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Endotypes of Prematurity and Phenotypes of Bronchopulmonary Dysplasia: Toward Personalized Neonatology
Maria Pierro1, Karen Van Mechelen2, Elke van Westering-Kroon2
1Neonatal and Paediatric Intensive Care Unit, M. Bufalini Hospital, AUSL Romagna, 47521 Cesena, Italy.
Insights
Bronchopulmonary dysplasia (BPD) arises from lung injury during development. Identifying distinct causes (endotypes) and BPD types (phenotypes) aids personalized treatment for premature infants.
Area of Science:
- Neonatology
- Pediatric Pulmonology
- Developmental Biology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants.
- It results from abnormal lung repair following antenatal and postnatal injuries.
- BPD pathogenesis is multifactorial and heterogeneous, involving various insults to developing lung structures.
Purpose of the Study:
- To explore the concept of endotyping prematurity and phenotyping BPD.
- To identify distinct pathways contributing to preterm birth and subsequent BPD.
- To align BPD classification with personalized medicine approaches.
Main Methods:
- Review of clinical, placental, and bacteriological data.
- Identification of two primary pathways leading to preterm birth before 32 weeks gestation: infection/inflammation and dysfunctional placentation.
- Categorization of proposed BPD phenotypes including parenchymal, airway, interstitial, congestive, vascular, and mixed.
Main Results:
- Two main pathways contributing to prematurity identified: infection/inflammation and dysfunctional placentation.
- Multiple BPD phenotypes proposed, reflecting diverse patterns of lung injury.
- Endotyping and phenotyping offer a framework for understanding BPD heterogeneity.
Conclusions:
- Understanding endotypes of prematurity and phenotypes of BPD is crucial.
- This approach supports the development of targeted therapies and prognostic strategies.
- Personalized medicine in BPD management is facilitated by endotyping and phenotyping.
Abstract:
Bronchopulmonary dysplasia (BPD), the chronic lung disease of prematurity, is increasingly recognized as the consequence of a pathological reparative response of the developing lung to both antenatal and postnatal injury. According to this view, the pathogenesis of BPD is multifactorial and heterogeneous with different patterns of antenatal stress (endotypes) that combine with varying postnatal insults and might distinctively damage the development of airways, lung parenchyma, interstitium, lymphatic system, and pulmonary vasculature. This results in different clinical phenotypes of BPD. There is no clear consensus on which are the endotypes of prematurity but the combination of clinical information with placental and bacteriological data enables the identification of two main pathways leading to birth before 32 weeks of gestation: (1) infection/inflammation and (2) dysfunctional placentation. Regarding BPD phenotypes, the following have been proposed: parenchymal, peripheral airway, central airway, interstitial, congestive, vascular, and mixed phenotype. In line with the approach of personalized medicine, endotyping prematurity and phenotyping BPD will facilitate the design of more targeted therapeutic and prognostic approaches.
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