The “developmental origins of health and disease” (DOHaD) hypothesis refers to the influence of early developmental exposures and fetal growth on the risk of chronic diseases in later periods. During fetal and early postnatal life, cell differentiation and tissue formation are influenced by several factors. The interaction between genes and environment in prenatal and early postnatal periods appears to be critical for the onset of multiple diseases in adulthood. Important factors influencing this interaction include genetic predisposition, regulation of gene expression, and changes in microbiota. Premature birth and intrauterine growth restriction (IUGR) are other important factors considered by the DOHaD hypothesis. Preterm birth is associated with impaired or arrested structural or functional development of key organs/systems, making preterm infants vulnerable to cardiovascular, respiratory, and chronic renal diseases during adulthood. Growth restriction, defined as impaired fetal growth compared to expected biological potential in utero, is an additional negative factor increasing the risk of subsequent diseases. Environmental factors implicated in the developmental programming of diseases include exposure to pollution, stress, drugs, toxic agents, nutrition, and exercise. The DOHaD may explain numerous conditions, including cardiovascular, metabolic, respiratory, neuropsychiatric, and renal diseases. Potential antenatal and postnatal preventive measures, interventions, and future directions are discussed.
Objective This study aimed to compare the safety and efficacy of intratracheal administration of budesonide and surfactant with surfactant alone for bronchopulmonary dysplasia (BPD) prevention in premature infants with respiratory distress syndrome.
Study Design A literature search was performed in MEDLINE, Embase, Cochrane, ClinicalTrials.gov, and gray literature. Assessment of quality was conducted using CASP tool, ROBIS tool, and GRADE framework.
Results A systematic review and meta-analysis and three observational studies were identified. Budesonide was associated with reduced incidence and severity of BPD, reduced mortality, patent ductus arteriosus, need for additional surfactant doses, hypotension, duration of invasive ventilation, hospital stays, salbutamol prescriptions, and hospitalizations in the first 2 years of life. The safety of budesonide on neurodevelopmental outcomes at 2 to 3 years of corrected age was reported.
Conclusion Budesonide might be associated with a reduction in BPD incidence and severity, without evidence of impaired neurodevelopment at 2 to 3 years of age. According to the GRADE framework, the level of evidence is low due to significant heterogeneity of studies and other bias.
Key Points
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