OBJECTIVE: Bronchopulmonary dysplasia (BPD) or chronic lung disease is one of the principal causes of mortality and morbidity in preterm infants. Early identification of infants at the greater risk of developing BPD may allow a targeted approach for reducing disease severity and complications. The trigger cause of the disease comprehends the impairment of the alveolar development and the increased angiogenesis. Nevertheless, the molecular pathways characterizing the disease are still unclear. Therefore, the use of the metabolomics technique, due to the capability of identifying instantaneous metabolic perturbation, might help to recognize metabolic patterns associated with the condition. METHODS: The purpose of this study is to compare urinary metabolomics at birth in 36 newborns with a gestational age below 29 weeks and birth weight <1500 g (very low birth weight - VLBW), admitted in Neonatal Intensive Care Unit (NICU) divided into two groups: the first group (18 cases) consisting of newborns who have not yet developed the disease, but who will subsequently develop it and the second group (18 controls) consisting of newborns not affected by BPD. Urine samples were collected within 24-36 h of life and immediately frozen at -80 °C. RESULTS: The (1)H-NMR spectra were analyzed using a partial least squares discriminant analysis (PLS-DA) model coupled with orthogonal Signal Correction. Using this approach it was possible with urine at birth to discriminate newborns that will be later have a diagnosis of BPD with a high statistics power. In particular, we found five important discriminant metabolites in urine in BPD newborns: lactate, taurine, TMAO, myoinositol (which increased) and gluconate (which decreased). CONCLUSION: These preliminary results seem to be promising for the identification of predictor's biomarkers characterizing the BPD condition. These data may suggest that BPD is probably the result of an abnormal development (respiratory bud, vascular tree, hypodysplasia of pneumocytes) and could be considered a congenital disease (genetics plus intrauterine epigenetics). Early identification of infants at the greater risk of developing BPD may allow a targeted approach for reducing disease severity and complications.
OBJECTIVE:Bronchopulmonary dysplasia (BPD) or chronic lung disease is one of the principal causes of mortality and morbidity in preterm infants. Early identification of infants at the greater risk of developing BPD may allow a targeted approach for reducing disease severity and complications. The trigger cause of the disease comprehends the impairment of the alveolar development and the increased angiogenesis. Nevertheless, the molecular pathways characterizing the disease are still unclear. Therefore, the use of the metabolomics technique, due to the capability of identifying instantaneous metabolic perturbation, might help to recognize metabolic patterns associated with the condition. METHODS: The purpose of this study is to compare urinary metabolomics at birth in 36 newborns with a gestational age below 29 weeks and birth weight <1500 g (very low birth weight - VLBW), admitted in Neonatal Intensive Care Unit (NICU) divided into two groups: the first group (18 cases) consisting of newborns who have not yet developed the disease, but who will subsequently develop it and the second group (18 controls) consisting of newborns not affected by BPD. Urine samples were collected within 24-36 h of life and immediately frozen at -80 °C. RESULTS: The (1)H-NMR spectra were analyzed using a partial least squares discriminant analysis (PLS-DA) model coupled with orthogonal Signal Correction. Using this approach it was possible with urine at birth to discriminate newborns that will be later have a diagnosis of BPD with a high statistics power. In particular, we found five important discriminant metabolites in urine in BPD newborns: lactate, taurine, TMAO, myoinositol (which increased) and gluconate (which decreased). CONCLUSION: These preliminary results seem to be promising for the identification of predictor's biomarkers characterizing the BPD condition. These data may suggest that BPD is probably the result of an abnormal development (respiratory bud, vascular tree, hypodysplasia of pneumocytes) and could be considered a congenital disease (genetics plus intrauterine epigenetics). Early identification of infants at the greater risk of developing BPD may allow a targeted approach for reducing disease severity and complications.
Authors: Antonio Noto; Giulia Pomero; Michele Mussap; Luigi Barberini; Claudia Fattuoni; Francesco Palmas; Cristina Dalmazzo; Antonio Delogu; Angelica Dessì; Vassilios Fanos; Paolo Gancia Journal: Ann Transl Med Date: 2016-11
Authors: Roberta L Keller; Rui Feng; Sara B DeMauro; Thomas Ferkol; William Hardie; Elizabeth E Rogers; Timothy P Stevens; Judith A Voynow; Scarlett L Bellamy; Pamela A Shaw; Paul E Moore Journal: J Pediatr Date: 2017-05-17 Impact factor: 4.406
Authors: Michael R La Frano; Johannes F Fahrmann; Dmitry Grapov; Theresa L Pedersen; John W Newman; Oliver Fiehn; Mark A Underwood; Karen Mestan; Robin H Steinhorn; Stephen Wedgwood Journal: Am J Physiol Lung Cell Mol Physiol Date: 2018-08-16 Impact factor: 5.464
Authors: María Álvarez-Fuente; Laura Moreno; Jane A Mitchell; Irwin K Reiss; Paloma Lopez; Dolores Elorza; Liesbeth Duijts; Alejandro Avila-Alvarez; Luis Arruza; Manuel Ramirez Orellana; Eugenio Baraldi; Patrizia Zaramella; Santiago Rueda; Álvaro Gimeno-Díaz de Atauri; Hercília Guimarães; Gustavo Rocha; Elisa Proença; Bernard Thébaud; Maria Jesús Del Cerro Journal: Pediatr Res Date: 2018-11-21 Impact factor: 3.756