Lower respiratory tract illness and RSV prophylaxis in very premature infants.
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AIMS: To determine the frequency of and the risk factors for readmissions for any lower respiratory tract illness (LRTI) and for respiratory syncytial virus (RSV) documented LRTI in children born very prematurely who had or had not received RSV prophylaxis. METHODS: Multicentre prospective longitudinal cohort study of 2813 infants, born between April 2000 and December 2000 at less than 33 weeks of gestational age, and followed until the end of the epidemic season. RESULTS: Among the 2256 children who had no bronchopulmonary dysplasia at 36 weeks of postmenstrual age and were not submitted to RSV prophylaxis, 27.4% were readmitted at least once for any reason during the epidemic season; 15.1% and 7.2% were readmitted at least once for any LRTI and RSV related LRTI, respectively. Children born at less than 31 weeks' gestation, having an intrauterine growth restriction, or living in a single mother family were at a significantly higher risk of readmission for LRTI in general as well as for RSV related LRTI. Of the 376 children submitted to prophylaxis, 28.2% were readmitted at least once for any LRTI and 6.1% for RSV related LRTI. CONCLUSION: One out of four children who had received no prophylaxis, was born very prematurely, and was without bronchopulmonary dysplasia at 36 weeks of postmenstrual age, was readmitted at least once for any reason. Roughly 50% and 20% of these readmissions were related to a LRTI and an RSV infection, respectively. Further epidemiological studies are warranted to assess the aetiology and impact of other respiratory pathogens on post-discharge readmission and respiratory morbidity in this population. (+info)
Pulmonary antioxidant concentrations and oxidative damage in ventilated premature babies.
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OBJECTIVE: To determine the relation between lipid peroxidation and the antioxidants ascorbate, urate, and glutathione in epithelial lining fluid in ventilated premature babies, and to relate the biochemical findings to clinical outcome. DESIGN: A cohort study conducted between January 1999 and June 2001. SETTING: A NHS neonatal intensive care unit. PATIENTS: An opportunity sample of 43 ventilated babies of less than 32 weeks gestation. MAIN OUTCOME MEASURES: The duration of supplementary oxygen according to the definition of bronchopulmonary dysplasia (BPD; oxygen dependency at 36 weeks gestational age). METHODS: Epithelial lining fluid was sampled by bronchoalveolar lavage. Ascorbate, urate, glutathione, and malondialdehyde (a marker of lipid peroxidation) were measured. RESULTS: Babies who developed BPD had significantly lower initial glutathione concentrations (mean (SEM) 1.89 (0.62) v 10.76 (2.79) microM; p = 0.043) and higher malondialdehyde concentrations (mean (SEM) 1.3 (0.31) v 0.345 (0.09) microM; p < 0.05) in the epithelial lining fluid than those who were not oxygen dependent. These variables were poor predictors of the development of BPD. Gestational age, endotracheal infection, and septicaemia had good predictive power. The level of oxidative damage was associated with the presence of endotracheal infection/septicaemia rather than inspired oxygen concentration. CONCLUSIONS: Endotracheal infection, septicaemia, and gestational age, rather than antioxidant concentrations, are the most powerful predictors of the development of BPD. (+info)
Dexamethasone increases plasma amino acid concentrations in bronchopulmonary dysplasia.
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Nine ventilated low birthweight babies were treated with dexamethasone (0.6 mg/kg/day). Appreciable suppression of weight gain was accompanied by uraemia and significant increases in the concentration of all amino acids except phenylalanine, tyrosine, threonine, and glutamate. Ornithine, citrulline, alanine, glutamine, and cystine concentrations increased threefold or more. The findings could not be explained by changes in dietary intake and presumably reflect pronounced catabolism, though the effects of dexamethasone on intermediary metabolism and membrane transport could also play a part. (+info)
Role of oxidative stress as physiopathologic factor in the preterm infant.
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Oxidative stress usually occurs when the production of damaging free radicals (ROS) and other oxidative molecules exceeds the capacity of the body's antioxidant defenses. This process is supposed to begin after the delivery, but it can even affect the fetus when maternal pregnancy diseases (i.e.: pre-eclampsia, eclampsia, maternal infections) occur and in the case of preterm delivery. Most living organisms have developed well integrated antioxidant defenses to prevent the potential negative role of the ROS, in order to scavenge them and to control their concentration. These mechanisms are deficient in preterm newborn. Many illnesses in preterm infants, including bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), brain injury such as hypoxic/ischemic encephalopathy, and intraventricular hemorrhage (IVH) are thought to be related to the action of ROS. This presumably occurs due to the fact that the antioxidant system of preterm infants is at the same time highly stressed and incompletely developed. Unfortunately, the clinical trials which tried to prevent oxidative stress using antioxidant agents failed their objective and therefore they cannot be considered as an effective therapy. The objective of this review is to clarify the role of oxidative stress in the development of the previous severe diseases in preterm infants, and its possible correlation with hyperbilirubemia. (+info)
Benefits of non invasive ventilation.
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Mechanical ventilation of the newborn infant has increased neonatal survival. However, this increased survival has come at the expense of increased morbidity, in the form of bronchopulmonary dysplasia, and at the cost of an expensive technology. Continuous positive airway pressure (CPAP) is accepted as conferring clinical benefit in supporting the recently extubated preterm infant and in the management of apnea of prematurity. Attention is now being drawn to physiologic and clinical evidence to support CPAP use, with or without early surfactant, as a primary treatment of hyaline membrane disease. The purpose of this review is to explore these proposed benefits of non invasive ventilation and place them in the context of current clinical evidence. (+info)
Low plasma retinol concentrations increase the risk of developing bronchopulmonary dysplasia and long-term respiratory disability in very-low-birth-weight infants.
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BACKGROUND: The effect of inadequate vitamin A during the neonatal period on lung status is still unknown. OBJECTIVE: We tested the hypothesis that low plasma retinol concentrations during the first month of life are independently associated with bronchopulmonary dysplasia (BPD) and long-term respiratory morbidity at 6 mo gestationally corrected age (ie, the age the infant would be had the pregnancy gone to term). DESIGN: Respiratory outcome information was obtained to 6 mo corrected age for a historical cohort of very-low-birth-weight neonates (<1250 g) who were admitted to intensive care over a 7-y period. Neonates with one or more plasma measurements of retinol concentrations < 0.35 micromol/L (<100 microg/L) on days 1-28 were classified as having low vitamin A. BPD was defined at day 28 by clinical and radiologic criteria and by use of supplemental oxygen at 36 wk postmenstrual age (PMA). Dependence on supplemental oxygen was used to identify long-term respiratory disability at 6 mo corrected age. Multivariate logistic regression analyses were conducted. RESULTS: Of the 350 study infants, 192 (55%) had low vitamin A status. BPD occurred in 52% of survivors at day 28 (173/331) and at 36 wk PMA (147/285). Fourteen percent (33/244) required oxygen support at 6 mo corrected age. Adjusted odds ratios of BPD with low vitamin A were 3.5 (95% CI: 1.7, 7.2) at day 28 and 1.7 (1.0, 2.7) at 36 wk PMA. At 6 mo corrected age, the adjusted odds ratio was 2.6 (1.1, 6.4) for respiratory disability with low vitamin A. CONCLUSION: Poor vitamin A status during the first month of life significantly increased the risk of developing BPD and long-term respiratory disability. (+info)
Inositol supplementation in premature infants with respiratory distress syndrome.
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BACKGROUND: Inositol influences cellular function and organ maturation. Feeding premature infants inositol-rich breast milk increases their serum inositol concentrations. Whether inositol supplementation benefits infants receiving fluids for parenteral nutrition, which are inositol-free, is not known. METHODS: We carried out a placebo-controlled, randomized, double-blind trial to determine the effects of administering inositol (80 mg per kilogram of body weight per day) during the first five days of life to 221 infants with respiratory distress syndrome who were receiving parenteral nutrition (gestational age, 24 to 32 weeks; birth weight, less than 2000 g). All the infants were treated with mechanical ventilation and some with surfactant as well. The primary end point was survival at 28 days without bronchopulmonary dysplasia. RESULTS: The 114 patients given inositol had significantly lower mean requirements for inspiratory oxygen (P less than 0.01) and mean airway pressure (P less than 0.05) from the 12th through the 144th hour of life than did the 107 infants given placebo. Eighty-one infants given inositol and 51 given placebo survived without bronchopulmonary dysplasia (71 vs. 55 percent; P = 0.005). In the 65 infants given surfactant, however, inositol had no effect on the degree of respiratory failure. Thirteen infants given inositol and 21 given placebo had retinopathy of prematurity (13 vs. 26 percent; P = 0.022); none of the infants given inositol had stage 4 disease, whereas 7 of those given placebo did (0 vs. 9 percent; P = 0.012). Among the infants given placebo, those who had poor outcomes (death, bronchopulmonary dysplasia, or stage 4 retinopathy of prematurity) had lower serum inositol concentrations during days 2 through 7 than those who had good outcomes (P less than 0.01). CONCLUSIONS: The administration of inositol to premature infants with respiratory distress syndrome who are receiving parenteral nutrition during the first week of life is associated with increased survival without bronchopulmonary dysplasia and with a decreased incidence of retinopathy of prematurity. (+info)
The Angiotensin Converting Enzyme Insertion/Deletion polymorphism is not associated with an increased risk of death or bronchopulmonary dysplasia in ventilated very low birth weight infants.
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BACKGROUND: The ACE gene contains a polymorphism consisting of either the presence (insertion, I) or absence (deletion, D) of a 287 bp alu repeat in intron 16. The D allele is associated with increased ACE activity in both tissue and plasma. The DD genotype is associated with risk of developing ARDS and mortality. The frequency of the D allele is higher in patients with pulmonary fibrosis, sarcoidosis and berylliosis. The role of this polymorphism has not been studied in the development of BPD in the premature newborn. METHODS: ACE I/D genotype was determined in 245 (194 African-American, 47 Caucasian and 4 Hispanic) mechanically ventilated infants weighing less than 1250 grams at birth and compared to outcome (death and/or development of BPD). RESULTS: The incidence of the D allele in the study population was 0.58. Eighty-eight (35.9%) infants were homozygous DD, 107 (43.7%) were heterozygous ID and 50 (20.4%) were homozygous II. There were no significant differences between genotype groups with respect to ethnic origin, birth weight, gestation, or gender. There was no effect of the ACE I/D polymorphism on mortality or development of BPD (O2 on 28 days or 36 weeks PCA). Secondary outcomes (intraventricular hemorrhage and periventricular leukomalacia) similarly were not influenced by the ACE ID polymorphism. CONCLUSIONS: The ACE I/D polymorphism does not significantly influence the development of BPD in ventilated infants less than 1250 grams. (+info)