ACD/MPV is a developmental disorder characterized by abnormal pulmonary vascular architecture—specifically, the misalignment of pulmonary veins and a paucity of alveolar capillaries. These anatomical deviations lead to profound pulmonary hypertension and hypoxemia immediately after birth. Historically, diagnosis relied primarily on post-mortem lung histology, severely limiting early identification and potential intervention. The study changes this paradigm by integrating advanced imaging modalities and genetic testing to enable earlier and more accurate diagnosis.

One of the study’s pivotal findings involved the elucidation of the precise histopathological mechanisms underlying ACD/MPV. The team meticulously analyzed lung biopsies from neonates with suspected disease, confirming the signature misalignment of small pulmonary veins adjacent to pulmonary arteries, a trait not found in typical pulmonary development. Additionally, they quantified the significant reduction in alveolar capillary density, which disrupts the delicate gas exchange interface essential for neonatal respiration. These histological markers now form the cornerstone of diagnostic criteria.

The genetic dimension of the study provides particularly exciting avenues for clinical translation. Using high-throughput sequencing technologies, the researchers uncovered novel pathogenic variants in FOXF1 and its enhancer regions—a gene known to regulate pulmonary vascular development during embryogenesis. The identification of these mutations, some of which had not been previously linked to ACD/MPV, offers a direct genetic hallmark that could facilitate prenatal diagnosis and genetic counseling for affected families.

Clinically, ACD/MPV presents a formidable challenge. Neonates often manifest severe, treatment-refractory pulmonary hypertension, leading to rapid decompensation. Conventional therapies, including inhaled nitric oxide and extracorporeal membrane oxygenation (ECMO), frequently fail to stabilize these infants. The study’s extensive clinical dataset highlights that early genetic screening, combined with prompt histological confirmation, could fundamentally alter management strategies. These findings emphasize the urgent need for the development of targeted therapies.

From a pathophysiological standpoint, the study provides a nuanced understanding of how misaligned pulmonary veins disrupt normal hemodynamics. Normally, pulmonary veins course independently through lung parenchyma to return oxygenated blood to the left atrium. In ACD/MPV, these veins run anomalously adjacent to the pulmonary arteries, leading to venous congestion and secondary vascular remodeling that culminates in irreversible pulmonary hypertension. Such insight is crucial for researchers designing novel interventional approaches.

The researchers also tackled the issue of disease heterogeneity. While most neonates with ACD/MPV experience fatal outcomes within the first month, a minority demonstrate a protracted clinical course. Intriguingly, the study correlates certain genetic variants with milder phenotypes, suggesting genotype–phenotype relationships that could predict prognosis. This discovery opens the door for more personalized care plans and nuanced counseling regarding life expectancy and treatment expectations.

Importantly, the collaborative effort unites pediatric pulmonologists, pathologists, geneticists, and neonatologists, representing a model for multidisciplinary approaches to rare pediatric diseases. Each center contributed vital case data that, when pooled, provided unprecedented statistical power and clinical insight. This collaborative design serves as a template for future research endeavors tackling similarly rare but lethal neonatal disorders.

On the technological frontier, the study explores the role of next-generation sequencing as a frontline diagnostic tool. Circulating fetal DNA assessment and rapid whole-exome sequencing postnatally emerged as promising diagnostic methodologies that circumvent the need for invasive lung biopsy. These minimally invasive approaches have the potential to revolutionize diagnosis, enabling clinicians to identify ACD/MPV quickly and implement supportive therapies or palliative care discussions earlier.

Furthermore, the authors discuss the implications for genetic counseling. Identification of de novo and inherited mutations in FOXF1 underscores the need to offer targeted counseling to families. Understanding mutation origin aids in recurrence risk assessment for subsequent pregnancies. Currently, genetic counseling is limited but the study’s findings pave the way for integrating molecular diagnostics into routine prenatal and postnatal care pathways.

The study also fuels hope for therapeutic innovation by illuminating developmental pathways. Given FOXF1’s critical role in lung vascular formation, future research may focus on gene therapy or molecular modulation to rectify aberrant vascular patterning. While such therapeutic strategies remain aspirational, mechanistic insights gained provide a solid foundation for translational research.

Moreover, the researchers advocate for the establishment of international registries to gather longitudinal clinical data. Long-term follow-up is needed to understand disease trajectory and outcomes in patients receiving different supportive measures. Continuous data accrual will assist in refining diagnostic thresholds and evaluating emerging therapies’ efficacy.

From an epidemiological perspective, the study estimates ACD/MPV incidence and reveals potential underdiagnosis due to lack of awareness and limited access to diagnostic resources. The authors call for heightened clinical vigilance when managing neonates with unexplained pulmonary hypertension, encouraging early genetic and histological assessment to avoid misclassification under more common diagnoses like persistent pulmonary hypertension of the newborn (PPHN).

In discussing limitations, the authors acknowledge that despite the study’s breadth, rare subtypes of ACD/MPV and overlapping pulmonary vascular disorders still present diagnostic challenges. They advocate for further multinational collaborations incorporating advanced imaging techniques such as micro-CT and MRI to capture subtle morphological variants.

Ultimately, this landmark study orchestrates a leap forward in understanding ACD/MPV’s complex biology, diagnosis, and clinical management. It stands as a testament to the power of collaborative research and multidisciplinary approaches trumping the insidious lethality of rare neonatal diseases. Neonatologists, pulmonologists, and geneticists now possess robust tools and knowledge that will save lives, transform care, and inspire novel treatments.

As the study garners international attention, the compelling data and clear clinical frameworks it offers may soon alter screening guidelines and therapeutic protocols worldwide. The dream that once seemed impossible—a timely diagnosis and effective treatment of alveolar capillary dysplasia with misalignment of pulmonary veins—is now closer than ever to becoming reality. This research embodies the relentless pursuit of innovation and compassion that defines modern pediatric medicine.

Subject of Research: Alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV) in neonates

Article Title: Alveolar capillary dysplasia with misalignment of pulmonary veins in neonates: a multicenter cohort study

Article References:
Sendi, P., Martinez, P., Kobaitri, K. et al. Alveolar capillary dysplasia with misalignment of pulmonary veins in neonates: a multicenter cohort study. Pediatr Res (2026). https://doi.org/10.1038/s41390-026-05265-0

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05265-0

Keywords: ACD/MPV, alveolar capillary dysplasia, pulmonary veins, neonatal pulmonary hypertension, FOXF1 mutations, neonatal respiratory failure, genetic diagnosis, pediatric pulmonology, pulmonary vascular development

The global incidence of CDH reveals its status as a relatively rare yet impactful birth defect. Epidemiological estimates place the incidence of this condition between approximately 1.7 and 5.7 cases per 10,000 live births, with a commonly reported prevalence figure of one in every 4,000 births. Despite its rarity, the burden on affected individuals and healthcare systems is substantial due to the complexity of respiratory support required and the long-term management of associated sequelae. Over recent decades, advances in neonatal intensive care and surgical interventions have contributed to a gradual decrease in mortality rates among infants born with CDH. However, survival is only part of the challenge, as many survivors face enduring respiratory and developmental challenges.

One of the most compelling aspects of CDH pathology is the disruption of lung development at a critical juncture—branching morphogenesis. This early phase of pulmonary formation involves the repetitive branching of epithelial tubes, establishing the vast network necessary for effective gas exchange. In CDH, this process is impeded by mechanical and biochemical alterations induced by the herniated abdominal contents occupying space within the thoracic cavity. The resultant reduction in alveolar units, the microscopic air sacs vital for oxygen and carbon dioxide exchange, compromises lung function from the outset. This structural inadequacy complicates efforts to ventilate affected neonates, who often require mechanical respiratory support.

Adding dimensional complexity is the impairment of vasculogenesis in CDH-affected lungs. Pulmonary blood vessels develop in conjunction with airways, and their abnormal formation contributes to heightened pulmonary vascular resistance. This physiological aberration lays the groundwork for pulmonary hypertension, imposing increased strain on the right heart and diminishing oxygen delivery. The confluence of hypoplastic airways and vascular abnormalities compounds the respiratory compromise experienced by these infants and challenges clinicians seeking to optimize ventilation strategies that minimize additional injury.

Mechanical ventilation, a lifesaving tool in neonatal intensive care units, presents unique challenges in infants with CDH. The immature and structurally compromised lungs are particularly vulnerable to ventilator-induced lung injury (VILI), a phenomenon where the mechanical forces applied during ventilation exacerbate lung damage and inflammation. The delicate balance between providing sufficient respiratory support and avoiding overstretching fragile lung tissues demands nuanced approaches tailored to the individual patient. VILI not only jeopardizes immediate recovery but can also precipitate chronic lung disease, extending the burden of illness into childhood and beyond.

While mortality rates in CDH have been decreasing, survivors often navigate a complex landscape of long-term respiratory morbidity. Chronic pulmonary sequelae can persist for years, and in some cases extend into adulthood, significantly impacting quality of life. These sequelae include ongoing difficulties with lung function, susceptibility to respiratory infections, and potential development of bronchopulmonary dysplasia (BPD), a chronic lung disease more commonly associated with prematurity but relevant here due to the fragile pulmonary milieu. The trajectory of lung health in CDH survivors reflects the intricate interplay of initial structural deficits, therapeutic interventions, and postnatal growth.

Beyond the respiratory system, CDH imposes multifaceted clinical challenges encompassing surgical repair, cardiovascular management, and developmental monitoring. The timing and approach to surgical intervention remain critical considerations, as premature surgery can exacerbate pulmonary hypertension, yet delayed repair prolongs compromised respiratory mechanics. Multidisciplinary teams involving neonatologists, surgeons, pulmonologists, and rehabilitation specialists are vital to optimizing outcomes. Understanding the interplay of mechanical ventilation strategies, pulmonary vascular resistance, and lung growth informs these clinical decisions and underpins ongoing research efforts.

Recent scientific inquiry has focused on advancing mechanical ventilation techniques to better accommodate the unique pathophysiology of CDH lungs. For instance, modalities that synchronize ventilator support with the patient’s own respiratory efforts show promise in reducing VILI and promoting more physiologic lung inflation. Such approaches recognize the heightened vulnerability of hypoplastic and dysplastic pulmonary tissues. The goal of minimizing additional injury while maximizing oxygen delivery is central to improving survival and decreasing long-term morbidity, highlighting the importance of individualized respiratory care in this population.

Research also delves into prenatal interventions aimed at mitigating the severity of CDH-related lung hypoplasia. Techniques such as fetal endoscopic tracheal occlusion (FETO) seek to stimulate lung growth by temporarily blocking the fetal trachea, thereby encouraging lung fluid retention and expansion. These pioneering interventions, performed in utero, represent a paradigm shift from reactive postnatal care to proactive fetal therapy. While outcomes are still being evaluated, fetal interventions offer hope of improving lung development and reducing the burden of respiratory failure post-birth.

Genetic and molecular investigations into CDH pathogenesis continue to unveil potential mechanisms underpinning diaphragmatic defects and associated pulmonary anomalies. Mutations affecting muscle development, extracellular matrix composition, and signaling pathways that regulate morphogenesis are under scrutiny. Understanding these molecular underpinnings could pave the way for targeted therapies that address root causes rather than solely managing clinical manifestations. Such discoveries hold promise for transforming the prognosis of affected infants through earlier diagnosis and molecularly guided treatments.

Despite advances in survival and technology, the landscape of CDH management remains fraught with uncertainty. Variability in presentation severity, response to treatment, and likelihood of complications demands robust, evidence-based guidelines that incorporate emerging data and real-world clinical experience. Registries and collaborative networks that consolidate patient data internationally are proving invaluable in refining knowledge and optimizing care protocols. The complexity of CDH exemplifies the challenges inherent in managing rare congenital diseases with multifactorial etiologies.

Furthermore, the psychosocial impact on families and patients is an integral consideration in CDH care. Navigating prolonged hospitalizations, uncertain prognoses, and potential developmental delays calls for comprehensive support systems encompassing psychological, social, and educational resources. Patient-centered care models that address quality of life and functional outcomes alongside medical management are critical in fostering holistic recovery and long-term well-being.

Looking ahead, the future of CDH treatment lies at the nexus of technological innovation, molecular medicine, and personalized care. Biotechnological advances such as regenerative medicine and bioengineered diaphragmatic patches offer tantalizing prospects for reconstructive therapies that restore diaphragm integrity and lung architecture. Concurrently, improved imaging techniques and biomarkers could enable earlier and more precise diagnosis, guiding bespoke treatment plans that reflect individual disease biology and progression patterns.

Ultimately, CDH stands as a poignant illustration of how congenital defects intersect with developmental biology, respiratory physiology, and clinical innovation. While substantial strides have been made in reducing mortality, the persistent challenge of minimizing chronic respiratory morbidity calls for continued investment in translational research. Interdisciplinary collaboration among scientists, clinicians, and families will be indispensable in unraveling the full spectrum of CDH and forging pathways toward improved outcomes for the most vulnerable infants.

As the global medical community advances efforts to understand and treat congenital diaphragmatic hernia, the imperative remains clear: to transform a once uniformly fatal condition into one that is not only survivable but compatible with a healthy, fulfilling life. This journey of discovery and care epitomizes the evolving nature of neonatal medicine — a marriage of cutting-edge science and compassionate clinical practice aimed at rewriting the narrative for infants born with this formidable challenge.

Subject of Research: Congenital diaphragmatic hernia (CDH) and its impact on lung development, respiratory morbidity, and mechanical ventilation challenges.

Article Title: NAVA use in infants with established bronchopulmonary dysplasia, congenital diaphragmatic hernia, and those on ECMO: a narrative literature review.

Article References:
Sanfilippo, M., Azzuqa, A., Kloesz, J. et al. NAVA use in infants with established bronchopulmonary dysplasia, congenital diaphragmatic hernia, and those on ECMO: a narrative literature review. J Perinatol (2026). https://doi.org/10.1038/s41372-026-02649-2

Image Credits: AI Generated

DOI: 17 April 2026

Congenital diaphragmatic hernia represents a complex clinical challenge, as its pathophysiology hinges not only on structural lung hypoplasia but also on pulmonary hypertension and cardiac dysfunction. Historically, the emphasis has been on lung development and ventilatory strategies, yet cardiovascular complications notably influence survival and morbidity. The research team harnessed advanced echocardiographic techniques to delineate the patterns in cardiac function that correspond to mortality and morbidities such as persistent pulmonary hypertension of the newborn and long-term neurodevelopmental impairments.

Utilizing high-resolution, prospective echocardiographic assessment, the study enrolled a cohort of infants diagnosed prenatally or shortly post-birth with CDH. Serial cardiac evaluations were meticulously performed in the immediate neonatal period, focusing on parameters such as right ventricular systolic pressure, tricuspid annular plane systolic excursion (TAPSE), and left ventricular ejection fraction. These metrics offer quantitative insights into the hemodynamic burden imposed by pulmonary vascular resistance and ventricular interdependence, both of which are pivotal in modulating clinical outcomes.

One of the most salient findings highlighted by the investigators was the prognostic significance of right ventricular function markers. Elevated right ventricular systolic pressure identified via echocardiography consistently correlated with increased incidence of extracorporeal membrane oxygenation (ECMO) requirement and mortality. This finding underscores the hypothesis that right ventricular afterload, a consequence of pulmonary hypertension, strains the cardiovascular system and underlies the cascade toward clinical deterioration in infants with CDH.

Moreover, the assessment of the interventricular septal configuration revealed critical insights into ventricular interaction. Altered septal geometry during systole and diastole suggested ventricular interdependency disruption, which clearly predicted hemodynamic instability. This mechanistic understanding advances neonatal care by pinpointing which patients are at escalated risk for cardiovascular collapse and may benefit from early pharmacological or surgical interventions targeting pulmonary vascular resistance.

Additional echocardiographic indicators, such as diminished TAPSE values, also emerged as predictors of adverse short-term outcomes. TAPSE, a measure of longitudinal right ventricular function, appeared instrumental in detecting subclinical ventricular dysfunction before overt heart failure manifestations. The use of this non-invasive parameter positions echocardiography as not only diagnostic but also prognostic, aligning with precision medicine paradigms in neonatal care.

These findings propel the role of echocardiography beyond traditional diagnostic domains into a pivotal prognostic realm. The study emphasizes the necessity of integrating comprehensive cardiac evaluation into the multidisciplinary management strategy for infants with CDH. As a result, cardiologists and neonatologists can jointly refine risk stratification models, tailor respiratory and hemodynamic support modalities, and monitor therapeutic efficacy dynamically.

Further elucidation through multivariate analysis confirmed that echocardiographic variables operated independently of conventional risk markers such as birth weight, gestational age, or lung-to-head ratio measured prenatally. This dissociation identifies cardiac function as an autonomous determinant of clinical trajectory, advocating for routine cardiac imaging as part of standardized postnatal assessments.

The implications of this study extend into shaping future clinical trials and therapeutic guidelines. Targeted therapies addressing right ventricular afterload reduction and functional support can now be more precisely timed, potentially enhancing survival rates and reducing long-term sequela in infants with CDH. Precision in patient selection for interventions like ECMO could also be refined, mitigating procedural risks and optimizing resource allocation.

Notably, the authors highlighted the potential for novel echocardiographic technologies, including speckle-tracking and three-dimensional imaging, to further enhance the characterization of cardiac mechanics in CDH. Such advanced modalities could augment the predictive accuracy and offer more nuanced insights into myocardial deformation patterns, expanding the clinical utility of bedside cardiac ultrasound.

Despite the promise, the authors caution that echocardiographic assessments require expertise and standardized protocols to ensure reproducibility and accuracy. Training initiatives and consensus guidelines may be necessary to embed these evaluation strategies into routine neonatal intensive care units globally, facilitating widespread adoption and impact.

In conclusion, this pivotal research underscores echocardiographic evaluation as an indispensable frontier in newborn care for congenital diaphragmatic hernia. By illuminating cardiac functional hallmarks that presage adverse clinical outcomes, the study redefines risk assessment and therapeutic stratagems, with the ultimate goal of improving survival and quality of life for affected infants. The integration of cardiovascular insights will indubitably enrich multidisciplinary management approaches and inspire further innovation in neonatal medicine.

As clinicians and researchers digest these findings, a new paradigm is emerging—one that acknowledges the heart’s centrality in the pathogenesis and prognosis of CDH. This evolution in understanding portends a future where precision diagnostics and targeted cardiac therapeutics transform neonatal outcomes, making what was once a dire diagnosis increasingly manageable and survivable.

Subject of Research: Echocardiographic predictors of adverse outcomes in infants with congenital diaphragmatic hernia

Article Title: Echocardiographic predictors of adverse outcomes in infants with congenital diaphragmatic hernia

Article References:
Ting, J.Y., Sehgal, A., Kuan, M.T.Y. et al. Echocardiographic predictors of adverse outcomes in infants with congenital diaphragmatic hernia. J Perinatol (2026). https://doi.org/10.1038/s41372-026-02670-5

Image Credits: AI Generated

DOI: 14 April 2026

Chronic pulmonary hypertension presents a formidable challenge in neonatal medicine, particularly among ELGANs, who are predisposed to multiple cardiopulmonary complications due to their underdeveloped lungs and cardiovascular systems. Current diagnostic standards for cPH rely heavily on echocardiographic assessments, which, while invaluable, can sometimes prove insufficiently sensitive or specific in this delicate cohort. The need for reliable, non-invasive biomarkers to aid early and accurate diagnosis has never been more urgent.

NT pro-BNP, a cardiac neurohormone released in response to ventricular stretch and pressure overload, has garnered considerable attention as a biomarker for various cardiovascular conditions in adults and older children. However, its role and diagnostic accuracy in ELGANs with suspected chronic pulmonary hypertension have remained underexplored until now. This retrospective cohort study spearheaded by Garcia-Gozalo and colleagues represents a critical step toward bridging this knowledge gap.

The research methodology involved a comprehensive review of medical records from a cohort of ELGANs, meticulously identifying those diagnosed with cPH based on standardized echocardiographic criteria. Plasma levels of NT pro-BNP were measured and analyzed in conjunction with clinical data, including gestational age, birth weight, respiratory support requirements, and comorbidities. Statistical models were employed to evaluate the sensitivity, specificity, and predictive values of NT pro-BNP levels for the diagnosis of chronic pulmonary hypertension.

One of the study’s pivotal findings is the establishment of a threshold NT pro-BNP level that optimally discriminates between ELGANs with and without cPH. This biomarker threshold demonstrated robust sensitivity and specificity, outperforming some existing diagnostic modalities. Notably, elevated NT pro-BNP levels correlated strongly with the severity of pulmonary hypertension and adverse clinical outcomes, hinting at its potential utility not merely as a diagnostic but also as a prognostic tool.

The implications of these findings are profound. Integrating NT pro-BNP measurement into routine screening protocols for ELGANs could facilitate earlier detection of cPH, allowing for prompt initiation of targeted therapies and closer monitoring. Such advances may reduce the incidence of complications associated with delayed diagnosis, including right ventricular dysfunction and exacerbated respiratory failure, ultimately improving survival rates and long-term quality of life.

Moreover, the non-invasive nature of NT pro-BNP testing offers a significant advantage in the fragile neonatal population. Blood sampling for biomarker analysis is minimally invasive compared to repeated echocardiographic studies, which require skilled operators and may be limited by operator variability and patient stability. NT pro-BNP assays can provide rapid results, enabling timely clinical decision-making in dynamic neonatal intensive care settings.

Interestingly, the study also sheds light on the pathophysiological processes underpinning chronic pulmonary hypertension in ELGANs. The elevated NT pro-BNP levels reflect the heightened cardiac strain induced by persistent pulmonary vascular resistance and impaired pulmonary vasodilation. This biochemical signature echoes the structural and functional cardiac remodeling observed in echocardiographic images, underscoring the intimate link between molecular signals and macroscopic pathology.

Despite these promising outcomes, the authors prudently emphasize the need for further prospective studies encompassing larger and more diverse neonatal populations to validate their findings. The variability in NT pro-BNP assays across laboratories and potential confounding factors such as concurrent infections or renal impairment warrant cautious interpretation. Nonetheless, this study lays a solid foundation for subsequent clinical trials aimed at refining biomarker-guided management strategies for cPH in ELGANs.

From a clinical perspective, the deployment of NT pro-BNP measurement could revolutionize the multidisciplinary approach required for managing ELGANs with pulmonary hypertension. Neonatologists, cardiologists, and pulmonologists may soon collaborate more intimately, using a tangible biomarker to calibrate treatment intensity, titrate pharmacologic interventions, and assess therapeutic responses. This could foster a paradigm shift in neonatal care, balancing vigilance with precision medicine.

While the biological underpinnings of NT pro-BNP elevation are complex, involving neurohormonal activation, myocardial stress, and inflammatory mediators, their quantification offers a window into the evolving cardiopulmonary landscape within the neonatal heart. This biomarker’s predictive capabilities, combined with traditional clinical and imaging data, may pave the way for integrated diagnostic algorithms, enhancing diagnostic accuracy and enabling personalized treatment plans.

Moreover, the study highlights the broader importance of biomarker discovery in neonatology, where diagnostic challenges are often compounded by the limited clinical expressivity of disease and the high vulnerability of patients. As neonatal medicine advances, leveraging molecular insights to supplement clinical acumen stands to markedly improve neonatal outcomes and reduce chronic morbidities linked to prematurity.

In the era of precision medicine, this investigation into NT pro-BNP’s diagnostic utility embodies a crucial step toward individualized care for ELGANs. By harnessing the power of biomarkers, clinicians may better navigate the complexities of chronic pulmonary hypertension, intercepting disease progression early and tailoring interventions that align with each neonate’s unique pathophysiology.

Ultimately, the convergence of advanced diagnostics, biomarker research, and neonatal expertise offers hope for transforming the prognosis of chronic pulmonary hypertension among the smallest patients. This study not only broadens scientific understanding but also charts a potential course for enhanced clinical protocols, underscoring the promise of translational research in addressing pressing neonatal challenges.

As ongoing research continues to unravel the intricate interplay between cardiopulmonary physiology and molecular indicators, NT pro-BNP may emerge as a cornerstone of neonatal pulmonary hypertension diagnosis. Its incorporation into clinical practice could signify a momentous stride in neonatal intensive care, reducing diagnostic uncertainty and fostering proactive, evidence-based management for fragile ELGANs worldwide.

In summary, the retrospective cohort study by Garcia-Gozalo et al. heralds a new chapter in neonatal cardiopulmonary diagnostics. By demonstrating the diagnostic accuracy of NT pro-BNP for chronic pulmonary hypertension in ELGANs, it invites the medical community to reconsider existing strategies and explore biomarker-informed pathways toward better neonatal outcomes. The findings inspire optimism that, through continued research and clinical innovation, the challenges posed by cPH in premature infants can be more effectively surmounted.

Subject of Research: Evaluation of NT pro-BNP as a diagnostic biomarker for chronic pulmonary hypertension in extremely low gestational age neonates (ELGANs < 28 weeks gestation).

Article Title: Can N-terminal pro-brain natriuretic peptide accurately diagnose chronic pulmonary hypertension among extremely low gestational age neonates: A Retrospective Cohort Study.

Article References:
Garcia-Gozalo, M., Jain, A., Weisz, D.E. et al. Can N-terminal pro-brain natriuretic peptide accurately diagnose chronic pulmonary hypertension among extremely low gestational age neonates: A Retrospective Cohort Study. J Perinatol (2025). https://doi.org/10.1038/s41372-025-02462-3

Image Credits: AI Generated

DOI: 13 November 2025