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Physiological Phenotyping of Respiratory Outcomes in Infants Born Premature

早产儿呼吸结果的生理表型

基本信息

批准号：
10383746
负责人：
Steven Herbert Abman
金额：
$ 74.85万
依托单位：
INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-03-01 至 2025-03-01
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10383746
关键词：
Adult Adult asthma Age Air Airway Disease Alveolar Area Asthma COPD Overlap Syndrome Biological Markers Blood Vessels Blood Volume Blood capillaries Bronchopulmonary Dysplasia Child Childhood Clinical Trials Design Data Development Diagnosis Diffusion Disease Disease Outcome Distal Early Intervention Echocardiography Educational workshop Environment Extremely low gestational age newborn Functional disorder Gases Gestational Age Growth Growth and Development function Impairment Incidence Infant Lung Lung diseases Measures Nature Outcome Oxygen Pattern Phenotype Physiological Premature Birth Premature Infant Proteomics Pulmonary Diffusing Capacity Pulmonary function tests Recovery Research Respiratory Disease Risk Role Secondary to Severities Signal Pathway Spirometry Structure of parenchyma of lung Surface Testing United States National Institutes of Health Vascular Diseases base clinical phenotype disease heterogeneity disorder subtype early childhood high risk improved improved functioning infancy injured airway innovation novel premature lungs pulmonary function pulmonary vascular disorder resilience respiratory respiratory morbidity specific biomarkers therapeutic target

项目摘要

With improved survival of extremely low gestational age newborns, a high incidence of bronchopulmonary dysplasia (BPD) and respiratory morbidities persist throughout childhood. Premature birth results in impaired lung alveolar and vascular growth and airways disease. The standard NIH definition of BPD, as based on the need for oxygen and respiratory support at 36 weeks gestational age, is imprecise and provides a poor surrogate for persistent respiratory problems throughout childhood. Importantly, premature infants even without the BPD diagnosis have persistent respiratory disease. Furthermore, BPD is not a homogenous respiratory disease, but represents a spectrum of airway and parenchymal abnormalities that likely contribute to different clinical phenotypes and to late respiratory morbidities after NICU discharge. However, the relative roles of small airways dysfunction and distal lung and vascular disease to late respiratory outcomes after preterm birth remain unknown. The importance of this problem has been further highlighted at recent NIH Workshops on prematurity and lung disease, which concluded that improved characterization of respiratory phenotypes after preterm birth is necessary to better understand disease heterogeneity and variability in outcomes; to accurately identify at risk infants for late disease; to improve specific therapeutic targets; and to enhance clinical trial design for early interventions. We have previously demonstrated reduced forced expiratory flows (FEF) and pulmonary diffusion capacity (DLCO) in BPD infants compared to full term controls; that decrements in FEF and DLCO are not well correlated with each other; and that each measure likely reflects different contributions to BPD pathophysiology and late respiratory morbidities. Therefore, we hypothesize that infant respiratory morbidities after preterm birth are highly variable due to differential impairment of airway, parenchymal and vascular development that can be characterized as distinct physiologic phenotypes; that the nature and severity of these specific impairments of lung function are strongly associated with increased respiratory morbidities during infancy; and that proteomic biomarkers can enhance the physiologic characterization of phenotype and prediction of late respiratory outcomes.

随着极低胎龄新生儿存活率的提高，支气管肺的发病率高