Impact on Neonatal Outcome and Anthropometric Growth in Very Low Birth Weight Infants with Histological Chorioamnionitis

Mu, Shu‐Chi; Lin, Cheng–Hui; Ma, Hui-Ju; Lee, Jing-Sheng; Lin, Ming-I; Lee, Chin-Cheng; Chen, Tong-Jong; Jow, Guey–Mei; Sung, Tseng-Chen

doi:10.1016/s0929-6646(08)60091-1

Cited by 38 publications

(34 citation statements)

References 21 publications

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“…Chorioamnionitis-exposed patients had either similar7 21 23 25 29 30 or decreased2 3 19 32 RDS incidences in most studies. While Elimian and colleagues reported an increase in RDS incidence, the difference disappeared after multivariate analysis 18.…”

Section: Respiratory Outcome After Chorioamnionitismentioning

confidence: 94%

Histological chorioamnionitis and respiratory outcome in preterm infants

Been

Zimmermann

2008

Archives of Disease in Childhood - Fetal and Neonatal Edition

138

123

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A considerable body of human and animal experimental evidence links antenatal inflammation to both accelerated maturation and adverse development of the lung. Initial reports suggest that in preterm infants histological chorioamnionitis is associated with a decreased incidence of respiratory distress syndrome (RDS), while the incidence of bronchopulmonary dysplasia (BPD) is increased. Considerable variation exists in the findings of subsequent human studies, largely dependent on differences in inclusion and exclusion criteria. Taking these differences into account, recent studies generally seem to confirm the effect of chorioamnionitis on RDS incidence, while no effect on BPD is seen. The increased use of antenatal steroids and the diminished effects of secondary pro-inflammatory hits seem to explain part of this change. Additional research is needed to explore these complex interactions and their underlying mechanisms, and evaluate the long term pulmonary effects of antenatal inflammation.

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Section: Respiratory Outcome After Chorioamnionitismentioning

confidence: 94%

Histological chorioamnionitis and respiratory outcome in preterm infants

Been

Zimmermann

2008

Archives of Disease in Childhood - Fetal and Neonatal Edition

138

123

View full text Add to dashboard Cite

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“…Multiple clinical studies have shown that chorioamnionitis is strongly linked with an increased risk for the development of bronchopulmonary dysplasia (BPD) (14,22,40,41,45,48,53,64,66), which is the chronic lung disease of infancy that follows premature birth and injury to the immature lung. Despite improvements in perinatal care, BPD remains one of the most significant sequelae of prematurity (5).…”

mentioning

confidence: 99%

Moderate postnatal hyperoxia accelerates lung growth and attenuates pulmonary hypertension in infant rats after exposure to intra-amniotic endotoxin

Tang¹,

Seedorf²,

Muehlethaler

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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-To determine the separate and interactive effects of fetal inflammation and neonatal hyperoxia on the developing lung, we hypothesized that: 1) antenatal endotoxin (ETX) causes sustained abnormalities of infant lung structure; and 2) postnatal hyperoxia augments the adverse effects of antenatal ETX on infant lung growth. Escherichia coli ETX or saline (SA) was injected into amniotic sacs in pregnant Sprague-Dawley rats at 20 days of gestation. Pups were delivered 2 days later and raised in room air (RA) or moderate hyperoxia (O 2, 80% O2 at Denver's altitude, ϳ65% O 2 at sea level) from birth through 14 days of age. Heart and lung tissues were harvested for measurements. Intraamniotic ETX caused right ventricular hypertrophy (RVH) and decreased lung vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2) protein contents at birth. In ETX-exposed rats (ETX-RA), alveolarization and vessel density were decreased, pulmonary vascular wall thickness percentage was increased, and RVH was persistent throughout the study period compared with controls (SA-RA). After antenatal ETX, moderate hyperoxia increased lung VEGF and VEGFR-2 protein contents in ETX-O2 rats and improved their alveolar and vascular structure and RVH compared with ETX-RA rats. In contrast, severe hyperoxia (Ն95% O 2 at Denver's altitude) further reduced lung vessel density after intra-amniotic ETX exposure. We conclude that intra-amniotic ETX induces fetal pulmonary hypertension and causes persistent abnormalities of lung structure with sustained pulmonary hypertension in infant rats. Moreover, moderate postnatal hyperoxia after antenatal ETX restores lung growth and prevents pulmonary hypertension during infancy. antenatal inflammation; vascular endothelial growth factor; bronchopulmonary dysplasia; persistent pulmonary hypertension of the newborn

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“…The percentage of CHA in our study was in the range of previously published studies. As shown in overview from Beer and Zimmerman (30), the increased incidence of BPD after prenatal inflammation was reproduced in 6 of 18 studies; furthermore, in only one study the results were adjusted for gestational age (31). Beside the importance of when the fetus is exposed to prenatal inflammation, the time of exposure to the intra-amniotic endotoxin is also important.…”

Section: Discussionmentioning

confidence: 96%