Editorial - (2021) Volume 11, Issue 6
Received: 16-Jun-2021
Published:
26-Jun-2021
, DOI: 10.37421/2161-105X.2021.11.548
Citation: Pramod A. "An Editorial on Bronchopulmonary Dysplasia." J Pulm Respir Med 11 (2021): 548.
Copyright: 2021 Pramod A. This is an open-access article distributed under the terms of the creative commons attribution license which permits unrestricted
use, distribution and reproduction in any medium, provided the original author and source are credited.
Bronchopulmonary dysplasia (BPD) is a chronic lung illness that affects mostly preterm babies and is caused by a mismatch between lung injury and healing in the developing lung. BPD is the most frequent respiratory morbidity among premature babies, affecting over 10,000 new-borns in the United States each year. The prevalence of BPD has remained fairly stable over the previous two decades, but the pathophysiology has changed as a result of significant improvements in the respiratory care of extremely low birth weight (ELBW) infants. We attempted to review and summarise the current knowledge on the pathogenesis and pathophysiology of BPD in this paper. Our goal is to provide information that will aid in the prevention and treatment of severe BPD in ELBW new-borns. Improved survival of infants born at the biological limits of viability has relied on developments in perinatal care over the past 50 years in the absence of effective therapies to prevent preterm births. Except for extremely preterm infants with poor prenatal care or catastrophic prenatal events that result in severe respiratory failure at birth, the vast majority of extremely preterm infants now survive, however they frequently acquire persistent lung disease called bronchopulmonary dysplasia (BPD; also known as chronic lung disease). BPD is the most common consequence of extreme preterm delivery, despite great attempts to reduce harmful but often life-saving postnatal treatments (such as oxygen, mechanical ventilation, and corticosteroids). BPD is now understood to be the result of an abnormal reparative response to both antenatal and recurrent postnatal pulmonary damage. As a result, lung development is significantly hampered, leading to chronic airway and pulmonary vascular disease, which can impact adult lung function. More knowledge of BPD's pathobiology will lead to a better understanding of disease mechanisms as well as lung repair and regeneration, paving the way for the development of new treatment targets. Simultaneously, clinical and translational research that improves illness phenotyping and allows for early identification of at-risk preterm new-borns could improve trial design and tailored therapy to improve preterm infant outcomes.
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