Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed a randomized, double-blind, controlled trial to determine whether vitamin A supplementation in a group of very low birth weight infants would reduce the incidence of bronchopulmonary dysplasia. Forty-nine infants (birth weight 700 to 1100 gm) requiring mechanical ventilation and supplemental oxygen at 96 hours age were randomly assigned to receive either 2000 IU retinyl palmitate (n = 27) or saline placebo (n = 22) intramuscularly every other day for up to 14 doses. There were no differences between treatment groups in the incidences of bronchopulmonary dysplasia at 31 days of postnatal age (vitamin A group 48%, placebo group 55%; p = 0.776), supplemental oxygen requirement at 34 weeks of postconceptional age, or other complications of prematurity. The vitamin A group had higher mean plasma vitamin A concentrations than the placebo group, but mean plasma vitamin A concentrations were greater than 20 micrograms/dl (suggesting sufficiency) in both groups after the first study week. By study day 28, only one fourth of the infants in either group had plasma vitamin A concentrations less than 20 micrograms/dl. In contrast to an earlier report, we found no change in the incidence of BPD with vitamin A supplementation. Our findings may reflect a low baseline incidence of vitamin A deficiency in the study population and recent changes in the respiratory care of very low birth weight infants. The latter may have lessened the potential impact of vitamin A deficiency on lung disease.
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PMID:Trial of vitamin A supplementation in very low birth weight infants at risk for bronchopulmonary dysplasia. 830 48

Studies were made of the vitamin A status of newborn as judged by cord serum vitamin A in relation to gestational age, birth weight, and maternal vitamin A status in 130 + 79 mother-infant pairs belonging to low and high income groups in urban Baroda. The mean values for maternal serum vitamin A (microgram/dl, mean +/- SE) in the two groups were 21.8 +/- 0.59 (n = 130) and 29.3 +/- 0.80 (n = 79), respectively. The corresponding values for cord serum vitamin A were 13.8 +/- 0.40 and 19.6 +/- 0.64 for full-term infants and 7.5 +/- 0.44 and 12.9 +/- 0.80 for premature infants. Even for comparable levels of maternal serum vitamin A, differences were found between income groups regarding birth weight and cord serum vitamin A. Mothers of premature infants had lower levels of serum vitamin A than those of full-term infants suggesting maternal vitamin A status to be one of the correlates of prematurity. Significant correlations were found between cord serum vitamin A, maternal serum vitamin A, gestational age, and growth status. These studies suggest that a poor vitamin A status is one of the features associated with a higher prevalence of prematurity and intrauterine growth retardation found in poorly nourished populations. These findings stress the importance of satisfactory vitamin A supplies to pregnant and nursing mothers to prevent vitamin A deficiency and growth retardation in the progeny.
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PMID:Vitamin A status of the newborn in relation to gestational age, body weight, and maternal nutritional status. 648 86

Research related to maternal-child transmission of human immunodeficiency virus (HIV) has been advanced by standardization of case definitions and transmission rate calculation methodologies as well as enhanced diagnostic options for detecting infant HIV-1 infection. Standardization guidelines have yielded vertical transmission rate estimates of 25-30% in developing countries and 14-25% in developed countries. Mathematical modeling suggests that 95% of infant infections occur later than the last 2 months before delivery. Serial polymerase chain reaction evaluation has identified a 7.7% risk of in utero transmission, a 17.6% risk of combined in utero and intrapartum transmission, and a 4.9% incidence of late postnatal transmission. The risk of transmission through breast feeding has been estimated at 14%, with increases with longer durations. Advanced maternal clinical HIV status, primary infection, decreased maternal cell-mediated immunity, placentitis, ascending genital infection during the peripartum period, and syncytium-inducing HIV-1 strains have been associated with higher rates of maternal-child transmission. Prematurity, lack of cellular immunity, and vitamin A deficiency may be infant risk factors. The finding in an AIDS Clinical Trial Group that zidovudine (AZT) treatment was associated with a 67.5% reduction in risk has prompted widespread use of this regimen in developed countries; however, AZT is expensive and logistically difficult to administer in most developing country contexts. Randomized clinical trials currently underway are assessing the benefits of cesarean section delivery, postpartum HIV-specific immunoglobulin administration to infants, avoidance of breast feeding or early weaning, and antenatal maternal vitamin A administration. Selected intervention strategies should be regionally designed to take into account variations in viral, host, and obstetric factors.
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PMID:Mother-to-child transmission of human immunodeficiency virus type 1. 902 9

During late pregnancy, the fetal lung stores surfactant in preparation for extrauterine life. Surfactant deficiency, most often due to prematurity, precipitates respiratory distress syndrome (RDS) of the neonate. Although vitamin A (retinol) and retinoic acid have been shown to enhance the synthesis of phospholipid surfactant components, their effect on surfactant-specific proteins is unclear. No attempt has been made to evaluate the consequences of vitamin A restriction on surfactant phospholipid storage or on the expression of the life-essential surfactant protein-B (SP-B). We induced in rats a partial vitamin A deficiency leading to a 30-60% reduction in blood retinol, a status compatible with maintenance of gestation and absence of gross abnormalities in offspring. At term, lung surfactant phospholipids were reduced by 21%, and the major surfactant phospholipid, disaturated phosphatidylcholine (DSPC), was reduced by 27% in vitamin A-deficient (VAD) fetuses. The decrease in surfactant phospholipids and DSPC correlated linearly with plasma retinol, and reached about 50% in fetuses with the lowest retinol concentrations; it was accompanied by reduced expression of the gene for fatty acid synthase, a key enzyme in the synthetic pathway for surfactant-phospholipid lipid precursors. The amounts of SP-A, SP-B, and SP-C messenger RNAs were decreased by 46%, 32%, and 28%, respectively, in VAD fetuses. Consistently, amounts of SP-A and SP-B proteins were diminished as assessed by Western blotting. The proportion of type II cells determined after SP-B labeling was unchanged in VAD as compared with control lungs. Vitamin A deficiency is therefore a cause of lung maturational delay. In view of its rather large incidence in human populations, it may represent an increased risk for RDS and an aggravating factor for prematurity.
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PMID:Mild vitamin A deficiency delays fetal lung maturation in the rat. 1038 96

Bronchopulmonary dysplasia (BPD) is a chronic lung disease of infancy which is associated with prematurity and early lung injury resulting from mechanical ventilation. Oxygen toxicity, barotrauma, and volutrauma play key roles in its pathogenesis. Parenteral administration of Vitamin A to the newborn is the current recommended preventive therapy for BPD. Vitamin A has been found to upregulate genes necessary for fetal lung growth and increase surfactant production in animal models. Supplementation of Vitamin A in late pregnancy increases the cord blood vitamin A levels proportionately. Hence, we hypothesize that Vitamin A supplementation during late pregnancy can decrease the incidence of BPD in newborns. This can be an effective adjunct to postnatal preventive therapy. Vitamin A supplementation in late pregnancy carries no risk of teratogenicity unlike in early pregnancy. Moreover, vitamin A deficiency in pregnancy is associated with depressed immune function leading on to increased infectious morbidity and can cause intrauterine growth retardation, low birth weight and anemia in newborns. Combining antenatal Vitamin A supplementation to the mother with postnatal supplementation to the newborn can effectively prevent BPD better than the traditional postnatal preventive therapy alone. It will also treat the highly prevalent vitamin A deficiency in pregnant mothers and newborns of the developing world.
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PMID:Vitamin A supplementation in late pregnancy can decrease the incidence of bronchopulmonary dysplasia in newborns. 2029 8