Hyaline membrane disease in black newborns: does fetal lung maturation occur earlier?

doi:10.1016/0028-2243(94)90031-0

European Journal of Obstetrics & Gynecology and Reproductive Biology

Volume 55, Issue 3, 30 June 1994, Pages 157-161

https://doi.org/10.1016/0028-2243(94)90031-0 Get rights and content

Abstract

Debate has developed among several authors about possible accelerated maturation of black fetuses in comparison with whites. In Guadeloupe, French West Indies, where 85% of the population is of black African-American origin, it has been noted that the incidence of hyaline membrane disease (HMD) represents a significant drop beginning after the 32nd week of gestation. Over a 3-year period, 419 black low-birthweight singleton newborns were admitted in the University Hospital's Neonatal Department covering 70% of all births of the island. The incidence of HMD was 50% among very low birthweight (< 1500 g) and 8.3% among moderate low birthweight (≥ 1500 g; P < 0.001). The incidence of HMD was 48.8% among the very preterm (< 32 weeks) and 7.8% ( $26331$ ) among the moderate preterm (≥32 weeks; P < 0.001). These differences were similar for appropriate for gestational age and small for gestational age infants. Significant differences remained after controlling for several maternal risk factors. These results suggest that the 32nd week of gestation represents a significant drop in the risk for respiratory distress syndrome in black premature compared with that reported in literature on European infants (34th week) and therefore may implicate different obstetrical decisions in the management of critical pregnancies in this population.

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To use a large current prospective cohort of infants <29 weeks to compare bronchopulmonary dysplasia (BPD) rates in black and white infants.
The Prematurity and Respiratory Outcome Program (PROP) enrolled 835 infants born in 2011-2013 at <29 weeks of gestation; 728 black or white infants survived to 36 weeks postmenstrual age (PMA). Logistic regression was used to compare BPD outcomes (defined as supplemental oxygen requirement at 36 weeks PMA) between the races, adjusted for gestational age (GA), antenatal steroid use, intubation at birth, and surfactant use at birth.
Of 707 black or white infants with available BPD outcomes, BPD was lower in black infants (38% vs 45%), even though they were of significantly lower GA. At every GA, BPD was more common in white infants. The aOR for BPD was 0.60 (95% CI, 0.42-0.85; P = .004) for black infants compared with white infants after adjusting for GA. Despite the lower rate of BPD, black infants had a higher rate of first-year post-prematurity respiratory disease (black, 79%; white, 63%).
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Race Effects of Inhaled Nitric Oxide in Preterm Infants: An Individual Participant Data Meta-Analysis
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One trial (Schreiber 2003)10 was a single-center study, but the other two (NOCLD, NEWNO)11,16 were multicenter trials involving a total of 54 different sites. Despite the similarity between racial groups in gestational age (Table III), it is possible that African American infants were more developmentally mature, as has been proposed based on population data for gestational age at delivery,32 and that maturity impacts responsiveness to iNO. However, this was not observed in our analysis by gestational age (data not presented).
To assess whether inhaled nitric oxide (iNO) improves survival without bronchopulmonary dysplasia (BPD) for preterm African American infants.
An individual participant data meta-analysis was conducted, including 3 randomized, placebo-controlled trials that enrolled infants born at <34 weeks of gestation receiving respiratory support, had at least 15% (or a minimum of 10 infants in each trial arm) of African American race, and used a starting iNO of >5 parts per million with the intention to treat for 7 days minimum. The primary outcome was a composite of death or BPD. Secondary outcomes included death before discharge, postnatal steroid use, gross pulmonary air leak, pulmonary hemorrhage, measures of respiratory support, and duration of hospital stay.
Compared with other races, African American infants had a significant reduction in the composite outcome of death or BPD with iNO treatment: 49% treated vs 63% controls (relative risk, 0.77; 95% CI, 0.65-0.91; P = .003; interaction P = .016). There were no differences between racial groups for death. There was also a significant difference between races (interaction P = .023) of iNO treatment for BPD in survivors, with the greatest effect in African American infants (P = .005). There was no difference between racial groups in the use of postnatal steroids, pulmonary air leak, pulmonary hemorrhage, or other measures of respiratory support.
iNO therapy should be considered for preterm African American infants at high risk for BPD. iNO to prevent BPD in African Americans may represent an example of a racially customized therapy for infants.
Race, prematurity and immaturity
2007, Early Human Development
Compared to white Europeans, Blacks and South Asians have a significantly shorter mean gestational length and a higher incidence of preterm birth. For any given gestational age before 37 weeks, Black and South Asian babies have less risk of respiratory distress syndrome, and the survival rate in Black babies is higher than white Europeans. From 37 weeks of gestation onwards, the perinatal mortality rate in Blacks is higher than in white Europeans, and this appears to be associated with a higher rate of meconium passage and respiratory morbidity. In full term South Asian babies, the late gestation rise in antepartum stillbirth occurs one week earlier than in white Europeans. These patterns remained significant even after adjusting for socioeconomic factors. This suggests that fetal maturity occurs earlier in gestation in Blacks and South Asians when compared to white European babies.
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The report by Avery and Mead established that developmentally regulated surfactant deficiency attributable to reduction in the dominant surfactant phospholipid, phosphatidylcholine, causes neonatal respiratory distress syndrome in premature infants [14–17]. Studies of different ethnic groups, gender, targeted gene ablation in murine lineages, and recent clinical reports of monogenic causes of neonatal respiratory distress syndrome have suggested strongly that genetic mechanisms contribute significantly to risk for respiratory distress syndrome in newborn infants [18–46]. In addition, despite improvement in neonatal survival attributable to surfactant replacement therapy, long-term respiratory morbidity has persisted [4,47–52].
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Regular paperHyaline membrane disease in black newborns: does fetal lung maturation occur earlier?

Abstract

Am J Obstet Gynecol

J Pediatr

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Obstet Gynecol

Am J Prev Med

Amniotic fluid lecithin/sphingomyelin ratio: comparison between an African and a north American community

Pediatrics

Assessment of gestational age and development at birth

Pediatr Clin North Am

Epidemiology and classification of acute, neonatal respiratory disorders. A prospective study

Acta Paediatr Scand

Epidemiology of hyaline membrane disease in the United States: analysis of national mortality statistics

Pediatrics

Regular paper
Hyaline membrane disease in black newborns: does fetal lung maturation occur earlier?