Recent advancements in biomarker identification and machine learning have significantly enhanced the prediction and diagnosis of Bronchopulmonary Dysplasia (BPD) and neonatal respiratory distress syndrome (nRDS) in preterm infants. Key predictors of BPD severity include elevated cytokines like Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α), as well as inflammatory markers such as the Neutrophil-to-Lymphocyte Ratio (NLR) and soluble gp130. Research into endoplasmic reticulum stress-related genes, differentially expressed genes, and ferroptosis-related genes provides valuable insights into BPD's pathophysiology. Machine learning models like XGBoost and Random Forest have identified important biomarkers, including CYYR1, GALNT14, and OLAH, improving diagnostic accuracy. Additionally, a five-gene transcriptomic signature shows promise for early identification of at-risk neonates, underscoring the significance of immune response factors in BPD. For nRDS, biomarkers such as the lecithin/sphingomyelin (L/S) ratio and oxidative stress indicators have been effectively used in innovative diagnostic methods, including attenuated total reflectance Fourier transform infrared spectroscopy (ATR-FTIR) and high-content screening for ABCA3 modulation. Machine learning algorithms like Partial Least Squares Regression (PLSR) and C5.0 have shown potential in accurately identifying critical health indicators. Furthermore, advanced feature extraction methods for analyzing neonatal cry signals offer a non-invasive means to differentiate between conditions like sepsis and nRDS. Overall, these findings emphasize the importance of combining biomarker analysis with advanced computational techniques to improve clinical decision-making and intervention strategies for managing BPD and nRDS in vulnerable preterm infants.

Neonatal respiratory distress syndrome (NRDS) is one of the most common diseases in neonatal intensive care units, with an incidence rate of about 7% among infants. Additionally, it is a leading cause of neonatal death in hospitals in China. The main mechanism of the disease is hypoxemia and hypercapnia caused by lack of surfactant.

To explore the effect of pulmonary surfactant (PS) combined with noninvasive positive pressure ventilation on keratin-14 (KRT-14) and endothelin-1 (ET-1) levels in peripheral blood and the effectiveness in treating NRDS.

Altogether 137 neonates with respiratory distress syndrome treated in our hospital from April 2019 to July 2021 were included. Of these, 64 control cases were treated with noninvasive positive pressure ventilation and 73 observation cases were treated with PS combined with noninvasive positive pressure ventilation. The expression of KRT-14 and ET-1 in the two groups was compared. The deaths, complications, and PaO2, PaCO2, and PaO2/FiO2 blood gas indexes in the two groups were compared. Receiver operating characteristic curve (ROC) analysis was used to determine the diagnostic value of KRT-14 and ET-1 in the treatment of NRDS.

The observation group had a significantly higher effectiveness rate than the control group. There was no significant difference between the two groups in terms of neonatal mortality and adverse reactions, such as bronchial dysplasia, cyanosis, and shortness of breath. After treatment, the levels of PaO2 and PaO2/FiO2 in both groups were significantly higher than before treatment, while the level of PaCO2 was significantly lower. After treatment, the observation group had significantly higher levels of PaO2 and PaO2/FiO2 than the control group, while PaCO2 was notably lower in the observation group. After treatment, the KRT-14 and ET-1 levels in both groups were significantly decreased compared with the pre-treatment levels. The observation group had a reduction of KRT-14 and ET-1 levels than the control group. ROC curve analysis showed that the area under the curve (AUC) of KRT-14 was 0.791, and the AUC of ET-1 was 0.816.

Combining PS with noninvasive positive pressure ventilation significantly improved the effectiveness of NRDS therapy. KRT-14 and ET-1 levels may have potential as therapeutic and diagnostic indicators.

Bronchopulmonary disease (BPD) is associated with long-term neurodevelopmental and cardiorespiratory complications, often requiring significant use of resources. To reduce this healthcare burden, it is essential that those at high risk of BPD are identified early so that strategies are introduced to prevent disease progression. Our aim was to discuss potential methods for improving early diagnosis in the first week after birth.

A narrative review was undertaken. The search strategy involved searching PubMed, Embase and Cochrane databases from 1967 to 2024. The results of potential biomarkers and imaging modes are discussed. Furthermore, the value of scoring systems is explored.

BPD occurs as a result of disruption to pulmonary vascular and alveolar development, thus abnormal levels of factors regulating those processes are promising avenues to explore with regard to early detection of high-risk infants. Data from twin studies suggests genetic factors can be attributed to 82% of the observed difference in moderate to severe BPD, but large genome-wide studies have yielded conflicting results. Comparative studies are required to determine which biomarker or imaging mode may most accurately diagnose early BPD development. Models which include the most predictive factors should be evaluated going forward.

The role of systemic inflammatory indices in the diagnosis of bronchopulmonary dysplasia (BPD) is unknown. The aim of the study was to determine the possible clinical utility of systemic inflammatory indices in the prediction of moderate to severe BPD.

Premature infants<32 weeks of gestational age were included in the study. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), pan-immune-inflammation value (PIV), and systemic inflammation response index (SIRI) were calculated at birth and at the time of diagnosis of BPD (at 36th weeks of postmenstrual age). The patients were divided into two groups as no or mild BPD and moderate or severe BPD.

A total of 1146 infants were included in the study, 957 in Group 1 and 189 in Group 2. The SIRI value was significantly higher in moderate or severe BPD both at birth and at the 36th week of postmenstrual age (p<0.001 and p<0.001, respectively). The AUC value of SIRI was 0.809 and the cut-off value was>0.98 in the predictivity of BPD at birth. The AUC value of SIRI was 0.842 and the cut-off value was>1.33 for the diagnosis of BPD at 36th week of postmenstrual age. After multiple logistic regression analysis, SIRI was shown to be a significant parameter for the diagnosis of BPD (OR 2.847, 95% CI 1.557-4.875).

SIRI may be a useful biomarker for predicting moderate to severe BPD and a marker of clinical importance in the follow-up of infants with BPD.

Bronchopulmonary dysplasia (BPD) is a major complication in preterm infants <32 weeks. We aimed to assess whether plasma levels of mid-regional pro-atrial natriuretic peptide (MR-proANP) and C-terminal pro-endothelin-1 (CT-proET-1) predict respiratory morbidity.

This was a prospective, two-center, observational cohort study. MR-proANP and CT-proET-1 were measured at day 7 (±2) of life. Associations with duration of supplemental oxygen and the composite outcome of moderate or severe BPD or death (BPD/death) were investigated.

Two hundred and twenty-nine infants <32 weeks were included (median gestational age [GA] 29.6 weeks [interquartile range 29.0-30.7], median birth weight 1150 g [IQR 840-1410]). MR-proANP and CT-proET-1 were associated with the duration of supplemental oxygen in univariable analysis (both p < 0.001) but not after adjusting for co-factors. Infants with BPD/death showed higher plasma levels of MR-proANP (623.50 pmol/L [IQR 458.50-881.38] vs. 308.35 pmol/L [IQR 216.72-538.10]; p < 0.001) and CT-proET-1 (255.40 pmol/L [IQR 202.60-311.15] vs. 198.30 pmol/L [IQR 154.70-297.95]; p = 0.015) compared to infants without BPD/death. Levels of both biomarkers were significantly associated with BPD/death in univariable models but not after adjusting for co-factors.

MR-proANP and CT-proET-1 are associated with the duration of supplemental oxygen and the composite outcome BPD/death, but their prognostic value does not complement that of clinical risk factors.

Plasma levels of MR-proANP and CT-proET-1, measured on day 7 of life (±2 days) are associated in univariable analyses with duration of supplemental oxygen and the combined outcome of BPD or death in VLGA infants. Associations between both biomarkers and respiratory morbidity do not persist in multivariable models, in particular when gestational age is included. MR-proANP and CT-proET-1 have limited additional value to predict respiratory morbidity in VLGA infants compared to clinical parameters.

This study is aimed at exploring the effect of pulmonary surfactant (PS) combined with noninvasive positive pressure ventilation on the levels of Keratin-14 (KRT-14) and Endothelin-1 (ET-1) in peripheral blood and the therapeutic effect of neonatal respiratory distress syndrome (NRDS). Altogether 137 cases of neonates with respiratory distress syndrome treated in our hospital from April 2016 to July 2018 were collected. Among them, 64 cases treated with noninvasive positive pressure ventilation were considered as the control group, and 73 cases treated with PS combined with noninvasive positive pressure ventilation were considered as the observation group. The expression of KRT-14 and ET-1 in the two groups was compared. The therapeutic effect, death, complications, and blood gas indexes PaO2, PaCO2, and PaO2/FiO2 in the two groups were compared. Receiver operating characteristic curve (ROC) was applied to analyze the diagnostic value of KRT-14 and ET-1 in the therapeutic effect of NRDS. The effective rate of the observation group was higher than that of the control group. After treatment, PaO2 and PaO2/FiO2 in both groups were notably higher than that before treatment, while PaCO2 was notably lower than that before treatment. And after treatment, the levels of PaO2 and PaO2/FiO2 in the observation group were remarkably higher than that in the control group; PaCO2 was notably lower than that in the control group. After treatment, the levels of KRT-14 and ET-1 in the two groups were remarkably lower than those before treatment, and the levels of KRT-14 and ET-1 in the observation group were considerably lower than those in the control group after treatment. ROC curve showed that the area under the curve (AUC) of KRT-14 was 0.791, and the AUC of ET-1 was 0.816. PS combined with noninvasive positive pressure ventilation can notably improve the therapeutic effect of NRDS. KRT-14 and ET-1 levels may be potential therapeutic diagnostic indicators.

Bronchopulmonary Dysplasia (BPD) is a pulmonary disease affecting newborns, commonly those with prematurity or low birth weight. Its pathogenesis involves underdevelopment of lung tissue with subsequent limitations in ventilation and oxygenation, resulting in impaired postnatal alveolarization. Despite advances in care with improved survival, BPD remains a prevalent comorbidity of prematurity. In severe cases, management may involve mechanical ventilation via tracheostomy. BPD's demand for multidisciplinary care compounds the challenges in management of this condition. Here, we review existing literature: the history of disease, criteria for diagnosis, pathogenesis, and modes of treatment with a focus on the severe subtype: that which is associated with pulmonary hypertension (PAH) for which tracheostomy is often required to facilitate long-term mechanical ventilation. We review the current recommendations for tracheostomy and decannulation.

Bronchopulmonary dysplasia (BPD), which remains a major clinical problem for preterm infants, is caused mainly by hyperoxia, mechanical ventilation and inflammation. Many approaches have been developed with the aim of decreasing the incidence of or alleviating BPD, but effective methods are still lacking. Gasotransmitters, a type of small gas molecule that can be generated endogenously, exert a protective effect against BPD-associated lung injury; nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H₂S) are three such gasotransmitters. The protective effects of NO have been extensively studied in animal models of BPD, but the results of these studies are inconsistent with those of clinical trials. NO inhalation seems to have no effect on BPD, although side effects have been reported. NO inhalation is not recommended for BPD treatment in preterm infants, except those with severe pulmonary hypertension. Both CO and H₂S decreased lung injury in BPD rodent models in preclinical studies. Another small gas molecule, hydrogen, exerts a protective effect against BPD. The nuclear factor erythroid-derived 2 (Nrf2)/heme oxygenase-1 (HO-1) axis seems to play a central role in the protective effect of these gasotransmitters on BPD. Gasotransmitters play important roles in mammals, but further clinical trials are needed to explore their effects on BPD.