• Clinical and Experimental Pediatrics
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• 제62권10호
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• pp.367-373
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• 2019

Bronchopulmonary dysplasia (BPD) is a chronic lung disease of preterm infants with multiple factors affected from prenatal to postnatal periods. Despite significant advances in neonatal care over almost 50 years, BPD rates have not decreased; in fact, they may have even increased. Since more preterm infants, even at periviable gestational age, survive today, different stages of lung development affect the pathogenesis of BPD. Hence, the definition of BPD has changed from "old" to "new." In this review, we discuss the various definitions of BPD, risk factors from the prenatal to postnatal periods, management strategies by phase, and future directions for research.

• Clinical and Experimental Pediatrics
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• 제52권1호
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• pp.6-13
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• 2009

Recent advances in perinatal care have resulted in improved survival of extremely low birth weight infants (ELBWI). However, bronchopulmonary dysplasia (BPD) remains one of the major complications in ELBWI. BPD was originally described over 40 years ago; the clinical characteristics, epidemiology, and pathogenesis of BPD have changed markedly through this period. In this article, I have reviewed recent progress in research concerning the clinical presentation and characteristics, epidemiology, and pathogenesis of BPD.

• Clinical and Experimental Pediatrics
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• 제60권7호
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• pp.203-207
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• 2017

Chorioamnionitis is an inflammation in the fetal membranes or placenta. When chorioamnionitis develops, fetal lungs are exposed to inflammatory cytokines and mediators via amniotic fluid. Because inflammation plays a pivotal role in the development of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, fetal lung inflammation induced by chorioamnionitis has been considered to be one of the major pathogenetic factors for BPD. Although there have been a number of studies that demonstrated the relationship between chorioamnionitis and BPD, there are still controversies on this issue. The controversies on the relationship between chorioamnionitis and BPD arise from not-unified definitions of chorioamnionitis and BPD, different study populations, and the proportion of contribution between inflammation and infectious microorganisms. The publication bias also contributes to the controversies. Clinical trials targeting chorioamnionitis or microorganisms that cause chorioamnionitis will answer on the actual relationship between chorioamnionitis and BPD and provide a novel prophylactic strategy against BPD based on that relationship.

• Neonatal Medicine
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• 제18권2호
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• pp.165-176
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• 2011

The pathologic hallmark of new bronchopulmonary dysplasia (BPD) is an arrest in alveolarization and vascular development. Alveoli are the fully mature gas-exchange units and alveolarization denotes the process through which the developing lung attains its fully mature structure. In human, alveolarization is mainly a postnatal event and begins in utero around 35 postmenstrual weeks and continues to 2 postnatal years. Beginning of respiration with very immature lungs as a result of preterm delivery renders the immature lung to be exposed to various injuries such as mechanical stretch, hyperoxia, infection/inflammation and leads to a disruption of normal alveolarization process, which is a main pathologic finding of BPD. Better understanding of the control mechanisms of normal alveolarization process should help us to figure out the pathophysiology of BPD and discover effective preventive or therapeutic measures for BPD. In this review, the pathologic evolution of BPD from 'old' to 'new' BPD, the detailed mechanisms of normal alveolarization, and the factors that disrupt normal alveolarization will be discussed.

• Neonatal Medicine
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• 제25권3호
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• pp.91-95
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• 2018

Bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH) is increasingly being recognized as a cause of morbidity and mortality in preterm infants. Recently, BPD-PH has also been shown to have additional long-term negative effects on neurodevelopmental outcomes and right ventricular function. Several significant risk factors associated with the development of BPD-PH have been identified. A screening strategy for BPD-PH is needed for infants presenting more than one risk factor. In addition, an early echocardiogram within 14 days of age may be a useful tool to identify infants at high-risk for BPD-PH. We have reviewed recent progress in research concerning clinical characteristics, presentation, and outcomes of BPD-PH and have suggested direction for future studies.

• Neonatal Medicine
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• 제18권2호
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• pp.177-181
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• 2011

Bronchopulmonary dysplasia (BPD) is characterized by arrest of vascular and alveolar development in premature infants. Recent advances in neonatology have increased the survival of immature babies. Consequently, the prevalence of BPD is increasing. Animal studies and autopsy findings of BPD have demonstrated interruption in vascular development and reversal of lung injury through promotion of vasculogenesis. Normal lung development is driven by temporal and spatial specific growth factors and cellto-cell signaling in vascular development. Lung injury through various pathways causes disruption in this complex interactive process and results in aberrant vascular development and subsequent BPD. By understanding the regulation of vascular growth of the lung, it would be possible to find new targets in the treatment and prevention of BPD in premature infants.

• Clinical and Experimental Pediatrics
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• 제53권6호
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• pp.688-693
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• 2010

An increase in the number of preterm infants and a decrease in the gestational age at birth have resulted in an increase in the number of patients with significant bronchopulmonary dysplasia (BPD) and secondary pulmonary hypertension (PH). PH contributes significantly to the high morbidity and mortality in the BPD patients. Therefore, regular monitoring for PH by using echocardiography and B-type natriuretic peptide (BNP) or N-terminal-proBNP must be conducted in the BPD patients with greater than moderate degree to prevent PH and to ensure early treatment if PH is present. In the BPD patients with significant PH, multi-modality treatment, including treatment for correcting an underlying disease, oxygen supply, use of diverse selective pulmonary vasodilators (inhaled nitric oxide, inhaled prostacyclins, sildenafil, and endothelin-receptor antagonist) and other methods, is mandatory.

• Tuberculosis and Respiratory Diseases
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• 제78권2호
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• pp.128-132
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• 2015

Bronchopulmonary dysplasia (BPD) is related to decreased lung function throughout life. However, the pathology and radiology pattern of BPD of adults are not documented well yet. In this case report, we present BPD case of an adult monozygotic twin showing nearly identical lesions on chest computed tomography (CT). CT images showed mixed areas of ground-glass and reticular opacities in both lungs. They had common histories of pneumonias requiring mechanical ventilations in period of infants. Pulmonary function test of one patient showed a pulmonary insufficiency with airway obstruction. Pathologic findings showed bronchiolar hyperplasia and peribronchiolar fibrosis which was similar to classic BPD patients. Our twin case report might help provide distinguishing pathology and radiology pattern of an adult pulmonary sequelaes of BPD. It might be reasonable to make close follow-up for BPD patients to evaluate the long-term outcomes of BPD survivors.

• Clinical and Experimental Pediatrics
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• 제64권1호
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• pp.37-43
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• 2021

Background: Animal studies have shown that a leukocyte influx precedes the development of bronchopulmonary dysplasia (BPD) in premature sheep. The CXC chemokine receptor 2 (CXCR2) pathway has been implicated in the pathogenesis of BPD because of the predominance of CXCR2 ligands in tracheal aspirates of preterm infants who later developed BPD. Purpose: To test the effect of CXCR2 antagonist on postnatal systemic and pulmonary inflammation and alveolarization in a newborn Sprague-Dawley rat model of BPD. Methods: Lipopolysaccharide (LPS) was injected intraperitoneally (i.p.) into the newborn rats on postnatal day 1 (P1), P3, and P5 to induce systemic inflammation and inhibit alveolarization. In the same time with LPS administration, CXCR2 antagonist (SB-265610) or vehicle was injected i.p. to investigate whether CXCR2 antagonist can alleviate the detrimental effect of LPS on alveolarization by attenuating inflammation. On P7 and P14, bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) were collected from the pups. To assess alveolarization, mean cord length and alveolar surface area were measured on 4 random nonoverlapping fields per animal in 2 distal lung sections at ×100 magnification. Results: Early postnatal LPS administration significantly increased neutrophil counts in BALF and PB and inhibited alveolarization, which was indicated by a greater mean cord length and lesser alveolar surface area. CXCR2 antagonist significantly attenuated the increase of neutrophil counts in BALF and PB and restored alveolarization as indicated by a decreased mean cord length and increased alveolar surface area in rat pups exposed to early postnatal systemic LPS. Conclusion: CXCR2 antagonist preserved alveolarization by alleviating pulmonary and systemic inflammation induced by early postnatal systemic LPS administration. These results suggest that CXCR2 antagonist can be considered a potential therapeutic agent for BPD that results from disrupted alveolarization induced by inflammation.

• Clinical and Experimental Pediatrics
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• 제58권11호
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• pp.415-420
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• 2015

Purpose: Bronchopulmonary dysplasia (BPD) is characterized by inflammation with proteolytic damage to the lung extracellular matrix. The results from previous studies are inconsistent regarding the role of proteinases and antiproteinases in the development of BPD. The aim of the present study was to investigate whether matrix metalloproteinase (MMP)-8, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-2, and TIMP-1 levels in the serum of preterm infants at birth are related to the development of BPD. Methods: Serum was collected from 62 preterm infants at birth and analyzed for MMP-8, MMP-9, TIMP-2, and TIMP-1 by using enzyme-linked immunosorbent assay. MMPs and TIMPs were compared in BPD (n=24) and no BPD groups (n=38). Clinical predictors of BPD (sex, birth weight, gestational age, etc.) were assessed for both groups. The association between predictors and outcome, BPD, was assessed by using multivariate logistic regression. Results: Sex, birth weight, and mean gestational age were similar between the groups. BPD preterm infants had significantly lower TIMP-2 levels at birth compared with no BPD preterm infants ($138.1{\pm}23.0ng/mL$ vs. $171.8{\pm}44.1ng/mL$, P=0.027). No significant difference was observed in MMP-8, MMP-9, and TIMP-1 levels between the two groups. Multivariate logistic regression analysis indicated that the TIMP-2 levels were predictive of BPD after adjusting for sex, birth weight, gestational age, proteinuric preeclampsia, and intraventricular hemorrhage (${\beta}=-0.063$, P=0.041). Conclusion: Low TIMP-2 serum levels at birth may be associated with the subsequent development of BPD in preterm infants.