Surfactant deficiency

For the treatment of lung surfactant deficiency in premature human infants suffering from respiratory distress syndrome, limited clinical trials were performed showing that liposomes in the lung-instilled intratracheally either as an aerosolized mist (Ivey et al., 1977) or as a suspension via an endotracheal tube (Fujiwara et al., 1980)—rapidly improved lung function. No adverse effects were observed as a result of the supplementation with surfactant-like material. It appears, therefore, that liposomes are a suitable system for the delivery of major phospholipid components of endogenous lung surfactant. 

Pulmonary gene therapy is attractive for the treatmment of chronic bronchitis, cystic fibrosis, a-1 antitrypsin deficiency, familial emphysema, asthma, pulmonary infections, surfactant deficiency, pulmonary hypertension, lung cancer, and malignant mesothelioma. The pulmonary endothelium may act as a bioreactor for the production and secretion of therapeutic proteins, such as clotting factors and erythropoietin into the blood circulation. There is a potential benefit for acquired lung diseases, as well as cancers, to be controlled and possibly treated by expression of cytokines, surfactant, antioxidant enzymes, or mucoproteins within lung cells. 

The linear dependence between the threshold dilution and the initial total phospholipid concentration (respectively, DPPC) found allows to determine the threshold dilution for a 100% probability for formation of NBF instead of Ct. Fig. 11.5 shows that if a sample dilution of 3.1 times is applied, then it is possible to detect almost all cases with a developed RDS. Therefore, the threshold dilution of 3.1 times allows to distinguish the mature from immature AF samples which gives a good reason to employ it in diagnosing of RDS, and respectively, to estimate the lung surfactant deficiency. Hence, the formation of black foam films from AF samples taken at different gestation weeks and diluted 3.1 times, indicates that there is no risk of RDS, while film rupture predicts an eventual RDS development. 

Pulmonary parenchymal immaturity Surfactant deficiency Antioxidant deficiencies Hyperoxic exposure Barotrauma... 

In 1959, surfactant deficiency was identified as the major pathogenic factor in respiratory distress syndrome in infants. Pulmonary surfactant is a complex mixture of phospholipids, neutral lipids, and specific proteins which spread as a monolayer at the air-liquid... 

These highly imaginative studies may duplicate some of the changes that occur during the liquid-to-gas transition at birth, and thus may explain some of the complications encountered and possibly provide new insights for the therapy of surfactant deficiency in idiopathic respiratory disease of the newborn. 

Neonatal respiratory distress syndrome (RDS) is predominantly a disease of surfactant deficiency. 

RDS, historically known as hyaline membrane disease (HMD), is more appropriately termed surfactant-deficiency RDS. RDS is associated with considerable morbidity and mortality. Before 35 weeks gestation, the risk of RDS and the severity of disease increase with greater degree of prematurity and, in the absence of appropriate antenatal interventions, occurs in over 50% of newborns of 30 weeks or less gestation. The Vermont Oxford Network experience for 1999 describes over 27,000 neonates below 1500 g from 325 neonatal intensive care unit (NICU) sites. The annual report noted that RDS occurred in over 80% of premature infants below 1000 g and that there was a gradual decline to about 42% of neonates with birth weights between 1400 and 1500 g. 

FIGURE 28-1. Chest x-ray demonstrating surfactant-deficient respiratory distress syndrome with ground glass appearance and air bronchograms. 

Calfactant is a lung surfactant. It is an extract of natural surfactant from calf lungs that restores lung surfactant in premature infants with lung surfactant deficiency causing respiratory distress syndrome (RDS). Calfactant is indicated in RDS in premature infants under 29 weeks of gestational age at high risk for RDS and for the treatment rescue of premature infants under 72 hours of age who develop RDS and require endotracheal inmbation. 

Another approach consists in the compensation of endogenous surfactant deficiency in treated water by means of biofouling incubation inside the filtration load. As was shown in [4], the surface-active metabolic products of different bacteria cells act as cofactors of bubble-film water treatment process. Rapid accumulation of endogenous surfactants in aqueous media occurs under favorable ecological conditions. An appropriate niche for aerobic reproduction of heterotrophic bacteria is any well-developed nontoxic granular material through which contaminated and oxygen-enriched water passes. Here, the water contaminants are a source of feed for bacteria cells. 

Phospholipidosis presents an alternative but rather benign effect of macrolides. Although it is reported in chronic macrolide therapy, there are no obvious negative effects and there is a possibility that it contributes to beneficial effects, notably in inflammatory bowel and eye diseases where additional phospholipids correct surfactant deficiencies. Various studies show that phospholipidosis resolves on discontinuation of macrolide therapy and there are no clinical reports of negative outcomes associated with it. Thus phospholipidosis is probably mechanistically linked to effects in immune cells and it seems to present therapeutic opportunities in phospholipid deficiencies rather than any obvious adverse effects in clinical practice. 

Loss of alveolar surfactant activity is likely to have pathophysiological consequences. These might include an increase in the work of breathing, owing to focal or widespread atelectasis (222) augmentation of pulmonary edema, consequent to a reduction in interstitial hydrostatic pressure (223) and increased susceptibility to infection, owing to loss of the antibacterial properties of surfactant (97). Because many of the adverse effects of surfactant deficiency can be reversed... 

Section 2.08.2.4) at ambient temperature than surfactant-deficient samples, which was traced back to increased surfactant mobility. This correlates with an inaease in the basal spacing between silicate platelets. In solid-state magic angle spinning (MAS), NMR spectra for phosphonium... 

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