TY - JOUR
T1 - Endotypes of Prematurity and Phenotypes of Bronchopulmonary Dysplasia
T2 - Toward Personalized Neonatology
AU - Pierro, Maria
AU - Van Mechelen, Karen
AU - van Westering-Kroon, Elke
AU - Villamor-Martínez, Eduardo
AU - Villamor, Eduardo
N1 - Funding Information:
The authors would like to thank Ester Ndayarinze for her contribution to the design of the figures.
Publisher Copyright:
© 2022 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2022/4/26
Y1 - 2022/4/26
N2 - 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.
AB - 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.
KW - CHILDREN
KW - COMPUTED-TOMOGRAPHY
KW - DIAGNOSIS
KW - EXTREMELY PRETERM INFANTS
KW - HYPERTENSION
KW - INTERSTITIAL LUNG-DISEASE
KW - NITRIC-OXIDE
KW - PULMONARY VEIN STENOSIS
KW - TRACHEOBRONCHOMALACIA
KW - VASCULAR DEVELOPMENT
KW - bronchopulmonary dysplasia
KW - endotype
KW - phenotype
KW - preterm birth
U2 - 10.3390/jpm12050687
DO - 10.3390/jpm12050687
M3 - (Systematic) Review article
C2 - 35629108
SN - 2075-4426
VL - 12
JO - Journal of Personalized Medicine
JF - Journal of Personalized Medicine
IS - 5
M1 - 687
ER -