Lung Injury and Bronchopulmonary Dysplasia in Newborn Infants

Christou, Helen; Brodsky, Dara

doi:10.1177/0885066604273494

Cited by 31 publications

(36 citation statements)

References 119 publications

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“…(a) genetic predisposition, including sex, race 27,28 and the effect of various genetic polymorphisms, such as those associated with the b2 adrenoceptor, Angiotensin Converting Enzyme (ACE) and glutathione S transferase alleles, [29][30][31][32] (b) preterm delivery per se, [33][34][35] (c) neonatal respiratory disorders and the various treatment strategies on the growing and differentiating lung, [1][2][3][4]27,[36][37][38][39][40] and (d) interactions between neonatal lung disease and the environment (including exposure to tobacco smoke, allergens and infections). 15,41 This in turn requires international consensus on which essential details should be recorded for infants recruited to such studies.…”

Section: The Next Steps?mentioning

confidence: 99%

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

Stocks

Coates

Bush

2006

Pediatric Pulmonology

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Summary. 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, multidisciplinary, 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. Pediatr Pulmonol.

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Section: The Next Steps?mentioning

confidence: 99%

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

Stocks

Coates

Bush

2006

Pediatric Pulmonology

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“…Preterm infants with severe bronchopulmonary dysplasia have reduced saccular airway and alveolar duct formation and have lower FGF-10 expression in their lungs (8,9). In adult patients, Fgf-10 haploinsufficiency can lead to abnormal pulmonary function and chronic obstructive pulmonary disease (10).…”

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confidence: 99%

Interactions between NF-κB and SP3 Connect Inflammatory Signaling with Reduced FGF-10 Expression

Carver

Plosa

Stinnett

et al. 2013

Journal of Biological Chemistry

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“…A n increase in survival of extremely preterm infants has been associated with an increased incidence of bronchopulmonary dysplasia (BPD) (1), which has become a major clinical challenge because of its serious health consequences. Surviving infants with BPD are at higher risk for recurrent respiratory infections, bronchial hyperreactivity, repeated hospitalizations, and neurodevelopmental abnormalities (1,2).…”

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confidence: 99%

Genetic Risk Factors of Bronchopulmonary Dysplasia

et al. 2008

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ABSTRACT:The aim of the study was to assess the association between bronchopulmonary dysplasia (BPD) and polymorphisms of genes coding for vascular endothelial growth factor (VEGF), transforming growth factor (TGF-␤1), insulin-like growth factor (IGF-1), and 5,10-methylenetetrahydrofolate reductase (MTHFR). A sample of 181 newborns with mean gestational age of 28 wk was prospectively evaluated. Molecular analysis of TGF-␤1 Ϫ800GϾA, Ϫ509CϾT, 10TϾC, 25GϾC, VEGF Ϫ460TϾC and 405GϾC and MTHFR 677CϾT polymorphisms were performed and the number of CA repeats in the promoter region of IGF-1 gene was assessed. The frequency of all TGF-␤1, IGF-1, and MTHFR polymorphisms, as well as the frequency of VEGF 405GϾC polymorphism was similar in all groups. The newborns with Ϫ460TT and Ϫ460CT genotypes were significantly overrepresented in the BPD groups compared with the no BPD group. Multivariate analysis revealed that carrying T allele increased the risk of BPD by 9% (95%CI: 2-14%) above the baseline risk established for given gestational age, length of oxygen therapy, and sex. Based on our data from a single center, we propose that VEGF Ϫ460TϾC polymorphism may influence the risk of BPD. A n increase in survival of extremely preterm infants has been associated with an increased incidence of bronchopulmonary dysplasia (BPD) (1), which has become a major clinical challenge because of its serious health consequences. Surviving infants with BPD are at higher risk for recurrent respiratory infections, bronchial hyperreactivity, repeated hospitalizations, and neurodevelopmental abnormalities (1,2).The current consensus is that BPD is a complex disease: the interaction of a susceptible host with a multitude of external risk factors underlies its pathogenesis. It is still unclear why BPD progresses to severe disease in one group of very low birth weight (VLBW) infants but regresses spontaneously in other infants with similar clinical characteristics. This difference in BPD development may result from differences in reactions to inflammatory stimuli and varied ability to tolerate oxidative stress and inflammation. Genetic foundations for the development of BPD are implicated in twin studies, which reveal highly significant concordance rates for BPD: 3.69-fold in monozygotic and 1.4-fold in dizygotic twins (3).The criteria for selection of BPD candidate genes in the present study were their potential involvement in angiogenesis and alveolarization regulating mechanisms, as well as their involvement in free radical elimination.The first factor worth examining is vascular endothelial growth factor (VEGF). VEGF is a relatively specific endothelial cell mitogen that regulates endothelial cell differentiation and angiogenesis, and plays a central role in vascular repair. VEGF has multiple roles in vascular development and maintenance and is essential for the formation of embryonic vasculature (4,5). The absence of VEGF results in impaired fetal lung microvascular development. The VEGF gene is also a good candidate because there are a consid...

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Lung Injury and Bronchopulmonary Dysplasia in Newborn Infants

Cited by 31 publications

References 119 publications

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

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

Interactions between NF-κB and SP3 Connect Inflammatory Signaling with Reduced FGF-10 Expression

Genetic Risk Factors of Bronchopulmonary Dysplasia

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