Respiratory Distress Syndrome Mortality In the United States, 1987 to 1995

Malloy, Michael H.; Freeman, Daniel

doi:10.1038/sj.jp.7200420

Cited by 42 publications

(39 citation statements)

References 8 publications

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“…The growing black-white inequality emerged despite the fact that, from the 1980s into the 1990s, rates of preterm birth and low birth weight increased among whites while the rates of these adverse birth outcomes declined slightly among blacks (Demissie et al 2001). Moreover, the well-documented survival advantage of preterm and very low birth weight black infants, compared to their white counterparts, seems to have eroded (Hamvas et al 1996;Kline et al 1989;Malloy and Freeman 2000;Ranganathan et al 2000;Russell 1986, 1990).…”

Section: Introductionmentioning

confidence: 85%

Absolute Change in Cause-Specific Infant Mortality for Blacks and Whites in the US: 1983–2002

Powers

Song

2009

Popul Res Policy Rev

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Section: Introductionmentioning

confidence: 85%

Absolute Change in Cause-Specific Infant Mortality for Blacks and Whites in the US: 1983–2002

Powers

Song

2009

Popul Res Policy Rev

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“…Although the incidence and severity of respiratory distress syndrome has been reduced with antenatal corticosteroid therapy, which hastens lung development, and postnatal replacement surfactant treatment, newborn respiratory distress remains a frequent occurrence in very low birth weight infants and a requirement for respiratory support often continues for many weeks (1,2). The clinical pattern after the first week of life frequently includes episodes of respiratory deterioration necessitating increased inspired oxygen or ventilatory support (3).…”

mentioning

confidence: 99%

Dysfunction of Pulmonary Surfactant in Chronically Ventilated Premature Infants

Merrill¹,

Ballard²,

Cnaan³

et al. 2004

Pediatr Res

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Infants of Ͻ30 wk gestation often require respiratory support for several weeks and may develop bronchopulmonary dysplasia (BPD), which is associated with long-term pulmonary disability or death in severe cases. To examine the status of surfactant in infants at high risk for BPD, this prospective study analyzed 247 tracheal aspirate samples from 68 infants of 23-30 wk gestation who remained intubated for 7-84 d. Seventy-five percent of the infants had one or more surfactant samples with abnormal function (minimum surface tension 5.1-21.7 mN/m by pulsating bubble surfactometer), which were temporally associated with episodes of infection (p ϭ 0.01) and respiratory deterioration (p ϭ 0.005). Comparing normal and abnormal surfactant samples, there were no differences in amount of surfactant phospholipid, normalized to total protein that was recovered from tracheal aspirate, or in relative content of phosphatidylcholine and phosphatidylglycerol. Contents of surfactant proteins (SP) A, B, and C, measured in the surfactant pellet by immunoassay, were reduced by 50%, 80%, and 72%, respectively, in samples with abnormal surface tension (p Յ 0.001). On multivariable analysis of all samples, SP-B content (r ϭ Ϫ0.58, p Ͻ 0.0001) and SP-C content (r ϭ Ϫ0.32, p Ͻ 0.001) were correlated with surfactant function. We conclude that most premature infants requiring continued respiratory support after 7 d of age experience transient episodes of dysfunctional surfactant that are associated with a deficiency of SP-B and SP-C. Infants born prematurely, particularly those of Յ30 wk gestation, are at high risk for lung disease. Although the incidence and severity of respiratory distress syndrome has been reduced with antenatal corticosteroid therapy, which hastens lung development, and postnatal replacement surfactant treatment, newborn respiratory distress remains a frequent occurrence in very low birth weight infants and a requirement for respiratory support often continues for many weeks (1, 2). The clinical pattern after the first week of life frequently includes episodes of respiratory deterioration necessitating increased inspired oxygen or ventilatory support (3). In some infants, lung disease progresses to BPD, which is defined as a continuing requirement for supplemental oxygen and/or positive pressure ventilatory support at 36 wk postmenstrual age (4). BPD occurs in approximately 30% of infants with birth weights Ͻ1000 g and is associated with long-term pulmonary and/or neurodevelopmental disability or death in severe cases (4, 5). The etiology of this progressive respiratory insufficiency is likely multifactorial, including oxygen toxicity, volutrauma associated with mechanical ventilation, infection, patent ductus arteriosus, and inflammation, and results in arrest of alveolar development and interstitial fibrosis (4).Pulmonary surfactant is a mixture of lipids and proteins produced by alveolar type II cells. The major phospholipid component, saturated phosphatidylcholine, forms a highly surface-active film in lung alveoli ...

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“…For the acetate group (n ϭ 13), all infants received simultaneous infusions of [1][2][3][4][5][6][7][8][9][10][11][12][13] For the glucose group (n ϭ 19), all infants received [U-13 C 6 ] glucose. The FSR from plasma glucose of total surfactant PC, analyzed by GC-C-IRMS, was previously published for this group (13).…”

Section: Study Populationsmentioning

confidence: 99%

“…Pulmonary surfactant is composed of ‫ف‬ 80% PL, with palmitate constituting ‫ف‬ 60-80% of the fatty acid composition. Infants born prematurely have a quantitative deficiency in surfactant that may result in respiratory distress syndrome (1)(2)(3). In animal studies, radioactively labeled tracers have been used to determine rates of surfactant synthesis and turnover (3)(4)(5).…”

mentioning

confidence: 99%

Metabolic kinetics of pulmonary surfactant in newborn infants using endogenous stable isotope techniques

Bohlin

Patterson

Spence

et al. 2005

Journal of Lipid Research

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We compared kinetic indices of pulmonary surfactant metabolism in premature infants (n ‫؍‬ 41) with respect to i ) tracer ([1-13 C 1 ]acetate, [U-13 C 6 ]glucose, and [1,2,3,4-13 C 4 ] palmitate), ii ) phospholipid (PL) pool (total PLs or disaturated PLs), or iii ) instrumentation [gas chromatography/ mass spectrometry (GC/MS) or GC-combustion-isotope ratio mass spectometry (GC-C-IRMS)]. Tracer incorporation was measured in PLs extracted from serial tracheal aspirates after a 24 h tracer infusion. The fractional catabolic rate (FCR), representing the total fractional turnover from all sources of surfactant production, was independent of tracer. The fractional synthesis rate of surfactant PL from plasma palmitate was significantly higher than that from palmitate synthesized de novo from acetate, and these two sources of palmitate together accounted for only half of the total surfactant production in preterm infants. [U-13 C 6 ]glucose showed significant recycling of the 13 C label in intermediary metabolism, distinguishable by GC-MS but not by GC-C-IRMS, resulting in a slower apparent FCR when GC-C-IRMS was used. The extracted PL pool did not affect the surfactant metabolic indices. We suggest that FCR should be used as a primary measure of surfactant turnover kinetics and that tracers labeling both de novo synthesis (acetate and glucose) and preformed pathways (plasma palmitate) can be used to partition the fractional contribution of each pathway to total production. -Bohlin, K., B.

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Respiratory Distress Syndrome Mortality In the United States, 1987 to 1995

Cited by 42 publications

References 8 publications

Absolute Change in Cause-Specific Infant Mortality for Blacks and Whites in the US: 1983–2002

Absolute Change in Cause-Specific Infant Mortality for Blacks and Whites in the US: 1983–2002

Dysfunction of Pulmonary Surfactant in Chronically Ventilated Premature Infants

Metabolic kinetics of pulmonary surfactant in newborn infants using endogenous stable isotope techniques

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