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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bronchopulmonary dysplasia of preterm infants has a multifactorial etiology. Pulmonary immaturity, oxygen toxicity, formation of oxygen radicals and mechanical lung trauma as well as additional factors (pulmonary hyperhydration, infection a.o.) may contribute to pulmonary damage. A pulmonary inflammatory reaction is thought to play a central role in the pathogenesis of chronic lung disease. It is characterized by the presence of inflammatory cells and various inflammatory mediators including proteases, chemoattractants, cytokines, leukotrienes and others. Due to the immaturity of several protective systems (antiproteases, antioxidants, surfactant system) the inflammatory response seems to be aggravated. Moreover, the magnitude and persistence of inflammation may eventually lead to pulmonary fibrosis.
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PMID:[Pathogenesis of bronchopulmonary dysplasia]. 852 53

Free radical-mediated oxidation of proteins may impair their function and cause cellular damage. We studied pulmonary protein oxidation and its association with the development of chronic lung disease in 61 newborn infants (mean gestational age 31.1 +/- 4.0, range 24-41 weeks) requiring intensive care with oxygen therapy. Protein oxidation was quantified as protein carbonylation in tracheal aspirates recovered daily during the first week of life. Mean carbonyl concentration was 3.5 +/- 1.6 mumol/mg protein. Negative correlations existed between protein carbonylation during days 2-4 and gestational age (day 2: r = -0.37, p = 0.01; day 3: r = -0.48, p = 0.001; and day 4: r = -0.33, p = 0.03). Patients who developed bronchopulmonary dysplasia showed significantly higher protein carbonylation on days 1-6 (all p < 0.05). In multiple regression analysis explaining bronchopulmonary dysplasia, using gestational age, inspired oxygen on days 1-3 and protein carbonylation on day 3 as independent variables, only protein carbonylation remained significant. We conclude that immaturity is the most important factor explaining free radical-mediated pulmonary protein oxidation in newborn infants and that oxidation of proteins is related to the development of chronic lung disease.
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PMID:Early protein oxidation in the neonatal lung is related to development of chronic lung disease. 858 Jun 30

Since the advent of surfactant therapy for hyaline membrane disease, the problems associated with this condition have been greatly reduced in severity and morbidity. However, many premature infants who recover from the biochemical problem of surfactant deficiency still suffer from structural immaturity of the lungs. This aspect of lung immaturity centers primarily around pulmonary hypoplasia, for these infants, because they are immature, have fewer than normal alveoli and thus cannot accomplish adequate gas exchange. As a result, they are placed on long-term ventilator therapy, which renders them susceptible to problems associated with hypoxia, oxygen toxicity, and barotrauma. Over the last two decades, we have learned a great deal about the pathophysiology of these problems, and we believe that the terminology used to describe them may now be less than accurate. We suggest that the it be adjusted to more correctly reflect the problems seen in these infants.
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PMID:Immature lung problems: can our nomenclature be more specific? 861 May 73

Bronchopulmonary dysplasia (BPD), a respiratory disorder first described in prematurely born infants with respiratory distress syndrome (RDS) treated with mechanical ventilation and oxygen supplementation, is the most common cause of chronic lung disease in infants. It is defined as the need for increased inspired oxygen at 28 days of age, and is observed with the highest frequency following premature delivery of very low birth weight infants. Indeed, an incidence of 48% has been recently reported in a population with a mean gestational age of 27 weeks. The etiology of BPD is multifactorial including lung immaturity, respiratory distress, oxygen therapy, and mechanical ventilation. Based on the current understanding of the pathogenesis of the disease, several therapeutical strategies are used. One of them is focused on the prevention of BPD by correcting surfactant deficiency in premature infants with RDS using exogenous surfactant, and also by improving the techniques of mechanical ventilation used for the management of RDS. Another approach which is being developed is focused on the factors involved in the processes of repair of the injured immature lung. These factors include the use of inhibitors of the inflammatory cascade, antioxidants, and inhibitors of fibrosis.
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PMID:[Bronchopulmonary dysplasia]. 876 16

For all 67 babies born in Greenland between January 1, 1990 and December 31, 1992 with a birthweight < 2000 g, birth certificates and clinical data were reviewed. The frequency of a birthweight of < 2000 g was 1.8%, which corresponds with Danish data. Twenty-four (35%) died. Compared with Danish babies, the stratified odds ratio for death was 5.16. There was a marked geographic variation, with the highest mortality in the less affluent remote districts. Respiratory insufficiency was the dominant cause of death, with immaturity the only other important cause. Due to lack of equipment in the smaller district hospitals, half of the babies dying from respiratory insufficiency received no other treatment than oxygen in an incubator. It is recommended that all district health centres are equipped with facilities for nasal continuous airway pressure, that the use of antibiotics is encouraged and that the introduction of surfactant replacement therapy is considered.
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PMID:Prematurity in Greenland. A study of infants with a birthweight below 2000 g. 883 71

A 480 g, 38-day-old female infant underwent ventriculo-peritoneal shunt surgery for hydrocephalus after intra-ventricular hemorrhage. The patient was born at a gestational age of 25 weeks and 5 days, weighing 600 g, as one of twins by a cesarean section. Although respiratory distress syndrome developed, it was relieved with surfactant. The esophagus was easily perforated by a gastric tube. At the age of 7 days, PDA was closed conservatively with indomethacin. Anesthesia was induced and maintained with fentanyl (induction dose 4 micrograms.kg-1, total dose 6 micrograms.kg-1) and vecuronium. Ventilation was controlled with oxygen and air (FIO2 0.21-0.25). The main problems encountered by anesthetists in the perioperative period were; fluid management (hyperkalemia, hyponatremia, infusion volume), bradycardia due to increased intracranial pressure, body temperature control (hypothermia), and transport to the operating room. In anesthesia for extremely low birth weight (extremely premature) infants, utmost care and proficient procedure are required because of their immaturity, fragility and smallness.
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PMID:[Anesthetic problems in a 480 g infant for ventriculo-peritoneal shunt surgery]. 886 31

To quantitate the developmental changes in selenium-dependent cellular glutathione peroxidase during the perinatal period, tissue sections from foetal (day 12 to day 22) and neonatal (day 6) rats were stained immunohistochemically using specific polyclonal antiserum. The intensity of the staining was quantified by fluorescence microscopy image analysis. There was a general trend of enriched glutathione peroxidase in the epithelial linings and metabolically active sites. Significant fluorescence was detected in cardiomyocytes, hepatocytes, renal tubular epithelium, bronchiolar epithelium and intestinal epithelium at day 15. The intensity increased in a stepwise manner thereafter. The overall increase in the intensity of staining in the heart, liver, kidneys, lungs and intestine was 1.5-, 2.3-, 1.6-, 1.7- and 3.0-fold, respectively. The phase of most rapid increase occurred during the foetal period in the liver, intestine and heart. In the kidneys and lungs, glutathione peroxidase increased significantly during foetal life, and to a similar extent postnatally. These results suggest that the intracellular H2O2-scavenging system develops during the foetal period as an essential mechanism for living under atmospheric oxygen conditions. The late development observed in the kidneys and lungs is consistent with the relative biological immaturity of these organs in full-term neonates.
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PMID:Immunohistochemical localization and quantitative analysis of cellular glutathione peroxidase in foetal and neonatal rat tissues: fluorescence microscopy image analysis. 886 49

Umbilical venous oxygen tension (UVPO2) and gestational age are negatively correlated antepartum. To see if the negative correlation between UVPO2 and gestational age would still be present postpartum, a retrospective study of all 7522 births at the University of Zurich Hospital from 1989 through 1992 was performed. The 6612 infants with UVPO2 values were divided into low and higher risk groups. Singletons between the 10th and 90th weight percentiles, born vaginally with cephalic presentation after spontaneous onset of labor from healthy mothers were considered low risk. All other births were considered higher risk. No correlations between UVPO2 and gestational age were found in any group studied (low risk, higher risk or total population). The higher risk group had a lower mean UVPO2 than the low risk group (p < .0001). Since there is a negative correlation before birth and none after birth, this indicates that some preterm infants may be subject to greater drops in UVPO2 during delivery than term infants. The magnitude of the drop increases with additional complications and immaturity. However, not all preterms have normal UVPO2 values for gestational age antepartum. Some preterms already have a low UVPO2 in utero and experience a drop in UVPO2 during delivery as well.
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PMID:Umbilical vein oxygen tension independent from gestational age at birth. 888 Jun 32

Noninfective acute respiratory disease develops in approximately 1% of all newborn infants and results in their admission to a critical care unit. Transient tachypnea of the newborn occurs as a result of a delay in the clearance of fetal lung liquid; however, respiratory distress syndrome, typically thought to be exclusively a problem of relative surfactant deficiency, is now suspected to be characterized by an even greater air space fluid burden from the inability to absorb fetal lung liquid. In vivo experiments have demonstrated that the lung epithelium secretes Cl and fluid throughout gestation and develops the ability to actively reabsorb Na+ only during late gestation. At birth, the mature lung switches from active Cl- (fluid) secretion to active Na+ (fluid) absorption in response to circulating catecholamines. Changes in oxygen tension augment the Na(+)-transporting capacity of the epithelium and increase gene expression for the epithelial Na+ channel (ENaC). The inability of the immature fetal lung to switch from fluid secretion to fluid absorption results, at least in large part, from an immaturity in the expression of ENaC, which can be upregulated by glucocorticosteroids. Both pharmacological blockade of the lung's epithelial Na+ channel and genetic knockout experiments using mice deficient in the ENaC pore-forming subunit have demonstrated the critical physiological importance of lung Na+ transport at birth. When Na+ transport is ineffective, newborn animals develop respiratory distress and hypoxemia, retain their fetal lung liquid and, in the case of the ENaC knockout mice, die. Bioelectrical studies of human infants' nasal epithelia demonstrate that both transient tachypnea of the newborn and respiratory distress syndrome have defective amiloride-sensitive Na+ transport. These results suggest that neonatal respiratory distress syndrome has, in addition to a relative deficiency in surfactant, defective Na+ transport, which plays a mechanistic role in the development of the disease.
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PMID:Immature epithelial Na+ channel expression is one of the pathogenetic mechanisms leading to human neonatal respiratory distress syndrome. 890 78

Our aim was to evaluate long-term effects of exogenous surfactant therapy on pulmonary functional outcome in children born very preterm. We examined 40 children aged 7-12 years who were born before 30 weeks of gestation with an immature surfactant system, and were randomized to one of three treatment groups: human surfactant given at birth (prophylactic), human surfactant given after development of neonatal respiratory distress syndrome (rescue), and placebo (air) treatment. Spirometric parameters of preterm born children were compared with those of 20 children born at term. In addition, spirometric parameters were monitored twice daily for 4 weeks using a home spirometer. All spirometric parameters were significantly lower in the preterm groups than in the controls, except for the forced vital capacity (FVC) in the prophylactically treated group. Bronchial obstruction was found in 53% of the prophylactically treated group, in 36% of the rescue group, in 67% of the placebo group, and in 0% of the control group. Peak expiratory flow (PEF) and FVC values were higher in those children who received surfactant compared with the placebo group (P < 0.05). In 16 children (40%) born preterm, a beta2-agonist induced an increase in PEF > or = 15% at least three times during 2 weeks of home monitoring; eight children (20%) had abnormal diurnal PEF variation. Multiple regression analysis indicated that the independent variables associated with favorable outcomes in spirometric parameters were surfactant therapy (P = 0.012-0.045) and short intubation time after birth (P = 0.0009-0.0044). Bronchial obstruction, responsiveness to a beta2-agonist, and high diurnal PEF variation are common in children born before 30 gestational weeks. Surfactant supplementation reducing the need for mechanical ventilation or supplementary oxygen after birth may decrease the severity of immaturity related bronchial obstruction in childhood.
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PMID:Effect of neonatal surfactant therapy on lung function at school age in children born very preterm. 955 10


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