Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this review I have emphasized the complicated events that occur during the course of RDS. RDS is initiated by an inadequate pool size of functional surfactant within a structurally and functionally immature lung. Obstetric and delivery room management apparently can significantly influence surfactant function and, therefore, the incidence of RDS, possibly by affecting the permeability properties of the pulmonary vascular endothelium and alveolar epithelium. The course and severity of RDS will be further influenced by neonatal care and other occurrences such as the presence or absence of a PDA. Many details of the biochemical and physiologic events that result in RDS have not been defined, so we are currently unable to quantitatively understand how all the various factors interact during the course of RDS to give the characteristic clinical course of the disease. Variations in the magnitude and timing of these interactions will likely explain the variable manifestations of respiratory failure in the tiny infant. Within the context of the pathophysiology of RDS, surfactant replacement therapy and HFV represent two new and very different approaches to treatment. Initial clinical trials of surfactant replacement therapy in infants with RDS are encouraging, and experience with animal models indicates that such an approach will work. Replacement therapy also makes sense if one considers what is known about surfactant metabolism during RDS. However, no standard, tested, and safe preparation of surfactant is available. If past experience is any guide, it may not be easy to develop an acceptable product for general use. HFV offers an opportunity to ventilate infants with relatively high mean airway pressures but without the use of high peak airway pressures. Early clinical trials suggest the technique will benefit some infants, however no ventilators for HFV are available for clinical use. In light of the low mortality from respiratory failure in RDS and a morbidity from RDS resulting mostly from the other diseases of prematurity, these new therapeutic approaches need to be thoroughly tested and understood before general clinical use.
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PMID:Respiratory distress syndrome--new therapeutic approaches to a complex pathophysiology. 636 46

The risk of central nervous, visual, and auditory damage increases from 2/1000 live births in the normal birthweight to > 200/1000 as birthweight falls below 1500 g. Such babies are most likely to be born preterm. Advances in infant care have led to increasing numbers of very-low-birthweight, preterm infants surviving to school age with moderate to severe brain damage. Steroids are one of the current treatments, but they cause significant, long-term problems. The evidence reported here suggests an additional approach to protecting the very preterm infant by supporting neurovascular membrane integrity. The complications of preterm, very-low-birthweight babies include bronchopulmonary dysplasia, retinopathy of prematurity, intraventricular hemorrhage, periventricular leukomalacia, and necrotizing enterocolitis, all of which have a vascular component. Arachidonic acid (AA) and DHA are essential, structural, and functional constituents of cell membranes. They are especially required for the growth and function of the brain and vascular systems, which are the primary biofocus of human fetal growth. Molecular dynamics and experimental evidence suggest that DHA could be the ligand for the retinoid X receptor (RXR) in neural tissue. RXR activation is an obligatory step in signaling to the nucleus and in the regulation of gene expression. Very preterm babies are born with minimal fat stores and suboptimal circulating levels of these nutrients. Postnatally, they lose the biomagnification of the proportions of AA and DHA by the placenta for the fetus. No current nutritional management repairs these deficits. The placental biomagnification profile highlights AA rather than DHA. The resultant fetal FA profile closely resembles that of the vascular endothelium and not the brain. Without this nourishment, cell membrane abnormalities would be predicted. We present a scientific rationale for a common pathogenic process in the complications of prematurity.
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PMID:The potential role for arachidonic and docosahexaenoic acids in protection against some central nervous system injuries in preterm infants. 1284 75