[Bronchopulmonary dysplasia].

V Zupan; D Leyronnas; M Dehan

Home/Archive/PubMed

PubMed · 1924971

[Bronchopulmonary dysplasia].

V Zupan·D Leyronnas·M Dehan

View original source ↗Export metadata ↓

Abstract

Bronchopulmonary dysplasia (BPD) is one of the most serious complications of neonatal intensive care. This chronic lung disease usually follows early pulmonary injuries. Surfactant defect, oxygen toxicity and barotrauma are three major factors leading to diffuse alveolar and bronchiolar damage, first step of BPD. BPD usually appears in preterm infants and correlates with degree of prematurity and the severity of neonatal distress syndrome. Infants with BPD frequently have poor outcome; the mortality rate is near 30%. The long-term survival prognosis is uncertain with a risk of bronchopathy in adulthood. Until date, current management of BDP is unsuccessful. New strategies are required to prevent neonatal respiratory distress syndrome and decrease its severity.

Explore related subjects

Bronchopulmonary Dysplasia Humans Infant, Newborn Prognosis Risk Factors English Abstract Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

V Zupan, D Leyronnas, M Dehan. 1991. [Bronchopulmonary dysplasia].. https://pubmed.ncbi.nlm.nih.gov/1924971/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Lung function in infants and young children with chronic lung disease of infancy: the next steps?

Over the past year, a series of papers have reviewed the literature concerning assessment and interpretation of lung function in infants and young children with chronic lung disease of infancy. This manuscript, which represents the final paper in that series, summarizes the findings to date and highlights key areas for future research. Despite the huge literature in this field, interpretation of results and their use in guiding clinical management are still limited by difficulties in 'normalizing data' according to body size and maturation and selection of appropriate control groups. Furthermore, sensitive tests that more closely reflect the underlying pathophysiology of 'new' bronchopulmonary dysplasia, together with simple and reliable methods of assessing lung maturity at birth and true oxygen requirements at specified time points are urgently required. Research in this field is also challenged by the need to separate the independent effects of genetic predisposition, gene-environment interactions, preterm delivery, neonatal respiratory disorders and various treatment strategies on the growing lung. The extent to which disruption of lung growth following premature exposure to the extra-uterine environment leads to an earlier or more aggravated decline in respiratory function in later adult life remains to be elucidated. Whatever its origin, given the increasing survival of smaller and more immature infants, the long term sequelae of neonatal lung disease, are likely to continue to change, requiring ongoing, carefully designed longitudinal studies. Future research strategies need to encompass a multicenter, multi-disciplinary, collaborative approach with closer links between clinicians and basic scientists, to ensure that the most relevant research questions are addressed using appropriate methodology and that findings are implemented into clinical practice in a more timely fashion.

Bronchopulmonary Dysplasia↗

PubMed2007

Single nucleotide polymorphisms of tumor necrosis factor-alpha and the susceptibility to bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of infancy. A "New" BPD has been characterized in preterm infants that may begin in utero, and then progress post-natally, resulting in arrested lung development and alveolar hypoplasia. Foundations for this "New" BPD may be derived from pro-inflammatory genes including tumor necrosis factor-alpha (TNFalpha). The hypothesis of the current study is that single nucleotide polymorphisms (SNPs) of the pro-inflammatory TNFalpha gene place preterm infants at increased risk for BPD. Preterm infants (105 in number) with birthweights <or=1 kg, who survived to at least 36 weeks postmenstrual age (PMA) or discharge were enrolled into this study. They were stratified for BPD according to their need for supplemental oxygen at 28 days and at 36 weeks PMA (non-, mild-, moderate-, or severe-BPD). DNA was extracted from these infants and subjected to analyses for the TNFalpha SNPs: -1,031, -863, -857, -308, and -238. The PHASE software (version 2.1) was used to reconstruct haplotypes and estimate their frequencies within the study population. Differences in birth weight (P < 0.001) and gestational age (P < 0.001), but not in racial distribution between the groups were found. Haplotype-specific analysis revealed no significant association between BPD severity and any of the 5-marker common haplotypes with 10 or more copies in this study population. Additionally, no significant association was observed in any three SNP haplotypes at -1,031, -863, and -857, and two SNP haplotypes at -308 and -238. We observed no association between BPD severity and the five TNFalpha SNPs investigated.

Bronchopulmonary Dysplasia↗

PubMed2006

Special circumstances: trophic feeds, necrotizing enterocolitis and bronchopulmonary dysplasia.

There are many unresolved issues regarding how to feed the extremely-low-birth-weight (ELBW) infant. Trophic feedings of small volumes of breast milk or formula do not appear to increase the incidence of necrotizing enterocolitis (NEC). For prevention of NEC, breast milk, antenatal steroids and fluid restriction each confers a benefit. Because the incidence of NEC is relatively low, to determine if a particular prevention strategy is effective, large numbers of infants would need to be enrolled in a prospective, randomized controlled trial, and such trials are rare. Candidate therapies for NEC prevention that warrant further study include oral immunoglobulins, probiotics, long-chain polyunsaturated fatty acids and arginine. Suboptimal nutrition in ELBW infants is common in the early postnatal period. This is also the most critical time for the development of bronchopulmonary dysplasia, when even brief periods of malnutrition have significant effects on lung development and growth.

Bronchopulmonary Dysplasia↗