SGA (Small for Gestational Age-SGA), whose health problems are studied intensively in recent years. In Bulgaria children with low birth weight in recent years is about 10%, which is well above the European average indicator--6.2%. In 2001. created International Advisory Board, composed of 42 people leading experts in obstetrics, perinatal and neonatal medicine, pediatricians endocrinologists, pharmacologists and epidemiologists, with the following main tasks: the definition of small for gestational age children, diagnosis of SGA, SGA children growth and role of growth hormone in their treatment. Subsequent meetings of this committee discuss consensus on SGA infants who acquire their final form at a meeting in Prague in 2009 Small for gestational age (SGA, SGA), is described children whose body weight and/or height is lower than the average by more than 2 standard deviations (< - 2SD). Some authors use the boundary 3rd, 5th, or 10th percentile, but most believe that the use of indicators (< - 2SD) comprises the largest percentage of newborns with fetal growth disorders. Small for gestational age children are divided into: newborn weight retardation (SGAW), growth retardation (SGAL), matched up in weight and height (SGAWL). "Intrauterine growth retardation" (Intra-Uterine Growth Retardation (IUGR) are born with fetal growth retardation, documented at least two ultrasound scans, one of which in the 1st trimester Intrauterine hypotrophy is the second most common cause of perinatal death after prematurity. Hypotrophy is present in about 53% of premature and stillborn at 26% of full-term stillborn children. The incidence of asphyxia in SGA intrapartum is about 50%. Neonatal care includes effective primary resuscitation, treatment of existing and prevention of complications anticipated adaptation. These children are subject to follow-up for later risk of socially significant diseases in the adult.
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PMID:[Small for gestational age newborns--definition, etiology and neonatal treatment]. 2380 77

This review highlights pitfalls and challenges in interpreting neonatal hormone reports. Pre-analytical errors contribute to nearly 50% of all errors. Modern chemiluminescence assay are more accurate, have lower risk of Hook's effect, but continue to have problems of assay interference. Liquid chromatography mass spectroscopy is gold standard for most hormone assays. Neonatal hypoglycemia diagnostic cut-offs are lower than adults. Random growth hormone testing is of value in diagnosing growth hormone deficiency in neonates. 17-hydroxy-progesterone testing in first three days of life for congenital adrenal hyperplasia (CAH) remains a challenge due to cross-reactivity with maternal circulating steroids, prematurity and lack of adrenal maturation. Both T4 and TSH testing is encouraged after 48 hours of delivery for diagnosing neonatal hypothyroidism; repeat testing should be done immediately for confirmation of diagnosis. There is an urgent need to develop age- sex- and ethnicity-based normative data for different hormone parameters in neonates. Laboratory should develop their own neonatal references and avoid using ranges from manufacturers. In neonatal endocrinopathies, the clinical scenario should primarily dictate the treatment formulation with hormonal assay to supplement treatment.
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PMID:Neonatal Endocrine Labomas - Pitfalls and Challenges in Reporting Neonatal Hormonal Reports. 2939 54


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