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      Chorioamnionitis appears not to be a Risk Factor for Patent Ductus Arteriosus in Preterm Infants: A Systematic Review and Meta-Analysis

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          Abstract

          The contribution of chorioamnionitis (CA) to mortality and morbidity in preterm infants is difficult to assess because observational studies frequently present significant differences in baseline characteristics of the infants exposed or non-exposed to CA. In an attempt to perform a thorough assessment of the possible association between CA and patent ductus arteriosus (PDA) in preterm infants, we conducted a meta-analysis in which adjusted odds ratios (ORs) were pooled and we analyzed the effects of potential confounders, such as gestational age (GA) or birth weight (BW). We identified 45 relevant studies (27186 patients, 7742 CA cases). Random effects meta-analysis of crude ORs showed a significant positive association between CA and PDA (OR 1.352, 95% CI 1.172 to 1.560). Adjusted ORs were reported in 11 studies (19577 infants). Meta-analysis of these studies showed a significant negative association between CA and PDA (OR 0.802, 95% CI 0.751 to 0.959). Meta-regression showed that the differences in GA or BW between the CA-exposed and non-exposed groups were significantly correlated with the effect size of the association between PDA and CA. In conclusion, our study confirms that confounders need to be taken into account when assessing the association between CA and clinical outcomes in preterm infants.

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          Most cited references65

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          Spurious precision? Meta-analysis of observational studies.

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            Chorioamnionitis as a risk factor for cerebral palsy: A meta-analysis.

            Chorioamnionitis has been implicated in the pathogenesis of cerebral palsy, but most studies have not reported a significant association. Cystic periventricular leukomalacia (cPVL) is believed to be a precursor of cerebral palsy in preterm infants. To determine whether chorioamnionitis is associated with cerebral palsy or cPVL and to examine factors that may explain differences in study results. Searches of MEDLINE (1966-1999), Index Medicus (1960-1965), Doctoral Dissertation Abstracts On-Line (1861-1999), bibliographies, and online conference proceedings (1999) were performed for English-language studies with titles or abstracts that discussed prenatal risk factors for cerebral palsy or cPVL. Of 229 initially identified publications, meta-analyses were performed on studies that addressed the association between clinical (n = 19) or histologic (n = 7) chorioamnionitis and cerebral palsy or cPVL in both preterm and full-term infants. Inclusion criteria were: presence of appropriate exposure and outcome measures, case-control or cohort study design, and provision of sufficient data to calculate relative risks (RRs) or odds ratios with 95% confidence intervals (CIs). Studies evaluating risk of cerebral palsy following maternal fever, urinary tract infection, or other maternal infection were collected, but not included in the meta-analysis. Information from individual studies was abstracted using standardized forms by 2 independent observers blinded to authors' names, journal titles, and funding sources. Using a random effects model, clinical chorioamnionitis was significantly associated with both cerebral palsy (RR, 1.9; 95% CI, 1.4-2.5) and cPVL (RR, 3.0; 95% CI, 2.2-4.0) in preterm infants. The RR of histologic chorioamnionitis and cerebral palsy was 1.6 (95% CI, 0.9-2.7) in preterm infants, and histologic chorioamnionitis was significantly associated with cPVL (RR, 2.1; 95% CI, 1.5-2.9). Among full-term infants, a positive association was found between clinical chorioamnionitis and cerebral palsy (RR, 4.7; 95% CI, 1.3-16.2). Factors explaining differences in study results included varying definitions of clinical chorioamnionitis, extent of blinding in determining exposure status, and whether individual studies adjusted for potential confounders. Our meta-analysis indicates that chorioamnionitis is a risk factor for both cerebral palsy and cPVL. JAMA. 2000;284:1417-1424.
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              Pregnancy disorders that lead to delivery before the 28th week of gestation: an epidemiologic approach to classification.

              Epidemiologists have grouped the multiple disorders that lead to preterm delivery before the 28th week of gestation in a variety of ways. The authors sought to identify characteristics that would help guide how to classify disorders that lead to such preterm delivery. They enrolled 1,006 women who delivered a liveborn singleton infant of less than 28 weeks' gestation at 14 centers in the United States between 2002 and 2004. Each delivery was classified by presentation: preterm labor (40%), prelabor premature rupture of membranes (23%), preeclampsia (18%), placental abruption (11%), cervical incompetence (5%), and fetal indication/intrauterine growth restriction (3%). Using factor analysis (eigenvalue = 1.73) to compare characteristics identified by standardized interview, chart review, placental histology, and placental microbiology among the presentation groups, the authors found 2 broad patterns. One pattern, characterized by histologic chorioamnionitis and placental microbe recovery, was associated with preterm labor, prelabor premature rupture of membranes, placental abruption, and cervical insufficiency. The other, characterized by a paucity of organisms and inflammation but the presence of histologic features of dysfunctional placentation, was associated with preeclampsia and fetal indication/intrauterine growth restriction. Disorders leading to preterm delivery may be separated into two groups: those associated with intrauterine inflammation and those associated with aberrations of placentation.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                28 November 2016
                2016
                : 6
                : 37967
                Affiliations
                [1 ]Department of Pediatrics, Maastricht University Medical Center (MUMC+), School for Oncology and Developmental Biology (GROW) , Maastricht, the Netherlands
                Author notes
                Article
                srep37967
                10.1038/srep37967
                5125028
                27892517
                79b48d25-1780-4444-af57-2120a0e28ad3
                Copyright © 2016, The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 27 June 2016
                : 03 November 2016
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