暂无摘要。

Bronchopulmonary dysplasia (BPD) poses a significant challenge as the most common late morbidity of preterm infants. This study aimed to evaluate airway abnormalities in infants with BPD who underwent flexible bronchoscopy (FB) to gain insights into the prevalence of upper airway obstruction and associated complications. A retrospective case-control study was conducted on BPD patients who underwent FB at a tertiary center between 2013 and 2023. BPD patients were matched (1:3) with a reference group based on age, gender, and ethnicity, who also had undergone FB. Demographic data, comorbidities, indications for FB, findings, and complications during and after FB were collected. The study included 50 BPD patients (mean age 1.26 ± 0.9 years, 58% males), and 150 controls. As expected, BPD patients had a lower gestational age, lower birth weight, and longer hospitalizations and were treated with more medications. Abnormal bronchoscopy findings were significantly more common in the BPD group compared to the reference group, with an increased rate of turbinate hypertrophy (OR [95% CI]: 3.44 [1.27-9.37], P = 0.014), adenoid hypertrophy (OR: 2.7 [1.38-5.29], P = 0.004), lingual tonsils (OR: 5.44 [1.29-27.4], P = 0.0024), subglottic stenosis (OR: 6.95 [2.08-27.1], P = 0.002), and tracheomalacia (OR: 2.98 [1.06-8.19], P = 0.034). Complications including desaturation (OR: 3.89 [1.32-11.7], P = 0.013) and PICU admission (OR: 16.6 [2.58-322], P = 0.011) were more frequent in the BPD than in the reference group.
CONCLUSIONS: The study revealed a high prevalence of structural anomalies leading to upper airway obstruction and complications in infants with BPD undergoing FB. These findings emphasize the importance of careful consideration and preparation for bronchoscopic procedures in this vulnerable population.
BACKGROUND: • Bronchopulmonary dysplasia (BPD) represents the most prevalent late morbidity among preterm infants. • Preterm infants diagnosed with BPD frequently undergo diagnostic procedures, including flexible and rigid bronchoscopies, to identify structural pathologies within the respiratory tract.
BACKGROUND: • A significantly higher prevalence of structural anomalies leading to upper airway obstruction was observed in the BPD group compared to controls. • The incidence of complications during flexible bronchoscopy was higher in the BPD group than in controls.

UNASSIGNED: This meta-analysis aims to evaluate the potential link between common variations in the Surfactant Protein-B (SFTPB) gene and the risk of bronchopulmonary dysplasia (BPD) in preterm neonates.
UNASSIGNED: All pertinent articles published prior to February 1, 2024, in PubMed, Web of Science, EMBASE, CNKI, and Scopus databases were reviewed.
UNASSIGNED: Nineteen case-control studies involving 1149 BPD cases and 1845 non-BPD controls, were analyzed. Combined data indicated a significant link between SFTPB -18 A > C and Intron 4 VNTR polymorphisms with increased BPD susceptibility, while the 1580 C > T polymorphism provides a protective impact on BPD initiation.
UNASSIGNED: Pooled data indicated a significant association between SFTPB -18 A > C and Intron 4 VNTR polymorphisms with increased BPD risk, whereas the 1580 C > T polymorphism confers protection. These findings suggest a genetic susceptibility to BPD, underscoring the complex interplay of different genetic elements in its development.

Bronchopulmonary dysplasia (BPD) is a common chronic lung disease in infants and the most frequent adverse outcome of premature birth, despite major efforts to minimize injury. It is thought to result from aberrant repair response triggered by either prenatal or recurrent postnatal injury to the lungs during development. Intrauterine inflammation is an important risk factor for prenatal lung injury, which is also increasingly linked to BPD. However, the specific mechanisms remain unclear. This review summarizes clinical and animal research linking intrauterine inflammation to BPD. We assess how intrauterine inflammation affects lung alveolarization and vascular development. In addition, we discuss prenatal therapeutic strategies targeting intrauterine inflammation to prevent or treat BPD.

Survival of preterm-born infants, especially at extremes of prematurity (less than 28 weeks gestation), is now common, particularly in the developed world. Despite advances in neonatal care, short-term respiratory morbidity, termed bronchopulmonary dysplasia (also called chronic lung disease of prematurity), remains an important clinical outcome. As survival during the neonatal period has improved, preterm-born individuals are now entering childhood, adolescence and adulthood in far greater numbers, and adverse longer-term respiratory outcomes following birth at an immature stage of lung development are becoming increasingly apparent. In this article, we shall review the background of the major respiratory complications in the neonatal period, bronchopulmonary dysplasia, and the current evidence regarding its prevention and management. In addition, we shall review the emerging literature on the respiratory morbidity experienced in childhood, adolescence, and adulthood by preterm-born survivors, with reduced lung function and a risk of developing chronic obstructive pulmonary disease in early adult life. As this population of preterm-born individuals increases, an understanding of the respiratory consequences of preterm birth will become increasingly important not only for neonatologists, paediatricians and paediatric pulmonologists but also for physicians and healthcare professionals involved in the care of adults who were born preterm.

OBJECTIVE: Bronchopulmonary dysplasia (BPD), a common complication of prematurity, is associated with impaired lung function and increased morbidity in childhood. These children display heterogeneous somatic growth patterns which may ultimately impact their risk for later respiratory disease. We aim to understand the relationship between socioenvironmental exposures and growth in this population.
METHODS: A retrospective longitudinal cohort study was conducted using participants (n = 616) enrolled in the Johns Hopkins Outpatient BPD Registry. Growth measurements between 0 and 36 months of age were obtained. Somatic growth measurements, both corrected and uncorrected for gestational age, were converted to z-scores using Center for Disease Control and Prevention normative data. Using a participant\'s residential zip code, we utilized the 2019 Area Deprivation Index (ADI), the Childhood Opportunity Index (COI) 2.0, and neighborhood food insecurity data from the Maryland Food Bank. Linear regression analysis was performed employing individual socioenvironmental measures as independent variables and growth z-scores as dependent variables in univariate analysis. Univariate analysis was repeated adjusting for gestational age, BPD severity, and the presence of a gastrostomy tube (GT).
RESULTS: Of the three measures analyzed, national COI (nCOI) showed a significant association with mean weight z-scores, mean ADI showed some association with mean weight z-scores, and the percentage of a community experiencing food insecurity showed no association with mean weight z-scores. After adjusting for gestational age, BPD severity, and presence of a GT, children living in areas of greater opportunity (higher nCOI values), had significantly lower weight z-scores at 12 months corrected and at 24 and 36 months uncorrected CONCLUSIONS: Our findings suggest that the COI 2.0, a multidimensional measure, captures more facets of an individual\'s social environment, as compared to the singular nature of a measure of food insecurity. There are several potential explanations for the phenomenon seen, and further understanding of this dynamic is crucial for designing effective interventions and policies to better address inequities in outcomes.

Bronchopulmonary dysplasia (BPD) is the most common sequela of prematurity and is characterized by alveolar simplification and lung angiogenesis failure. The aim of this study was to explore the immune signatures of BPD. Differentially expressed gene analysis and immune infiltration analysis were conducted to identify key immune cell types and related genes by using the mRNA-seq dataset GSE25286. The expression patterns of key genes were validated in the scRNA-seq dataset GSE209664 and in experiments. The cell-cell crosstalk of key immune cells was explored with CellChat. We found that differentially expressed genes between BPD mice and controls were mostly enriched in leukocyte migration and M1 macrophages were highly enriched in BPD lungs. Hub genes (Cybb, Papss2, F7 and Fpr2) were validated at the single-cell level, among which the downregulation of Cybb was most closely related to macrophage infiltration. The reduced mRNA and protein levels of Cybb were further validated in animal experiments. Colocalization analysis of Cybb and macrophage markers demonstrated a significant decrease of Cybb in M1 macrophages. Cell-cell crosstalk found that alveolar epithelial cells interacted actively with macrophages through MIF-(CD74 + CD44) signalling. In conclusion, M1 macrophages played important roles in promoting BPD-like lung injury, which was correlated with a specific reduction of Cybb in macrophages and the potential activation of MIF signalling.

OBJECTIVE: The guidelines recommend early caffeine administration for preterm infants requiring non-invasive mechanical ventilation since earlier treatment is associated with better outcomes. The objective was to evaluate the impact of early caffeine therapy (within 24 hours after birth) on respiratory outcomes in very preterm infants who were initially receiving invasive mechanical ventilation.
METHODS: This was an observation cohort study from 1 January 2018 to 31 December 2022 based on a database that was prospectively collected and maintained. Infants who initially received invasive mechanical ventilation were divided into two groups based on the timing of caffeine initiation: within the first 24 hours after birth (early) and within 48 hours of birth or later (late). Generalised linear mixed models with a random effect model for the centre were used to assess the impact of different caffeine initiation times on neonatal outcomes.
RESULTS: Among the cohort of 9880 infants born at <32 weeks gestation, 2381 were eligible for this study (early initiation: 1758 (73.8%) and late initiation: 623 (26.2%)). For infants born at more than 28 weeks of gestation, the adjusted generalised linear mixed model showed that the duration of invasive mechanical ventilation was 1.34 (95% CI -2.40 to -0.27) days shorter and the incidence of moderate-to-severe bronchopulmonary dysplasia (BPD) was lower (adjusted OR 0.63; 95% CI 0.41 to 0.96) in the early caffeine group compared with the late caffeine group.
CONCLUSIONS: In very preterm infants who initially receive invasive mechanical ventilation, early administration of caffeine within 24 hours after birth can shorten the duration of invasive mechanical ventilation, reduce the incidence of moderate-to-severe BPD and improve respiratory outcomes. The very early initiation of caffeine treatment does not appear to be associated with any adverse outcomes.
BACKGROUND: ChiCTR1900025234.

Bronchopulmonary dysplasia (BPD) is a lung complication of premature births. The leading causes of BPD are oxidative stress (OS) from oxygen treatment, infection or inflammation, and mechanical ventilation. OS activates alveolar myeloid cells with subsequent myeloperoxidase (MPO)-mediated OS. Premature human neonates lack sufficient antioxidative capacity and are susceptible to OS. Unopposed OS elicits inflammation, endoplasmic reticulum (ER) stress, and cellular senescence, culminating in a BPD phenotype. Poor nutrition, patent ductus arteriosus, and infection further aggravate OS. BPD survivors frequently suffer from reactive airway disease, neurodevelopmental deficits, and inadequate exercise performance and are prone to developing early-onset chronic obstructive pulmonary disease. Rats and mice are commonly used to study BPD, as they are born at the saccular stage, comparable to human neonates at 22-36 weeks of gestation. The alveolar stage in rats and mice starts at the postnatal age of 5 days. Because of their well-established antioxidative capacities, a higher oxygen concentration (hyperoxia, HOX) is required to elicit OS lung damage in rats and mice. Neutrophil infiltration and ER stress occur shortly after HOX, while cellular senescence is seen later. Studies have shown that MPO plays a critical role in the process. A novel tripeptide, N-acetyl-lysyltyrosylcysteine amide (KYC), a reversible MPO inhibitor, attenuates BPD effectively. In contrast, the irreversible MPO inhibitor-AZD4831-failed to provide similar efficacy. Interestingly, KYC cannot offer its effectiveness without the existence of MPO. We review the mechanisms by which this anti-MPO agent attenuates BPD.

Bronchopulmonary dysplasia (BPD) remains the most common respiratory disorder of prematurity for infants born before 32 weeks of gestational age (GA). Early and prolonged exposure to chronic hypoxia and inflammation induces pulmonary hypertension (PH) with the characteristic features of a reduced number and increased muscularisation of the pulmonary arteries resulting in an increase in the pulmonary vascular resistance (PVR) and a fall in their compliance. BPD and BPD-associated pulmonary hypertension (BPD-PH) together with systemic hypertension (sHTN) are chronic cardiopulmonary disorders which result in an increased mortality and long-term problems for these infants. Previous studies have predominantly focused on the pulmonary circulation (right ventricle and its function) and developing management strategies accordingly for BPD-PH. However, recent work has drawn attention to the importance of the left-sided cardiac function and its impact on BPD in a subset of infants arising from a unique pathophysiology termed postcapillary PH. BPD infants may have a mechanistic link arising from chronic inflammation, cytokines, oxidative stress, catecholamines, and renin-angiotensin system activation along with systemic arterial stiffness, all of which contribute to the development of BPD-sHTN. The focus for the treatment of BPD-PH has been improvement of the right heart function through pulmonary vasodilators. BPD-sHTN and a subset of postcapillary PH may benefit from afterload reducing agents such as angiotensin converting enzyme inhibitors. Preterm infants with BPD-PH are at risk of later cardiac and respiratory morbidities as young adults. This paper reviews the current knowledge of the pathophysiology, diagnosis, and treatment of BPD-PH and BPD-sHTN. Current knowledge gaps and emerging new therapies will also be discussed.