REVIEW PAPER
Pathophysiological mechanisms and pharmacological methods of prevention and treatment of bronchopulmonary dysplasia in preterm infants
 
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1
Department of Neonatology and Neonatal Intensive Care Unit, Independent Public Healthcare, Puławy, Poland
2
Department of Veterinary Hygiene, Voivodship Veterinary Inspectorate, Lublin, Poland
CORRESPONDING AUTHOR
Sławomir Jan Wątroba   

Department of Neonatology and Neonatal Intensive Care Unit, Independent Public Healthcare, Puławy, Bema 1, 24-100, Puławy, Poland
 
J Pre Clin Clin Res. 2019;13(4):170–178
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Bronchopulmonary dysplasia (BPD) is a respiratory disease that is characterized by long-term respiratory failure and mainly affects premature infants with low birth weight (LBW), undergoing mechanical ventilation (MV) or requiring long-term oxygen therapy. In Europe, among newborns with birth weight <1500g, the incidence of BPD is around 15%.

Objective:
The purpose of this review was to analyze the pathophysiological mechanisms involved in the development of BPD in premature newborns and to discuss the current possibilities of pharmacological prevention and treatment of BPD.

Description of the state of knowledge:
The BPD pathogenesis is multifactorial. Lung damage is the result of barotrauma and volutrauma due to high-performance MV, actions of reactive oxygen species (ROS) and infectious agents. Currently used methods of pharmacological treatment of severe forms of BPD are mainly based on systemic steroid therapy and can not be considered completely effective and free of side effects.

Conclusions:
Despite the widespread use of proper pharmacotherapy and dynamic development of new methods of respiratory therapy, mortality in BPD is estimated at around 10% – 20%. Infants with BPD are much more exposed to respiratory infections caused by respiratory syncytial virus (RSV), which may result in the development of bronchial hyperresponsiveness and bronchial asthma. Among children with BPD there are significantly higher cognitive and behavioral deficits compared to healthy children, and cerebral palsy is also significantly more common.

ABBREVIATIONS
AA – arachidonic acid; AAP COFN – Committee on Foetus and Newborn of the American Academy of Pediatrics; ACTH – adrenocorticotropin; ADH – vasopressin, antidiuretic hormone; ASMC – airway smooth muscle cells; BPD – bronchopulmonary dysplasia; BTN – betamethasone; C AT – catalase; CC10 – Clara cell 10 kDa protein; CLD – chronic lung disease; COX – cyclooxygenase; CPAP – continuous positive airway pressure; CPS FNC – Fetus and Newborn Committee of the Canadian Pediatric Society; DEX – dexamethasone; ELBW – extremely low birth weight; ENA-78 – epithelial protein activating neutrophils; EURAIL – Europe Against Immature Lung; FC – fludrocortisone; FiO2 – oxygen concentration in the breathing mixture; FTP – fluticasone propionate; GCSs – glucocorticosteroids; GM-CSF – granulocyte and macrophage colony-stimulating factor; GPx – glutathione peroxidase; HC – hydrocortisone; HO. – hydroxyl radical; HO2. – hydroperoxide radical; IFN-γ – gamma interferon; ILs – interleukins; IRDS – respiratory distress syndrome; IUGR – intrauterine growth retardation; IVH – intraventricular haemorrhage; LBW – low birth weight; LTs – leukotrienes; MAS – meconium aspiration syndrome; MIP-1 – macrophage inflammatory protein-1; MMPs – metalloproteinases; MRI – magnetic resonance imaging; MV – mechanical ventilation; n- CPAP – continuous positive airway pressure – nasal method; NEC – necrotizing enterocolitis; O2. – superoxide anion; PD – prednisone; PDA – patent ductus arteriosus; PDGF – platelet-derived growth factor; PGs – prostaglandins; PIP– peak inspiratory pressure; PLA-2 – phospholipase A-2; PMA – postmenstrual age; PVL – periventricular leukomalacia; ROP – retinopathy of prematurity; ROS – reactive oxygen species; RSV – respiratory syncytial virus; SIP – spontaneous gastrointestinal perforation; SOD – superoxide dismutase; TG F -1β – transforming growth factor 1β; TIMP – tissue inhibitor of metalloproteinases; TNF-α – tumor necrosis factor α.
 
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