Does prenatal diagnosis modify neonatal treatment and early outcome of children with esophageal atresia?

Garabédian, Charles; Sfeir, Rony; Langlois, Carole; Bonnard, Arnaud; Khen-Dunlop, Naziha; Gelas, Thomas; Michaud, Laurent; Auber, F.; Gottrand, Frédéric; Houfflin‐Debarge, V.; Piolat, C.; Lemelle, J.L.; Fouquet, Virginie; Habonima, Edouard; Becmeur, F.; Poli-Mérol, M.L.; Breton, A; Petit, Thierry; Podevin, Guillaume; Lavrand, F.; Allal, H.; López, Manuel; Elbaz, F.; Merrot, Thierry; Michel, J.-L.; Buisson, Philippe; Sapin, Emmanuel; Delagausie, P.; Pélatan, C.; Gaudin, J.; Weil, Dominique; Vries, P. de; Jaby, Olivier; Lardy, H.; Aubert, D.; Borderon, Corinne; Fourcade, Laurent; Geiss, S; Bréaud, Jean; Pouzac, Myriam; Echaïeb, A.; Laplace, Christophe

doi:10.1016/j.ajog.2014.09.030

Cited by 38 publications

(41 citation statements)

References 32 publications

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“…These 2 indirect signs were frequently observed in the prenatal group (in more than 95% of cases). However, the positive predictive value of these 2 signs is low (between 40% and 56%), and the prenatal sonographic diagnosis can be improved by direct visualization of the fluid‐filled, blind‐ending esophagus during fetal swallowing or upper neck “pouch sign.” This sign was described in 46% of our prenatal group, a rate similar to that reported by Brantberg et al (ie, visible esophageal pouch in 43% of 21 cases of prenatally diagnosed EA) and higher than in our first study, which included all EA types . Furthermore, in France, a sonographic evaluation is systematically recommended during the third trimester (at about 32 weeks gestation).…”

Section: Discussionsupporting

confidence: 87%

“…Esophageal atresia type A is a specific version of EA that includes complete disruption of the esophagus without a tracheoesophageal fistula. It is the second most common EA type and the most frequently diagnosed antenatally; it also has a worse postnatal prognosis compared with type C . Due to the rarity of this malformation, no study to date has evaluated the influence of prenatal diagnosis on outcome.…”

Section: Discussionmentioning

confidence: 99%

“…In previous studies, we evaluated the impact of prenatal EA diagnosis on neonatal management and outcome at the age of 1 year, regardless of EA type . In that study, because of the low prevalence of EA type A, we were unable to focus specifically on this type, even though it has the highest rate of prenatal diagnosis (82.2%) and a higher neonatal morbidity than EA type C. Other studies evaluating prenatal EA diagnosis and its impact on neonatal outcome have had the same limitations or were conducted on a patient sample …”

Section: Introductionmentioning

confidence: 99%

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Management and outcome of neonates with a prenatal diagnosis of esophageal atresia type A: A population‐based study

et al. 2018

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Management and outcome of neonates with a prenatal diagnosis of esophageal atresia type A: A population‐based study

et al. 2018

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“…We acknowledge this weakness that may artificially reduce our reported performance of MRI and biochemistry. A recent study showed that prenatal diagnosis of EA does not modify the 1‐year outcome; however, prenatal diagnosis of EA allows prenatal counseling of the parents and prevents postnatal transfers . Moreover, prenatal diagnosis of EA allows to focus on associated malformation, which impacts on prognosis.…”

Section: Discussionmentioning

confidence: 99%

Performance of prenatal diagnosis in esophageal atresia

et al. 2015

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“…59 New preventive measures by targeting cellular organelle stress may be also effective to ameliorate birth defects caused by factors other than diabetes. 60–66 …”

Section: Commentmentioning

confidence: 99%

Type 2 diabetes mellitus induces congenital heart defects in murine embryos by increasing oxidative stress, endoplasmic reticulum stress, and apoptosis

Reece

Zhong

et al. 2016

American Journal of Obstetrics and Gynecology

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BACKGROUND Maternal type 1 and 2 diabetes mellitus are strongly associated with high rates of severe structural birth defects, including congenital heart defects. Studies in type 1 diabetic embryopathy animal models have demonstrated that cellular stress-induced apoptosis mediates the teratogenicity of maternal diabetes leading to congenital heart defect formation. However, the mechanisms underlying maternal type 2 diabetes mellitus–induced congenital heart defects remain largely unknown. OBJECTIVE We aim to determine whether oxidative stress, endoplasmic reticulum stress, and excessive apoptosis are the intracellular molecular mechanisms underlying maternal type 2 diabetes mellitus–induced congenital heart defects. STUDY DESIGN A mouse model of maternal type 2 diabetes mellitus was established by feeding female mice a high-fat diet (60% fat). After 15 weeks on the high-fat diet, the mice showed characteristics of maternal type 2 diabetes mellitus. Control dams were either fed a normal diet (10% fat) or the high-fat diet during pregnancy only. Female mice from the high-fat diet group and the 2 control groups were mated with male mice that were fed a normal diet. At E12.5, embryonic hearts were harvested to determine the levels of lipid peroxides and superoxide, endoplasmic reticulum stress markers, cleaved caspase 3 and 8, and apoptosis. E17.5 embryonic hearts were harvested for the detection of congenital heart defect formation using India ink vessel patterning and histological examination. RESULTS Maternal type 2 diabetes mellitus significantly induced ventricular septal defects and persistent truncus arteriosus in the developing heart, along with increasing oxidative stress markers, including superoxide and lipid peroxidation; endoplasmic reticulum stress markers, including protein levels of phosphorylated-protein kinase RNA-like endoplasmic reticulum kinase, phosphorylated-IRE1α, phosphorylated-eIF2α, C/EBP homologous protein, and binding immunoglobulin protein; endoplasmic reticulum chaperone gene expression; and XBP1 messenger RNA splicing, as well as increased cleaved caspase 3 and 8 in embryonic hearts. Furthermore, maternal type 2 diabetes mellitus triggered excessive apoptosis in ventricular myocardium, endocardial cushion, and outflow tract of the embryonic heart. CONCLUSION Similar to those observations in type 1 diabetic embryopathy, maternal type 2 diabetes mellitus causes heart defects in the developing embryo manifested with oxidative stress, endoplasmic reticulum stress, and excessive apoptosis in heart cells.

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Does prenatal diagnosis modify neonatal treatment and early outcome of children with esophageal atresia?

Cited by 38 publications

References 32 publications

Management and outcome of neonates with a prenatal diagnosis of esophageal atresia type A: A population‐based study

Management and outcome of neonates with a prenatal diagnosis of esophageal atresia type A: A population‐based study

Performance of prenatal diagnosis in esophageal atresia

Type 2 diabetes mellitus induces congenital heart defects in murine embryos by increasing oxidative stress, endoplasmic reticulum stress, and apoptosis

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