Background: Neonatal respiratory distress syndrome (NRDS), if caused by a lack of pulmonary surfactant (PS), leads to progressive alveolar collapse. Glucocorticoids have anti-inflammatory and anti-allergic effects and can reduce bronchial and pulmonary edema. This research hopes to systematically evaluate the efficacy and safety of animal-derived PS combined with the glucocorticoid drug budesonide in the treatment of NRDS.
Methods: Electronic databases (i.e., Wanfang, Weipu, CNKI, PubMed, Embase, Cochrane Library) were searched from inception until May 30th, 2021. Studies relevant to the treatment of pulmonary surfactant combined with budesonide in the treatment of neonatal respiratory distress syndrome were identified. Consequently, all the studies that met the inclusion criteria were considered qualified for screening. For the meta-analysis, all data were analyzed using RevMan 5.3 software. Furthermore, subgroup analysis was performed to evaluate the administration method of budesonide (nebulized inhalation, intratracheal instillation) combined with intratracheal instillation of pulmonary surfactant.
Results: A total of 10 articles were included in this study, involving 527 children. This meta-analysis suggests that the treatment of intratracheal infusion of pulmonary surfactant combined with budesonide therapy can effectively (I) reduce the time of mechanical ventilation (OR =-1.72,95% CI: -2.44 to -1.01, P<0.00001); (II) reduce the length of stay (OR =-5.17, 95% CI: -9.35 to -0.99, P=0.02); (III) reduce the incidence of bronchopulmonary dysplasia (BPD) (OR =0.52, 95% CI: 0.39-0.68, P<0.00001); and (IV) reduce the incidence of BPD (RR =0.73, 95% CI: 0.40-1.35, P=0.32). There was no significant difference in the incidence of retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), patent ductus arteriosus (PDA), or sepsis between the experimental group and the control group.
Discussion: The treatment of animal-derived pulmonary surfactant combined with budesonide can effectively shorten the hospital stay and reduce the time of invasive mechanical ventilation and the incidence of BPD. Meanwhile, it does not increase the risk of related complications or death. This approach can be applied clinically.
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http://dx.doi.org/10.21037/tp-22-8 | DOI Listing |
AAPS PharmSciTech
January 2025
Department of Mechanical and Nuclear Engineering, Virginia Commonwealth University, Richmond, VA, United States of America.
The administration of surfactant aerosol therapy to preterm infants receiving continuous positive airway pressure (CPAP) respiratory support is highly challenging due to small flow passages, relatively high ventilation flow rates, rapid breathing and small inhalation volumes. To overcome these challenges, the objective of this study was to implement a validated computational fluid dynamics (CFD) model and develop an overlay nasal prong interface design for use with CPAP respiratory support that enables high efficiency powder aerosol delivery to the lungs of preterm infants when needed (i.e.
View Article and Find Full Text PDFGen Physiol Biophys
January 2025
Institute of Histology and Embryology, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic.
Pulmonary alveolar proteinosis (PAP) is a rare disease characterised by excessive accumulation of surfactant components in alveolar macrophages, alveoli, and peripheral airways. The accumulation of surfactant is associated with only a minimal inflammatory response but can lead to the development of pulmonary fibrosis. Three clinical forms of PAP are distinguished - primary, secondary and congenital.
View Article and Find Full Text PDFAlveolar type 2 (AT2) cells maintain lung health by acting as stem cells and producing pulmonary surfactant. AT2 dysfunction underlies many lung diseases, including interstitial lung disease (ILD), in which some inherited forms result from the mislocalization of surfactant protein C (SFTPC) variants. Lung disease modeling and dissection of the underlying mechanisms remain challenging due to complexities in deriving and maintaining human AT2 cells ex vivo.
View Article and Find Full Text PDFJ Rheumatol
January 2025
J.A. Sparks, MD, MMSc, Brigham and Women's Hospital, Division of Rheumatology, Inflammation, and Immunity and Harvard Medical School, Boston, Massachusetts, USA.
Objective: To investigate baseline and change of pulmonary damage biomarkers (serum Krebs von den Lungen 6 [KL-6], human surfactant protein D [hSP-D], and matrix metalloproteinase 7 [MMP-7]) with rheumatoid arthritis-associated interstitial lung disease (RA-ILD) progression.
Methods: In the Korean Rheumatoid Arthritis Interstitial Lung Disease (KORAIL) cohort, a prospective cohort, we enrolled patients with RA and ILD confirmed by chest computed tomography imaging and followed annually. ILD progression was defined as worsening in physiological and radiological domains of the 2022 American Thoracic Society, European Respiratory Society, Japanese Respiratory Society, and Latin American Thoracic Society guideline for progressive pulmonary fibrosis (PPF).
Phytomedicine
December 2024
Univ Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Azinhaga de S. Comba, Coimbra 3000-548, Portugal; Univ Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), Coimbra, Portugal; Clinical Academic Centre of Coimbra (CACC), Coimbra, Portugal.
Background: Pulmonary Arterial Hypertension (PAH) is characterized by pulmonary vascular remodelling, often associated with disruption of BMPR2/Smad1/5 and BMPR2/PPAR-γ signalling pathways that ultimately lead to right ventricle failure. Disruption of intercellular junctions and communication and a pro-angiogenic environment are also characteristic features of PAH. Although, current therapies improve pulmonary vascular tone, they fail to tackle other key pathological features that could prevent disease progression.
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