-
American Journal of Respiratory Cell... Mar 2021
Topics: Animals; Diet; Dietary Carbohydrates; Feeding Behavior; Mice; Pulmonary Surfactants; Surface-Active Agents
PubMed: 33428544
DOI: 10.1165/rcmb.2020-0582ED -
NeoReviews Oct 2021Noninvasive ventilation is frequently used in the treatment of infants with respiratory distress syndrome. This practice is often effective in higher gestational age... (Review)
Review
Noninvasive ventilation is frequently used in the treatment of infants with respiratory distress syndrome. This practice is often effective in higher gestational age neonates, but can be difficult in those with lower gestational ages as surfactant deficiency can be severe. While noninvasive ventilation avoids the negative effects of intubation and ventilator-induced lung injury, failure of this mode of support does occur with relative frequency and is primarily caused by the poorly compliant, surfactant-deficient lung. Because of the potential problems associated with laryngoscopy and intubation, neonatologists have developed various methods to deliver surfactant in minimally invasive ways with the aim of improving the success of noninvasive ventilation. Methods of minimally invasive surfactant administration include various thin catheter techniques, aerosolization/nebulization, and the use of a laryngeal mask airway/supraglottic airway device. The clinician should recognize that currently the only US Food and Drug Administration-approved device to deliver surfactant is an endotracheal tube and all methods reviewed here are considered off-label use. This review will focus primarily on surfactant administration through laryngeal or supraglottic airways, providing a review of the history of this technique, animal and human trials, and comparison with other minimally invasive techniques. In addition, this review provides a step-by-step instruction guide on how to perform this procedure, including a multimedia tutorial to facilitate learning.
Topics: Humans; Infant, Newborn; Intubation, Intratracheal; Laryngeal Masks; Pulmonary Surfactants; Respiratory Distress Syndrome, Newborn; Surface-Active Agents; United States
PubMed: 34599065
DOI: 10.1542/neo.22-10-e673 -
Pediatric Pulmonology Feb 2023Patients with inherited pulmonary surfactant metabolism disorders have a wide range of clinical outcomes and imaging findings. Response to current anti-inflammatory... (Observational Study)
Observational Study
BACKGROUND
Patients with inherited pulmonary surfactant metabolism disorders have a wide range of clinical outcomes and imaging findings. Response to current anti-inflammatory therapies has been variable and efficacy is unclear.
OBJECTIVE
To describe and compare genetic, clinical, histological, and computed tomography (CT) outcomes in a cohort of patients with variants in the genes encoding surfactant protein C (SP-C) or adenosine triphosphate-binding cassette transporter A3 (ABCA3) in Argentina.
METHODS
Observational cohort retrospective study. Patients carrying variants in genes encoding SP-C and ABCA3 proteins were included.
RESULTS
Fourteen patients met the inclusion criteria: SFTPC n = 6, ABCA3 n = 8 (seven were heterozygous and one compound heterozygous). Neonatal respiratory distress was more frequent and severe in neonates with variants in the ABCA3 gene. The onset of the disease occurred in infancy before the age of 20 months in all cases. Patients with ABCA3 pathogenic variants had a severe clinical course, while long-term outcomes were more favorable in individuals with SFTPC variants. Initial CT findings were ground glass opacities and intraparenchymal cysts in both groups. Over time, signs of lung fibrosis were present in 57% of patients with ABCA3 variants and in 33% of the SFTPC group. The efficacy of anti-inflammatory interventions appears to be poor, especially for patients with ABCA3 pathogenic variants.
CONCLUSIONS
Clinical, histological, and radiological features are similar in patients with SFTPC and ABCA3 variants; however, the latter have more severe clinical course. Current anti-inflammatory regimens do not appear to stop the progression of the disease.
Topics: Infant, Newborn; Humans; Infant; Pulmonary Surfactants; Surface-Active Agents; Retrospective Studies; Argentina; Pulmonary Surfactant-Associated Protein C; Mutation; Disease Progression; ATP-Binding Cassette Transporters
PubMed: 36324278
DOI: 10.1002/ppul.26225 -
Pediatrics and Neonatology Mar 2023The role of prematurity and pulmonary inflammation in the pathogenesis of bronchopulmonary dysplasia (BPD) is very well-defined. However, there is limited knowledge...
BACKGROUND
The role of prematurity and pulmonary inflammation in the pathogenesis of bronchopulmonary dysplasia (BPD) is very well-defined. However, there is limited knowledge about whether the level of prematurity and surfactant therapy alter the pulmonary cytokines and endothelial growth factor (VEGF).
METHODS
This study analyzed the VEGF and cytokines, including interleukin (IL)-1β, IL-6, IL-8, and IL-10, and tumor necrosis factor α (TNF-α) in the tracheal aspirate (TA) of preterm infants obtained before (within 2 h after birth) and 10-12 h after the administration of the first dose of surfactant. TA was collected from 40 infants of 35 or fewer weeks of gestation, including extremely (Group 1, n = 19), very (Group 2, n = 13), and moderate/late (Group 2, n = 8) preterm neonates. In addition to univariate analysis, controlled regression models estimated the association of perinatal factors with the tested parameters and their role in the development of BPD.
RESULT
We recorded significantly lower post-partum levels of VEGF and higher IL-8, IL-1β, and TNF-α in the TA of Group 1 infants than in Group 2 and 3. Compared to the infants in Group 2 and 3, the post-surfactant increases of pulmonary VEGF, IL-8, IL-10, and TNF-α were more significant in Group 1. All tested parameters in Group 1 and 2 infants, before and after surfactant administration, were comparable. BPD was recorded in nearly 60% of the extremely preterm survivors and was significantly predicted by increased IL-8 before, and elevated TNF-α level after surfactant administration.
CONCLUSION
This study indicates the association of birth at extremely preterm gestation with reduction in pulmonary VEGF and exacerbation of pro-inflammatory cytokines followed by greater elevation post-surfactant administration levels of VEGF, IL-8, TNF-α, and IL-10 than in neonates born with gestational age of 28-35 weeks.
Topics: Infant; Pregnancy; Female; Infant, Newborn; Humans; Infant, Premature; Interleukin-10; Inflammation Mediators; Tumor Necrosis Factor-alpha; Surface-Active Agents; Interleukin-8; Vascular Endothelial Growth Factor A; Cytokines; Pulmonary Surfactants; Bronchopulmonary Dysplasia; Pneumonia
PubMed: 36224067
DOI: 10.1016/j.pedneo.2022.03.022 -
Journal of Perinatology : Official... Sep 2022Advances in perinatal management have led to improvements in survival rates for premature infants. It is known that the transitional period soon after birth, and the... (Review)
Review
Advances in perinatal management have led to improvements in survival rates for premature infants. It is known that the transitional period soon after birth, and the subsequent weeks, remain periods of rapid circulatory changes. Preterm infants, especially those born at the limits of viability, are susceptible to hemodynamic effects of routine respiratory care practices. In particular, the immature myocardium and cardiovascular system is developmentally vulnerable. Standard of care (but essential) respiratory interventions, administered as part of neonatal care, may negatively impact heart function and/or pulmonary or systemic hemodynamics. The available evidence regarding the hemodynamic impact of these respiratory practices is not well elucidated. Enhanced diagnostic precision and therapeutic judiciousness are warranted. In this narrative, we outline (1) the vulnerability of preterm infants to hemodynamic disturbances (2) the hemodynamic effects of common respiratory practices; including positive pressure ventilation and surfactant therapy, and (3) identify tools to assess cardiopulmonary interactions and guide management.
Topics: Hemodynamics; Humans; Infant; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Intermittent Positive-Pressure Ventilation; Pulmonary Surfactants; Respiratory Distress Syndrome, Newborn
PubMed: 35690691
DOI: 10.1038/s41372-022-01422-5 -
Clinics in Perinatology Mar 2024Pulmonary hypertension (PH) in preterm neonates has multifactorial pathogenesis with unique characteristics. Premature surfactant-deficient lungs are injured following... (Review)
Review
Pulmonary hypertension (PH) in preterm neonates has multifactorial pathogenesis with unique characteristics. Premature surfactant-deficient lungs are injured following exposure to positive pressure ventilation and high oxygen concentrations resulting in variable phenotypes of PH. The prevalence of early PH is variable and reported to be between 8% and 55% of extremely preterm infants. Disruption of the lung development and vascular signaling pathway could lead to abnormal pulmonary vascular transition. The management of early PH and the off-label use of selective pulmonary vasodilators continue to be controversial.
Topics: Infant; Infant, Newborn; Humans; Hypertension, Pulmonary; Lung; Infant, Extremely Premature; Positive-Pressure Respiration; Pulmonary Surfactants
PubMed: 38325940
DOI: 10.1016/j.clp.2023.11.005 -
Medical Hypotheses Nov 2020Pulmonary surfactant is considered to be one of the soaps. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the other enveloped viruses become very weak...
Pulmonary surfactant is considered to be one of the soaps. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the other enveloped viruses become very weak against surfactant. The SARS virus binds to angiotensin-converting enzyme (ACE2) receptor and causes pneumonia. In the lung, the ACE2 receptor sits on the top of lung cells known as alveolar epithelial type II (AE2) cells. These cells play an important role in producing surfactant. Pulmonary surfactant is believed to regulate the alveolar surface tension in mammalian lungs. To our knowledge, AE2 cells are believed to act as immunoregulatory cells; however, pulmonary surfactant itself has not been believed to act as a defender against the enveloped viruses. This study hypothesises that pulmonary surfactant may be a strong defender of enveloped viruses. Therefore, old coronaviruses merely cause pneumonia. On the contrary, new SARS-CoV-2 can suppress the production of surfactant that binds to the ACE2 of AE2 cells. The coronavirus can survive in the lung tissue because of the exhaustion of pulmonary surfactant.
Topics: Ambroxol; Angiotensin-Converting Enzyme 2; Bromhexine; COVID-19; Clinical Trials as Topic; Crystallography, X-Ray; Humans; Models, Theoretical; Phagocytosis; Pneumonia, Viral; Pregnenediones; Pulmonary Alveoli; Pulmonary Surfactants; SARS-CoV-2; Surface Tension; Surface-Active Agents; COVID-19 Drug Treatment
PubMed: 32590326
DOI: 10.1016/j.mehy.2020.110020 -
Ugeskrift For Laeger Nov 2021This review gives a summary of the development of a method to measure lung surfactant on gastric aspirate at birth in premature infants with the purpose to threat... (Review)
Review
This review gives a summary of the development of a method to measure lung surfactant on gastric aspirate at birth in premature infants with the purpose to threat respiratory distress syndrome early with targeted surfactant. Machine learning was used to create the algorithm, and a point-of-care spectrometer was constructed for use in the delivery room. The sensitivity was 91% and specificity 79% in a clinical trial. The same method was used to measure surfactant in tracheal fluid in patients with COVID-19 since lung surfactant may be diminished in these patients.
Topics: COVID-19; Humans; Infant; Infant, Newborn; Pulmonary Surfactants; Respiratory Distress Syndrome, Newborn; SARS-CoV-2; Surface-Active Agents
PubMed: 34761742
DOI: No ID Found -
Colloids and Surfaces. B, Biointerfaces Feb 2023Inhalation of harmful vaping additives has led to a series of lung illnesses. Some of the selected additives such as vitamin E acetate, and related molecules like...
Inhalation of harmful vaping additives has led to a series of lung illnesses. Some of the selected additives such as vitamin E acetate, and related molecules like vitamin E and cannabidiol, may interfere with the function of the lung surfactant. Proper lipid organization in lung surfactant is key to maintaining low surface tensions, which provides alveolar stability and effective gas exchange throughout respiration. Physiological surfactants, such as bovine lipid extract surfactant used to treat neonatal respiratory distress syndrome, serve as a good model for examining the potential effects of vape additives on proper function. We have found that all additives impede the surfactants' ability to efficiently reach high surface pressures as these systems displayed numerous shoulders throughout compression with accompanying defects to lipid organization. Moreover, the formation of lipid bilayer stacks in the film are hindered by the additives, most notably with vitamin e acetate. Loss of these stacks leave the film prone to buckling and collapse under high compression that occurs at the end of expiration. The data suggest that the additives may interfere with both proper lipid organization and the surfactant protein function.
Topics: Animals; Cattle; Pulmonary Surfactants; Surface-Active Agents; Vaping; Lung; Lipid Bilayers; Acetates
PubMed: 36630771
DOI: 10.1016/j.colsurfb.2023.113132 -
Cells Apr 2021Mucopolysaccharidosis IIIA (MPS IIIA) is a lysosomal storage disease with significant neurological and skeletal pathologies. Respiratory dysfunction is a secondary...
Mucopolysaccharidosis IIIA (MPS IIIA) is a lysosomal storage disease with significant neurological and skeletal pathologies. Respiratory dysfunction is a secondary pathology contributing to mortality in MPS IIIA patients. Pulmonary surfactant is crucial to optimal lung function and has not been investigated in MPS IIIA. We measured heparan sulphate (HS), lipids and surfactant proteins (SP) in pulmonary tissue and bronchoalveolar lavage fluid (BALF), and surfactant activity in healthy and diseased mice (20 weeks of age). Heparan sulphate, ganglioside GM3 and bis(monoacylglycero)phosphate (BMP) were increased in MPS IIIA lung tissue. There was an increase in HS and a decrease in BMP and cholesteryl esters (CE) in MPS IIIA BALF. Phospholipid composition remained unchanged, but BALF total phospholipids were reduced (49.70%) in MPS IIIA. There was a reduction in SP-A, -C and -D mRNA, SP-D protein in tissue and SP-A, -C and -D protein in BALF of MPS IIIA mice. Captive bubble surfactometry showed an increase in minimum and maximum surface tension and percent surface area compression, as well as a higher compressibility and hysteresis in MPS IIIA surfactant upon dynamic cycling. Collectively these biochemical and biophysical changes in alveolar surfactant are likely to be detrimental to lung function in MPS IIIA.
Topics: Animals; Biophysical Phenomena; Bronchoalveolar Lavage Fluid; Cholesterol; Chromatography, Liquid; G(M3) Ganglioside; Gene Expression Regulation; Heparitin Sulfate; Lysophospholipids; Mice, Inbred C57BL; Monoglycerides; Mucopolysaccharidosis III; Phospholipids; Pulmonary Alveoli; Pulmonary Surfactants; Reference Standards; Tandem Mass Spectrometry; Mice
PubMed: 33918094
DOI: 10.3390/cells10040849