Respiratory Distress Syndrome and the Induction of Fetal Lung Maturity by the Use of Glucocorticoids

Jones, Mary Brewer

doi:10.1111/j.1552-6909.1977.tb00507.x

Cited by 3 publications

(1 citation statement)

References 24 publications

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“…Loss or insuffiency of HIF-2α culminate in impaired pulmonary development, decreased surfactant production, ARDS and even neonatal death [103]. Prenatal and post natal exposure to glucocorticoids (betamethasone, dexamethasone and cortisol) have been demonstrated by various studies, to be helpful for epithelial cell maturation and improved amounts of pulmonary surfactant and suppressed inflammatory response [104,105,106,107]. Other elements that retard IUG include Chest wall anomalies, diaphragmatic hernia, Oligohydroamnios, Rhesus Isoimmunization, Renal anomalies, Myotonic Dystrophy, Anecephaly, Maternal diabetes, Alcohol and Nicotine, while sex hormones and several growth factors discussed in molecular mechanisms of lung growth are also known to affect fetal and neonatal lung development [23].…”

Section: Factors Effecting Pulmonary Developmentmentioning

confidence: 99%

Molecular and Physiological Determinants of Pulmonary Developmental Biology: a Review

Hameed¹,

Sherkheli²,

Hussain³

et al. 2013

AJBR

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The lungs undergo an extensive endodermal diverging morphogenesis along with alveogenesis, angiogenesis, and vasculogenesis to secure a sufficient diffusion surface for gaseous exchange. Any aberration in the course of normal development inculcating structural and functional abnormalities of lungs in antenatal life has potential morbidity in adult life. Factors such as IUGR, nutrient deficiency, FLM, Hypoxemia, ETS, surfactant deficiency, allergy and infections can adversely affect in-utero lungs development. Peculiar local and systemic inflammatory immune responses may elicit persistent architectural and physiological abnormalities. Lung surfactant produced by AEC-II cells is a mixture of phospholipids, surfactant proteins, and neutral lipids. Surfactant lowers alveolar surface tension, a crucial step for the prevention of alveolar collapse. Surfactant proteins are part of the innate immune defense of the lung. Surfactant deficiency and dysfunction is known to implicate a number of respiratory diseases especially allergic asthma and NRDS. The present article provides a state of the art review of the current knowledge of biology of normal lung development, its anatomical and molecular aspects, factors that regulate normal organogenesis of pulmonary system and molecular basis of respiratory allergic disorders including asthma.

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Section: Factors Effecting Pulmonary Developmentmentioning

confidence: 99%

Molecular and Physiological Determinants of Pulmonary Developmental Biology: a Review

Hameed¹,

Sherkheli²,

Hussain³

et al. 2013

AJBR

View full text Add to dashboard Cite

show abstract

Factors influencing surfactant composition in the newborn infant

Obladen¹

1978

Eur J Pediatr

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In order to evaluate the surfactant maturation of the neonate, tracheal aspirates were analyzed in 84 newborn infants with 12h of birth. Using 2-dimensional thin-layer chromatography, 9 different phospholipids were identified. Dynamic surface tension measurements were performed with a modified Wilhelmy balance. Five different groups of infants with typical phospholipid patterns were characterized: i.e., 1. Normal term newborn. 2. RDS in the preterm infant. 3. Acceleration of lung maturity in preterm infants without RDS. 4. Retardation in term infants with RDS. 5. Therapeutic induction of pulmonary maturity in preterm infants following maternal glucocorticoid administration. Mature lung effluent contains high concentrations of phosphatidylcholine (PC) and phsophatidylglycerol (PG). In infants with RDS, PC is low and PG absent. Accelerated lung maturity was observed after chronic prenatal stress, such as prolonged rupture of the membranes, chronic vaginal bleeding, and maternal hepatitis or drug addiction. Retardation of pulmonary maturity was seen in infants with alpha-1-AT-deficiency, maternal diabetes and maternal hypothyroidism. Administration of methylprednisolone to the mother 24 h to 72h before birth induced both the synthesis of PC and PG in the preterm infants, resulting in an almost full-term phospholipid pattern as early as 31 weeks of gestation. The significance of these factors on the pathogenesis of RDS is discussed.

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Measurement of cortisol and other factors in cord blood: Possible use in predicting future illness and as a guide to individual preventive medicine

Levina

1980

Medical Hypotheses

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Respiratory Distress Syndrome and the Induction of Fetal Lung Maturity by the Use of Glucocorticoids

Cited by 3 publications

References 24 publications

Molecular and Physiological Determinants of Pulmonary Developmental Biology: a Review

Molecular and Physiological Determinants of Pulmonary Developmental Biology: a Review

Factors influencing surfactant composition in the newborn infant

Measurement of cortisol and other factors in cord blood: Possible use in predicting future illness and as a guide to individual preventive medicine

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