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Biomarkers for Bronchopulmonary Dysplasia in the Preterm Infant.

Rivera L, Siddaiah R, Oji-Mmuo C, Silveyra GR, Silveyra P - Front Pediatr (2016)

Bottom Line: Over the past few decades, the incidence of BPD has significantly raised as a result of improved survival of VLBW infants requiring mechanical ventilation.Due to the current lack of effective treatment available for BPD and PH, research is currently focused on primary prevention strategies, and identification of biomarkers for early diagnosis, that could also represent potential therapeutic targets.We also present a brief summary of the information available on current strategies and guidelines to prevent and diagnose BPD and PH, as well as their pathophysiology, risk factors, and experimental therapies currently available.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, The Pennsylvania State University College of Medicine , Hershey, PA , USA.

ABSTRACT
Bronchopulmonary dysplasia (BPD) is a chronic inflammatory lung disease of very-low-birth-weight (VLBW) preterm infants, associated with arrested lung development and a need for supplemental oxygen. Over the past few decades, the incidence of BPD has significantly raised as a result of improved survival of VLBW infants requiring mechanical ventilation. While early disease detection is critical to prevent chronic lung remodeling and complications later in life, BPD is often difficult to diagnose and prevent due to the lack of good biomarkers for identification of infants at risk, and overlapping symptoms with other diseases, such as pulmonary hypertension (PH). Due to the current lack of effective treatment available for BPD and PH, research is currently focused on primary prevention strategies, and identification of biomarkers for early diagnosis, that could also represent potential therapeutic targets. In addition, novel histopathological, biochemical, and molecular factors have been identified in the lung tissue and in biological fluids of BPD and PH patients that could associate with the disease phenotype. In this review, we provide an overview of biomarkers for pediatric BPD and PH that have been identified in clinical studies using various biological fluids. We also present a brief summary of the information available on current strategies and guidelines to prevent and diagnose BPD and PH, as well as their pathophysiology, risk factors, and experimental therapies currently available.

No MeSH data available.


Related in: MedlinePlus

Pathophysiology of pulmonary hypertension (PH) secondary to bronchopulmonary dysplasia (BPD). A combination of antenatal and postnatal factors leads to the development of bronchopulmonary dysplasia (BPD). Disruption of vascular growth is caused by hypoxemia and vascular remodeling with posterior increase of vascular resistance. These changes lead to pulmonary vascular disease with increases vasoreactivity, vascular tone, and pulmonary vascular resistance. Thus, development of PH is a multifactorial consequence of BPD, which results in hemodynamic instability and long-lasting health consequences.
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Figure 2: Pathophysiology of pulmonary hypertension (PH) secondary to bronchopulmonary dysplasia (BPD). A combination of antenatal and postnatal factors leads to the development of bronchopulmonary dysplasia (BPD). Disruption of vascular growth is caused by hypoxemia and vascular remodeling with posterior increase of vascular resistance. These changes lead to pulmonary vascular disease with increases vasoreactivity, vascular tone, and pulmonary vascular resistance. Thus, development of PH is a multifactorial consequence of BPD, which results in hemodynamic instability and long-lasting health consequences.

Mentions: A complex signaling between the developing lung epithelium and the adjacent vascular endothelium results in normal development of lung vasculature. These signaling pathways involve molecules, such as VEGF and endothelial nitric oxide (eNO), which in animal models have been found to increase progressively during pulmonary vascular growth in the last half of gestation (38). Other preliminary studies have demonstrated a pharmacological inhibition of VEGF receptors that leads to attenuation of vascular growth and abnormal vasodilator capacity of pulmonary blood vessels (39, 40). This increased pulmonary vascular vasoreactivity leads to increased overall vascular resistance that is exaggerated even with minor left to right shunt of blood via patent ductus arteriosus (PDA), cardiac (patent foramen ovale, arterial receptor defect, ventricular septal defect) or intrapulmonary arteriovenous pulmonary vessels that results in a marked vasoconstrictor response and greater hemodynamic instability (Figure 2).


Biomarkers for Bronchopulmonary Dysplasia in the Preterm Infant.

Rivera L, Siddaiah R, Oji-Mmuo C, Silveyra GR, Silveyra P - Front Pediatr (2016)

Pathophysiology of pulmonary hypertension (PH) secondary to bronchopulmonary dysplasia (BPD). A combination of antenatal and postnatal factors leads to the development of bronchopulmonary dysplasia (BPD). Disruption of vascular growth is caused by hypoxemia and vascular remodeling with posterior increase of vascular resistance. These changes lead to pulmonary vascular disease with increases vasoreactivity, vascular tone, and pulmonary vascular resistance. Thus, development of PH is a multifactorial consequence of BPD, which results in hemodynamic instability and long-lasting health consequences.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4814627&req=5

Figure 2: Pathophysiology of pulmonary hypertension (PH) secondary to bronchopulmonary dysplasia (BPD). A combination of antenatal and postnatal factors leads to the development of bronchopulmonary dysplasia (BPD). Disruption of vascular growth is caused by hypoxemia and vascular remodeling with posterior increase of vascular resistance. These changes lead to pulmonary vascular disease with increases vasoreactivity, vascular tone, and pulmonary vascular resistance. Thus, development of PH is a multifactorial consequence of BPD, which results in hemodynamic instability and long-lasting health consequences.
Mentions: A complex signaling between the developing lung epithelium and the adjacent vascular endothelium results in normal development of lung vasculature. These signaling pathways involve molecules, such as VEGF and endothelial nitric oxide (eNO), which in animal models have been found to increase progressively during pulmonary vascular growth in the last half of gestation (38). Other preliminary studies have demonstrated a pharmacological inhibition of VEGF receptors that leads to attenuation of vascular growth and abnormal vasodilator capacity of pulmonary blood vessels (39, 40). This increased pulmonary vascular vasoreactivity leads to increased overall vascular resistance that is exaggerated even with minor left to right shunt of blood via patent ductus arteriosus (PDA), cardiac (patent foramen ovale, arterial receptor defect, ventricular septal defect) or intrapulmonary arteriovenous pulmonary vessels that results in a marked vasoconstrictor response and greater hemodynamic instability (Figure 2).

Bottom Line: Over the past few decades, the incidence of BPD has significantly raised as a result of improved survival of VLBW infants requiring mechanical ventilation.Due to the current lack of effective treatment available for BPD and PH, research is currently focused on primary prevention strategies, and identification of biomarkers for early diagnosis, that could also represent potential therapeutic targets.We also present a brief summary of the information available on current strategies and guidelines to prevent and diagnose BPD and PH, as well as their pathophysiology, risk factors, and experimental therapies currently available.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, The Pennsylvania State University College of Medicine , Hershey, PA , USA.

ABSTRACT
Bronchopulmonary dysplasia (BPD) is a chronic inflammatory lung disease of very-low-birth-weight (VLBW) preterm infants, associated with arrested lung development and a need for supplemental oxygen. Over the past few decades, the incidence of BPD has significantly raised as a result of improved survival of VLBW infants requiring mechanical ventilation. While early disease detection is critical to prevent chronic lung remodeling and complications later in life, BPD is often difficult to diagnose and prevent due to the lack of good biomarkers for identification of infants at risk, and overlapping symptoms with other diseases, such as pulmonary hypertension (PH). Due to the current lack of effective treatment available for BPD and PH, research is currently focused on primary prevention strategies, and identification of biomarkers for early diagnosis, that could also represent potential therapeutic targets. In addition, novel histopathological, biochemical, and molecular factors have been identified in the lung tissue and in biological fluids of BPD and PH patients that could associate with the disease phenotype. In this review, we provide an overview of biomarkers for pediatric BPD and PH that have been identified in clinical studies using various biological fluids. We also present a brief summary of the information available on current strategies and guidelines to prevent and diagnose BPD and PH, as well as their pathophysiology, risk factors, and experimental therapies currently available.

No MeSH data available.


Related in: MedlinePlus