Chorioamnionitis and Cerebral Palsy

Shatrov, Jobe; Birch, Samuel C. M.; Lam, Lawrence T.; Quinlivan, Julie A.; McIntyre, Sarah; Mendz, George L.

doi:10.1097/aog.0b013e3181e90046

Cited by 258 publications

(158 citation statements)

References 34 publications

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“…Prematurity in the setting of rupture of membranes has important implications in neonatal morbidity, especially at earlier gestational ages when amniotic and fetal infection is the leading known cause of preterm birth. There is a twofold increase in the risk of cerebral palsy when clinical chorioamnionitis is present [21], and survival without major morbidity (<10%) is a rare event at such earlier gestational ages [9].…”

Section: Discussionmentioning

confidence: 99%

Previable preterm rupture of membranes: gestational and neonatal outcomes

Margato

Martins

Júnior

et al. 2011

Arch Gynecol Obstet

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Section: Discussionmentioning

confidence: 99%

Previable preterm rupture of membranes: gestational and neonatal outcomes

Margato

Martins

Júnior

et al. 2011

Arch Gynecol Obstet

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“…Perinatal inflammation has been associated with a number of adverse neurological outcomes in preterm infants such as white matter injury, intraventricular hemorrhage, cystic periventricular leukomalacia and cerebral palsy [23,70,71,72]. Maternal intrauterine infection and inflammation can induce a production of proinflammatory cytokines in the fetal brain such as tumor necrosis factor-α (TNF-α) and interleukins (IL)-1, IL-6, and IL-8.…”

Section: Discussionmentioning

confidence: 99%

Chorioamnionitis as a Risk Factor for Retinopathy of Prematurity: A Systematic Review and Meta-Analysis

Mitra

Aune²,

Speer³

et al. 2014

Neonatology

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Background: The role of chorioamnionitis (CA) in the development of retinopathy of prematurity (ROP) has not been well established. Objective: To conduct a systematic review and meta-analysis of the association between CA and ROP in preterm infants. Data Sources: The authors searched MEDLINE, Embase, CINAHL, Cochrane Central Register of Controlled Trials and PubMed, reviewed reference lists of relevant articles, abstracts and conference proceedings (Society for Pediatric Research, European Society for Paediatric Research 1990-2012), sought results of unpublished trials, and contacted the primary authors of relevant studies. Study Selection: Studies were included if they had a comparison group, examined preterm infants, and reported primary data that could be used to measure the association between exposure to CA and the development of ROP. Data Extraction: Two reviewers independently screened the search results, applied inclusion criteria and assessed methodological quality using the Newcastle-Ottawa Scale. One reviewer extracted data and a second reviewer checked data extraction. Summary relative risks (RRs) were calculated using a random effects model. Data Synthesis: We identified 1,249 potentially relevant studies from the electronic databases. Twenty-seven studies involving 10,590 preterm neonates with 2,562 cases of ROP were included. Taking into account all included studies without adjusting for gestational age (GA), CA was significantly associated with ROP (any stage) [summary RR 1.33 (95% CI 1.14-1.55, I² = 77%, p_{heterogeneity} < 0.0001)], and a borderline significant association was observed for severe ROP (stage ≥3) [summary RR 1.27 (95% CI 0.99-1.63, I² = 74%, p_{heterogeneity} < 0.0001)]. There was no publication bias with Begg's test. However, subgroup analysis of studies adjusting for GA showed no significant association on CA with ROP [summary RR 0.98 (95% CI 0.77-1.26, I² = 0%, p_{heterogeneity} = 0.89)]. Conclusion: Unadjusted analyses showed that CA was significantly associated with ROP (any stage) as well as with severe ROP (stage ≥ 3). However, the association disappeared on analysis of studies adjusting for GA. Hence, CA cannot be definitively considered as a risk factor for ROP, and further studies should adjust for potential confounding factors and report results by stage to clarify the association with severe ROP.

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“…It is now recognized that the etiology of preterm brain injury is likely multifactorial. While HI is likely to be important, there is now compelling evidence that exposure to infection and secondary inflammation, both before and after birth, is highly associated with preterm brain injury and deficits in neuronal architecture and function in later life [2,3,4,5,6,7,8,9]. …”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-Induced Preconditioning Attenuates Apoptosis and Differentially Regulates TLR4 and TLR7 Gene Expression after Ischemia in the Preterm Ovine Fetal Brain

Dhillon

Gunn

Jung³

et al. 2015

Dev Neurosci

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Acute exposure to subclinical infection modulates subsequent hypoxia-ischemia (HI) injury in a time-dependent manner, likely by cross-talk through Toll-like receptors (TLRs), but the specific pathways are unclear in the preterm-equivalent brain. In the present study, we tested the hypothesis that repeated low-dose exposure to lipopolysaccharide (LPS) before acute ischemia would be associated with induction of specific TLRs that are potentially neuroprotective. Fetal sheep at 0.65 gestation (term is ∼145 days) received intravenous boluses of low-dose LPS for 5 days (day 1, 50 ng/kg; days 2-5, 100 ng/kg) or the same volume of saline. Either 4 or 24 h after the last bolus of LPS, complete carotid occlusion was induced for 22 min. Five days after LPS, brains were collected. Pretreatment with LPS for 5 days decreased cellular apoptosis, microglial activation and reactive astrogliosis in response to HI injury induced 24 but not 4 h after the last dose of LPS. This was associated with upregulation of TLR4, TLR7 and IFN-β mRNA, and increased fetal plasma IFN-β concentrations. The association of reduced white matter apoptosis and astrogliosis after repeated low-dose LPS finishing 24 h but not 4 h before cerebral ischemia, with central and peripheral induction of IFN-β, suggests the possibility that IFN-β may be an important mediator of endogenous neuroprotection in the developing brain.

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Chorioamnionitis and Cerebral Palsy

Cited by 258 publications

References 34 publications

Previable preterm rupture of membranes: gestational and neonatal outcomes

Previable preterm rupture of membranes: gestational and neonatal outcomes

Chorioamnionitis as a Risk Factor for Retinopathy of Prematurity: A Systematic Review and Meta-Analysis

Lipopolysaccharide-Induced Preconditioning Attenuates Apoptosis and Differentially Regulates TLR4 and TLR7 Gene Expression after Ischemia in the Preterm Ovine Fetal Brain

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